Troponin Clues: An Academic Reappraisal of Cardiac and Coronary Artery Pathologies in Sudden Death among Medicolegal Autopsies

Troponin Clues: An Academic Reappraisal of Cardiac and Coronary Artery Pathologies in Sudden Death among Medicolegal Autopsies | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Troponin Clues: An Academic Reappraisal of Cardiac and Coronary Artery Pathologies in Sudden Death among Medicolegal Autopsies Oi Chia YAP, Mohamad Aznool Haidy AHSORORI, Faridah MOHD NOR, and 2 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8452675/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Introduction: Sudden cardiac death (SCD) accounts for an estimated 15% to 20% of all deaths globally and is a leading cause of mortality. Methods: A cross-sectional study over 1-year (2023) recruiting medicolegal autopsy cases that were conducted in the Department of Forensic Medicine, Hospital Sultanah Aminah Johor Bahru (HSAJB), Malaysia. The relationship between point-of-care troponin I level and myocardial infarction (MI) was analysed. The morphology of the heart and coronary artery in cardiac death was also recorded. Results: A total of 143 cases were analyzed. Cardiac death was responsible for 78.2% of SCD. The leading cause of cardiac death was coronary atherosclerosis (31.1%). Significant association was demonstrated between SCD and the age group of 36–59 years old (p<0.001) and Malay ethnicity (p=0.017). No significant association between SCD and sex. Notably, a significant difference in troponin I levels between MI and non-MI cases (p=0.004), with the majority of MI cases (71.7%) showing elevated troponin I levels. No significant difference was observed in troponin I levels between acute and subacute and healed MI (p=0.763). The most common gross and histopathological finding in the coronary arteries was uncomplicated coronary atherosclerosis (41.3% gross; 70.0% histopathology). Fibrosis was the predominant macroscopic (50.8%) and microscopic (82.0%) finding in the heart. Conclusion: Coronary atherosclerosis and its complications were identified as the most common causes of cardiac death. It is plausible to consider using troponin I as an auxiliary investigation rather than as a sole diagnostic tool for MI, while exercising caution during the interpretation of results. coronary artery forensic heart sudden cardiac death Troponin I Figures Figure 1 BACKGROUND Sudden cardiac death (SCD) accounts for an estimated 15% to 20% of all deaths globally and is a leading cause of mortality worldwide. 1 The World Health Organization (WHO), according to the International Classification of Diseases, version 11 (ICD-11) defines sudden death as non-violent and not otherwise explained death occurring instantaneously or less than 24 hours from the onset of symptoms. 2 These cases generally refer to the death of apparently healthy individuals who are not under close medical care, although they may have an underlying medical illness which does not incapacitate them prior to this. 3,4 In this study, a temporal limitation between the onset of symptoms and the death, i.e. 24 hours, was not applied. The United States has an annual incidence of 60 per 100,000 cases of SCD, in which roughly 300,000–400,000 SCD occur each year. Based on death certificate data, SCD accounts for up to 15% of deaths in Western nations. 5 In Klang Valley, Malaysia, natural death constituted 37.8% of the medicolegal autopsies in the year 2014. Of all the natural causes of sudden death, cardiovascular diseases account for 75.8%. Coronary artery disease contributes for 60% of SCD, whereas the remaining SCD cases are attributed to ischaemic heart disease, acute myocardial infarction (MI), cardiomyopathy and hypertensive heart disease. 6 Often, SCD is the first and only symptom a deceased person displays and is the most frequent cause of death from heart disease. The sudden, unexpected nature of SCD, as well as its high incidence and fatality, renders it a major unsolved issue in the fields of emergency medicine and public health. Forensic pathology examinations and detailed autopsies are essential for diagnosing SCD. A timely diagnosis and early intervention of coronary artery disease may potentially lower the mortality of SCD. 7 Although troponin had been proposed by the European Society of Cardiology and the American College of Cardiology as a marker of choice for post-mortem diagnosis of MI, its use in forensic medical diagnosis had not been thoroughly demonstrated. Among the three isoforms of the troponin complex, namely, troponin I, T and C, troponin I and T isoforms are exclusive to myocardial cells, and these differences have enabled the development of highly sensitive in-vivo diagnostic methods. 8 The results of Rahimi et al. ’s 2018 study in Malaysia indicated that troponin T is neither specific nor useful as a cardiac biomarker. Consequently, it may not serve as a useful post-mortem diagnostic tool. 9 As earlier studies on troponin skewed towards laboratory settings, this research project focused on the point-of-care setting of troponin I, which gives the advantage of shorter turnaround time and does not require advanced training for the operating personnel. METHODS This study aims to compare the troponin I level between MI and non-MI in cardiac death, to demonstrate the epidemiology of SCD in Johor Bahru and provide a database on the frequency of morphological observations on the heart and coronary artery among cardiac death cases, hence aiding in the prompt diagnosis and prevention of SCD. Study population A cross-sectional study was conducted over one year, from January 2023 to December 2023, on medicolegal autopsy cases in the Department of Forensic Medicine at Hospital Sultanah Aminah Johor Bahru (HSAJB). A Police 61 order was issued by investigating police officers to government medical officers to perform medicolegal post-mortem examinations. Informed consent was obtained from the next of kin or guardians of the subjects by the doctors. The inclusion criteria were all medicolegal autopsies conducted during the study period for individuals aged 18 years and above, with samples selected through simple random sampling. One exclusion criterion was cases of SCD or suspected cardiac death without troponin I results or gross or histopathological findings of the heart and coronary arteries, such as bodies in advanced decomposition, skeletonized remains, charred bodies, or haemolyzed/clotted blood samples for troponin I. Other exclusion criteria included post-mortem cases with incomplete reports or data, unidentified bodies, and bodies with no next of kin or guardian to provide informed consent. Sudden cardiac death (SCD) is defined as natural, unexpected death in apparently well individuals. 2–4 In this study, a temporal limitation between the onset of symptoms and the death, i.e. 24 hours, was not applied. In this study, cardiac death refers to natural death cases where the death is due to heart disease/pathology, for example, MI. Non-cardiac death refers to natural death cases where the death is not attributed to heart pathology/disease, but to other organs, for instance, pneumonia. Unnatural death indicates death that is not brought upon by natural disease, for instance, head injury due to a road traffic collision and hanging. For every decedent, the following data, which consisted of age, sex, ethnicity, cause and manner of death, were collected. For cardiac death or death that was suspected to be due to heart disease, data regarding troponin I level, gross and histopathological findings of the heart and coronary artery and toxicology result were gathered. Biochemical analysis About 3–5 ml of blood was routinely drawn from femoral/subclavian/jugular veins during post-mortem examination of every subject that was suspected of having cardiac pathology. The blood was put into an ethylenediaminetetraacetic acid (EDTA) tube. The blood sample was then processed on an analyzer, Quidel Triage Meter Pro, which used a point-of-care fluorescence immunoassay method immediately. The analyzer gave exact numerical values for results of ≤ 10 ng/ml, while for results above 10 ng/ml, the results were issued as a range, which was > 10 ng/ml. The cut-off value of post-mortem troponin I is at 9.5 ng/mL. 10 The test had fulfilled the quality control (QC) recommendation from the manufacturer of the device and also the current Clinical Laboratory Improvement Amendments (CLIA) guidelines. 11 Gross and histopathological examination of the heart and the coronary artery For gross examination of the heart, the significant coronary artery occlusion by atheromatous plaques and/or thrombus is defined as ≥ 75% luminal occlusion on cross-sectioning. Heart weight exceeding 500 g in a male and 400 g in a female is regarded as cardiomegaly. The weight of the subjects was not taken into consideration in determining cardiomegaly in this study. The thickness of the left and right ventricles is measured at the midventricular level, without taking into account the trabeculae and papillary muscles. Normal range for the thickness of the ventricles is 12–15 mm for the left ventricular wall and 3–5 mm for the right ventricular wall. 12 With respect to the histopathological examination of the heart, a minimum two representative sections were taken from the heart, where a sample was obtained from the left ventricle/interventricular septum and right ventricle, respectively. A minimum of one representative section from the main coronary artery was taken. Tissue processing was done after the samples were fixed in 10% formalin. After the tissue blocks were sectioned, they were adhered to the slides and stained with hematoxylin and eosin (H&E) stain. All histological sections were examined under a microscope for any pathology by the medical officer and forensic pathologist in charge. Myocardial infarction (MI) is defined as the death of myocardial tissue that is caused by ischaemia, which is the reduction or cessation of blood flow to myocytes to a degree that oxygen delivery is not adequate to meet the metabolic demands of the cells. 12 Acute MI is characterized by the presence of contraction band necrosis and pyknosis of nuclei with or without interstitial oedema, hypereosinophilia of cytoplasm and waviness of myocyte fiber in the earliest stage; and polymorphonuclear leukocytes infiltration and coagulative necrosis in the inflammatory stage. Subacute or healing MI is depicted by well-established granulation tissues with new blood vessels and collagen deposition, and/or increased collagen deposition with decreased cellularity. A healed MI demonstrates dense collagenous scar without cellular infiltration 13 Statistical analysis The data were analyzed using the Statistical Package for the Social Sciences (SPSS) software (version 29.0), with parameters tabulated using frequencies and percentages. The association between age, sex, and ethnicity with SCD was analyzed using the Pearson Chi-Square test. The Pearson Chi-Square test was also used to interpret the association between MI and non-MI cases with troponin I levels, as well as the association between acute MI and subacute and healed (non-acute) MI. A p-value of less than 0.05 was considered statistically significant. RESULTS A total of 157 medicolegal autopsy cases from HSAJB were recruited in the study. Fourteen cases were excluded due to the unavailability of troponin I results, mostly due to haemolysis and decomposition of the blood samples, or the lack of histopathological findings of the heart and coronary arteries in cardiac death cases. This resulted in a final sample of 143 cases. The medicolegal autopsy cases were classified into two main groups: SCD (cardiac death and non-cardiac death) and non-SCD (unnatural death). Cardiac deaths were further subdivided into MI (acute, subacute, and healed MI) and non-MI groups, and into acute MI and non-acute MI (subacute and healed infarction) based on histopathological findings. Prevalence of sudden cardiac death and cardiac death Among the 143 medicolegal autopsy cases, the prevalence of SCD was 54.6%, while the prevalence of cardiac death was 42.7%. Cardiac death accounted for 78.2% of all SCD cases. Cause and manner of death SCD (54.6%) accounted for the majority of medicolegal autopsy cases, compared to unnatural deaths (45.5%) (Table 1 ). Among the three subgroups, unnatural death was the most prevalent at 45.5%, followed by cardiac death at 42.7%, and non-cardiac death at 11.9%. Table 1 Cause of death for medicolegal autopsies in the year 2023 Cause of death No. (%) (n = 143) Natural death (Sudden cardiac death (SCD)) 78 (54.6) Cardiac death 61 (42.7) Non-cardiac death 17 (11.9) Others 8 (5.6) Central nervous system disorder 6 (4.2) Respiratory disease 3 (2.1) Unnatural death (Non-sudden cardiac death) 65 (45.5) Road traffic collision 50 (35.0) Hanging 5 (3.5) Poisoning/drug-related death 5 (3.5) Blunt injury 2 (1.4) Stab/slash injury 2 (1.4) Fall from height 1 (0.7) Insert Table 1 The most common cause of death in the cardiac death subgroup was coronary atherosclerosis (31.1%), with no histopathological evidence of acute MI (Table 2 ). This was followed by acute MI due to coronary atherosclerosis (24.6%) and acute MI due to coronary artery thrombosis or complicated coronary atherosclerosis (14.8%). Overall, coronary atherosclerosis and its complications were the leading causes of cardiac death, accounting for 85.2% of cases. Table 2 Cause of death among cardiac death Cause of death for cardiac death cases N (%) (n = 61) Coronary atherosclerosis 19 (31.1) Acute myocardial infarction due to coronary atherosclerosis 15 (24.6) Acute myocardial infarction due to coronary artery thrombosis or complicated coronary atherosclerosis 9 (14.8) Coronary artery thrombosis or complicated coronary atherosclerosis 4 (6.6) Cardiac tamponade due to ruptured aortic dissection 3 (4.9) Acute myocardial infarction with non-obstructive coronary arteries 2 (3.3) Ischaemic heart disease 2 (3.3) Sudden arrhythmic death syndrome 2 (3.3) Cardiac tamponade due to ruptured acute myocardial infarction due to coronary atherosclerosis 1 (1.6) Coronary artery anomaly 1 (1.6) Myocarditis 1 (1.6) Cardiomyopathy 1 (1.6) Cardiac sarcoidosis 1 (1.6) Insert Table 2 Following natural death (54.6%), the second most common manner of death in medicolegal autopsy cases at HSAJB was accidental death (37.1%), followed by suicide (4.9%), misadventure (2.1%), homicide (0.7%), and unascertained causes (0.7%). Sociodemographic data and their association with sudden cardiac death Among the 143 cases, male subjects comprised the majority, with 123 cases (86.0%), while female subjects accounted for 20 cases (14.0%). Both SCD and unnatural deaths (non-SCD) predominantly involved males (85.9–86.2%) compared to females. However, there was no significant association between SCD and sex (p = 0.965). SCD (54.5%) and unnatural deaths (45.5%) were equally represented among male subjects. The largest proportion of medicolegal autopsy cases were from the age group of 36–59 years (54.5%), followed by 18–35 years (37.1%) and those aged 60 years and above (8.4%). There was a significant association between SCD and age (p < 0.001), with the 36–59 years age group (69.2%) being the most prevalent in SCD cases. Conversely, the most common age group for unnatural deaths was 18–35 years (53.8%). The majority of subjects were Malay (37.8%), with the remainder comprising Chinese (29.3%), Indian (23.1%), and other ethnicities (10.5%). Malays were the predominant ethnicity in SCD cases (42.3%), followed by Chinese (29.5%), and both Indian and other ethnicities (14.1% each). There was a significant association between SCD and ethnicity (p = 0.017), with SCD being most common among Malays. Troponin I level in cardiac death cases Association between myocardial infarction and non-myocardial infarction with troponin I level Among the 61 cases of cardiac death, elevated troponin I (≥ 9.5 ng/ml) was observed in 39 cases (63.9%), while 22 cases (36.1%) had normal troponin I levels (< 9.5 ng/ml) (Table 3 ). A significant difference in troponin I levels was found between MI and non-MI cases (p = 0.004). Most MI cases (71.7%) exhibited elevated troponin I levels, whereas a majority of non-MI cases (87.5%) had normal troponin I levels. The MI subgroup was the primary contributor to elevated troponin I cases (97.4%; 38 cases). Table 3 Relationship between myocardial infarction and non-myocardial infarction with troponin I Histopathological findings of heart Troponin I level (ng/ml) No. (%) No. (%) (n = 61) Chi-square value (χ 2 ) p-value < 9.5 (n = 22) ≥ 9.5 (n = 39) Myocardial infarction a 15 (28.3) 38 (71.7) 53 (86.9) 10.564 0.004 b, * Non-myocardial infarction 7 (87.5) 1 (12.5) 8 (13.1) a Myocardial infarction subgroup consisted of acute, subacute and healed myocardial infarction. b Pearson Chi-square with continuous correction. *p < 0.05 Insert Table 3 Association between acute myocardial infarction and subacute and healed (non-acute) myocardial infarction with troponin I level Among the 53 cases of MI, elevated troponin I was observed in 38 cases (71.7%) (Table 4 ). A minority of MI cases (28.3%) had normal troponin I levels despite histopathological evidence of MI. No significant difference was found between acute and subacute and healed (non-acute) MI regarding troponin I levels (p = 0.763). Both acute (73.3%) and subacute and healed MI (69.6%) showed a tendency for elevated troponin I. Table 4 Relationship between acute myocardial infarction and subacute and healed (non-acute) myocardial infarction with troponin I Histopathological findings of heart Troponin I level (ng/ml) No. (%) No. (%) (n = 53) Chi-square value (χ 2 ) p-value < 9.5 (n = 15) ≥ 9.5 (n = 38) Acute myocardial infarction 8 (26.7) 22 (73.3) 30 (56.6) 0.091 0.763 Subacute and healed myocardial infarction 7 (30.4) 16 (69.6) 23 (43.4) Insert Table 4 Gross and histopathological findings of coronary arteries The majority of coronary arteries (53.8%) exhibited no pathology. The most common gross pathology found in the coronary arteries was uncomplicated coronary atherosclerosis (Fig. 1 ), present in 41.3% of specimens, followed by coronary artery thrombosis (3.3%) and intraplaque hemorrhage (0.9%). A significant proportion of cardiac death cases with coronary atherosclerosis exhibited critical coronary artery occlusion (61.2%). This significant occlusion was most frequently observed in the left anterior descending artery (LAD) (48.2%), followed by the right coronary artery (RCA) (23.5%) and the left circumflex artery (LCX) (22.4%). Insert Fig. 1 No microscopic pathology was found in 6.3% of the sampled coronary arteries. The predominant histopathological finding in coronary arteries was uncomplicated coronary atherosclerosis, present in 70.0% of specimens, followed by intraplaque hemorrhage (12.5%) and coronary artery thrombosis (3.8%). Gross and histopathological findings of heart Among the examined hearts, 70.5% exhibited gross pathology, while 29.5% showed no gross pathology. Fibrosis was the most common gross finding, observed in 50.8% of samples, followed by cardiomegaly (19.7%) and hemorrhage (16.4%) (Table 5 ). Table 5 Prevalence of gross heart findings in adults aged 18 years and above Gross findings of the heart Total No. (%) (n = 61) Presence of gross finding of the heart 43 (70.5) Fibrosis 31 (50.8) Cardiomegaly 12 (19.7) Haemorrhage 10 (16.4) Thinning of ventricular wall 8 (13.1) Thickened left ventricular wall 7 (11.5) Dilated appearance of the heart chamber 7 (11.5) Thickened interventricular septum 5 (8.2) Others 5 (8.2) Cardiac tamponade 4 (6.6) Pale myocardium 4 (6.6) Mottled appearance 4 (6.6) Thickened right ventricular wall 2 (3.3) Yellow-tan discolouration 2 (3.3) Ruptured myocardium 1 (1.6) Replacement/infiltration of myocardium by fats 1 (1.6) No gross finding of the heart 18 (29.5) Insert Table 5 Histopathological findings were present in 91.8% of the examined hearts, with only 8.2% showing no microscopic findings (Table 6 ). Interstitial/replacement fibrosis was the most frequently observed microscopic finding, noted in 82.0% of cases, followed by contraction band/coagulative necrosis (34.4%), and infiltration by inflammatory cells (26.3%) (Fig. 1 ). Table 6 Histopathological findings of the heart Histopathological findings of the heart Total No. (%) (n = 61) Presence of histopathological finding of the heart 56 (91.8) Interstitial/replacement fibrosis 50 (82.0) Contraction band/coagulative necrosis 21 (34.4) Infiltration by inflammatory cells 16 (26.3) Hypertrophy of myocytes 15 (24.6) Perivascular fibrosis 14 (23.0) Haemorrhage 13 (21.3) Granulation tissue 12 (19.7) Interstitial oedema 9 (14.8) Myocyte hypereosinophilia 8 (13.1) Waviness of myocytes 4 (6.6) Replacement/infiltration of myocardium by fats 4 (6.6) Others 4 (6.6) Myocardial bridging 2 (3.3) Mural thrombus 1 (1.6) Ruptured myocardium 1 (1.6) No histopathological finding of the heart 5 (8.2) Insert Table 6 DISCUSSION Sudden cardiac death (SCD) remains a significant issue in public health and emergency medicine and is a major contributor to medicolegal autopsy cases globally. The Department of Forensic Medicine at HSAJB, one of only two autopsy centers in Johor Bahru with a population of approximately 1.71 million, reported a SCD prevalence of 54.6%. 14 This is notably higher compared to other studies, which have reported prevalence rates ranging from 30% to 37.8%. 6,15 Additionally, cardiac diseases were the leading cause of SCD, accounting for 78.2% of cases in this study. This finding aligns with previous studies by Kumar et al. (2007) and Rahimi et al. (2018), which reported cardiac diseases as responsible for 64.9% to 75.8% of SCDs. 6 , 16 Our study revealed that the most common cause of cardiac death was ischaemic heart disease/coronary atherosclerosis, accounting for 85.2% of cases, which was consistent with findings from previous studies, which reported rates between 75% and 80%. 17,18 One factor contributing to the high prevalence of SCD in this study is the increase in obesity and diabetes rates globally during the early 2000s, which are key risk factors for coronary atherosclerosis. 19 The low health screening rates among Malaysians, ranging from 10% to 49.7%, may also contribute to the high prevalence of cardiac death. 20 , 21 Additionally, the majority of cardiac death cases in this study were individuals aged 36–59 years (73.8%), a group where ischaemic heart disease/coronary atherosclerosis is more prevalent compared to congenital heart anomalies, cardiomyopathy, myocarditis, and arrhythmic disorders. 18 , 22 The study's findings align with those observed in Western societies, where approximately 15% of overall SCD is attributed to non-ischemic structural heart diseases, such as cardiomyopathy and infiltrative diseases like sarcoidosis and amyloidosis. 23 , 24 In this study, 3.3% of cardiac death cases had negative autopsies with a presumptive cause of sudden arrhythmic death syndrome, though genetic studies were not performed. This percentage is lower than reported by Murakoshi et al. and Winkel et al. (10–29%). 25,26 The difference may be because individuals under 35 years old, who are commonly affected by sudden arrhythmic death syndrome, represented only 18.0% of cardiac death cases in this study. Notably, all cases of sudden arrhythmic death syndrome in this study involved two men under 35 years old. This study found a male predominance in SCD cases; however, no significant association between SCD and sex was established. The male-to-female ratio in SCD cases ranged from 4.8 to 5, as reported by Ding et al. and Eckart et al . 7,27 . A Malaysian study from 2020 reported an even greater male predominance, with a 39-fold difference. 28 Researchers suggest that this male predominance may be attributed to the protective effects of oestrogen, which has both immediate and long-term impacts, including athero-protective effects on serum lipid concentrations and direct effects on blood vessels. 29 A significant association between SCD and age was observed, with the majority of cases occurring in individuals aged 36–59 years. This contrasts with other studies that report an increased incidence of SCD with advancing age. 28 , 30 This discrepancy may be due to the lower rate of medicolegal autopsies for SCD cases among individuals aged 60 years and above at our center. Our study also found a significant association between SCD and ethnicity, with SCD being more prevalent among Malays. This finding differs from studies by Kumar et al. and Ly et al. , which reported higher SCD prevalence among Indians and Chinese in Malaysia. 16 , 28 INTERHEART research suggests that Indians in Asia face a higher risk of developing cardiac disease earlier in life compared to other races due to a shared history of diabetes, which is closely linked to cardiac disease. 31 , 32 The cultural and genetic diversity among Malaysia's multi-ethnic population may contribute to unique cardiovascular morbidity and mortality risks that differ from those observed in Western populations. 33 Ismail et al. found higher associations of hypertension and left bundle branch block in Malays and aborigines, while Indians showed a higher association with left ventricular ejection fraction ≤ 40%. 34 Cardiac troponin is released swiftly from myocytes following myocardial damage and can be detected in the blood within 3–4 hours. It typically peaks after 16–18 hours and remains detectable for up to 10–21 days, which aids in diagnosis. 10 , 35 Our study found a significant difference between MI and non-MI cases in terms of troponin I levels, with a majority of MI cases (71.7%) exhibiting elevated levels. This finding aligns with Ooi et al. , who found that the troponin I levels in MI group differed significantly from those of the no-pathology group. 36 However, our result is in contrast with the finding of preceding study by Banon et al. which demonstrated that there were no statistically significant differences between ischaemic deaths and non-ischaemic death for high-sensitivity troponin I. 37 Factors contributing to false-negative results in our study included autolysis, microbial degradation, and the natural metabolic processes that occur post-mortem, despite troponin I typically increasing in a time-dependent manner, particularly if the post-mortem interval exceeds 48 hours. 10 Our study did not find a significant difference between acute and subacute and healed (non-acute) MI in relation to troponin I levels. Both acute (73.3%) and subacute and healed MI (69.6%) cases showed elevated troponin I levels. We have been unable to find similar preceding research for this parameter to compare our results. However, Ooi et al. found a significant difference between the troponin I level and the odds ratios for acute and subacute MI with healed MI, which was in contrast with our study. 36 The false-positive result in our study could be due to post-mortem time-dependent increases in troponin levels. Additionally, cardiac troponin can be detected in the blood earlier (about 3 hours) compared to the earliest histopathological changes, such as coagulative necrosis, which are detectable within the first 6 to 12 hours. 10 , 13 Furthermore, troponin I can persist in the blood for up to 10–21 days, which may result in false positives as the MI progresses from the acute to subacute phase. Other potential sources of analytical interference, such as heterophilic antibodies, fibrin clots, and haemolysis, should also be considered when interpreting post-mortem troponin I results 35 , 38 In this study, the most prevalent coronary artery pathology was uncomplicated coronary atherosclerosis, observed in 41.3% of cases. Complications of this condition, including intraplaque hemorrhage and coronary artery thrombosis, were the next most frequent pathologies. These results align with findings from Wagh et al . 39 However, our results differ from those of Waller et al. , who reported tunneled coronary arteries (myocardial bridging) (23.1%) as the most common cardiac pathology, as opposed to atherosclerotic coronary heart disease (20.6%). 40 This discrepancy may be attributed to differences in study populations. Our study found that the left anterior descending artery (LAD) was the most commonly affected artery (37.6%), which is consistent with findings from Shubhangi et al. and Wagh et al . 39,41 Fibrosis was notably the most frequent finding in our study, present in 50.8% of gross specimens and 82.0% of histopathological specimens. This was followed by acute MI changes. These results are consistent with studies by Nisha et al. and Wagh et al. , where fibrosis was more commonly observed than acute MI. 39,42 In contrast, a 2018 study in India found cardiac adiposity (23.0%) to be the most common cardiac morphology, followed by atherosclerotic coronary heart disease (21.1%) and left ventricular hypertrophy (19.0%). 43 The high prevalence of fibrosis in cardiac death cases in our study suggests that many subjects had a history of previous MI, regardless of the cause and whether they were symptomatic, before their deaths. This finding highlights the chronic nature of their cardiac pathology, which could have been identified through regular health screenings or medical consultations during the progression of their diseases. LIMITATION OF STUDY Difference in the post-mortem interval and haemolysis of the post-mortem blood samples were among the factors and interferences that pose limitation in this study. There remains the issue of clinically validated cut-off concentrations in post-mortem samples of point-of-care troponin I, thus further work is necessary to establish appropriate diagnostic cut-off values in the respective forensic laboratory. The statistical interpretation of the study could be limited by the small sample size of female participants. CONCLUSION Coronary atherosclerosis and its complications were the most common causes of cardiac death, predominantly affecting individuals aged 36–59 years and those of Malay ethnicity. Therefore, annual health screenings and awareness campaigns should be specifically targeted towards Malay individuals aged 36 and older to help prevent SCD. This study demonstrated that although there was a significant difference in troponin I levels between MI and non-MI cases, however, no significant difference was found between acute with subacute and healed (non-acute) MI in relation to troponin I levels. Consequently, it is plausible to consider using troponin I as an auxiliary investigation rather than as a sole diagnostic tool for MI while exercising caution during interpretation of result. Abbreviations SCD Sudden cardiac death MI myocardial infarction WHO World Health Organization EDTA ethylenediaminetetraacetic acid CLIA Clinical Laboratory Improvement Amendments LAD left anterior descending artery RCA right coronary artery LCX left circumflex artery Declarations Ethical approval and consent to participate The data were obtained from the post-mortem reports. Ethical clearance had been obtained from the Medical Research & Ethics Committee, Ministry of Health Malaysia (Reference number: 22-02449-F23) and Research Ethics Committee of the Faculty Medicine, Universiti Kebangsaan Malaysia (Reference number: UKM PPI/111/8/JEP-2022-653). Informed consent was obtained from the next of kin or guardian of all the studied subjects in the study. Consent for publication We would also like to thank the Director General of Health Malaysia for his permission to publish this article. Funding None References Hayashi M, Shimizu W, Albert CM. The spectrum of epidemiology underlying sudden cardiac death. Circ Res. 2015 Jun 5;116(12):1887-906. doi: 10.1161/CIRCRESAHA.116.304521. World Health Organization. ICD-11 for mortality and morbidity Statistics. [Internet]. 2019. [cited 2022 April 17]. Available from: https://Icd.Who.Int/Browse11/l-m/En#/Http%3a%2f%2fid.Who.Int%2ficd%2fentity%2f859971440 Buja LM, & Butany, J. Cardiovascular Pathology. 5 th ed. 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Eur Heart J. 2015 Nov 1;36(41):2793-2867. doi: 10.1093/eurheartj/ehv316 Chugh SS, Jui J, Gunson K, et al. Current burden of sudden cardiac death: Multiple source surveillance versus retrospective death certificate-based review in a large U.S. community. J Am Coll Cardiol. 2004 Sep 15;44(6):1268-75. doi: 10.1016/j.jacc.2004.06.029. Zheng ZJ, Croft JB, Giles WH, Mensah GA. Sudden cardiac death in the United States, 1989 to 1998. Circulation. 2001 Oct 30;104(18):2158-63. doi: 10.1161/hc4301.098254. Murakoshi N, Aonuma K. Epidemiology of arrhythmias and sudden cardiac death in Asia. Circ J. 2013;77(10):2419-31. doi: 10.1253/circj.cj-13-1129. Winkel BG, Holst AG, Theilade J, et al . Nationwide study of sudden cardiac death in persons aged 1-35 years. Eur Heart J. 2011 Apr;32(8):983-90. doi: 10.1093/eurheartj/ehq428. Eckart RE, Shry EA, Burke AP et al. Sudden death in young adults: An autopsy-based series of a population undergoing active surveillance. J Am Coll Cardiol. 2011 Sep 13;58(12):1254-61. doi: 10.1016/j.jacc.2011.01.049. Ly CK, Nadesan K, Samberkar SP, Byard RW, Samberkar PN. Ethnic variability in mortality from ischaemic heart disease/cardiomegaly in Malaysia. Med Leg J. 2021 Mar;89(1):37-39. doi: 10.1177/0025817220960597. Winkel BG, Risgaard B, Bjune T, et al. Gender differences in sudden cardiac death in the young-a nationwide study. BMC Cardiovasc Disord. 2017 Jan 7;17(1):19. doi: 10.1186/s12872-016-0446-5. Shuvy M, Qiu F, Lau G, et al . Temporal trends in sudden cardiac death in Ontario, Canada. Resuscitation. 2019 Mar;136:1-7. doi: 10.1016/j.resuscitation.2019.01.010. Jha AK, Varosy PD, Kanaya AM, et al. Differences in medical care and disease outcomes among black and white women with heart disease. Circulation. 2003 Sep 2;108(9):1089-94. doi: 10.1161/01.CIR.0000085994.38132.E5. Rodriguez CJ, Allison M, Daviglus ML, et al. Status of cardiovascular disease and stroke in Hispanics/Latinos in the United States: a science advisory from the American Heart Association. Circulation. 2014 Aug 12;130(7):593-625. doi: 10.1161/CIR.0000000000000071. Dans A, Ng N, Varghese C, Tai ES, Firestone R, Bonita R. The rise of chronic non-communicable diseases in Southeast Asia: Time for action. Lancet. 2011 Feb 19;377(9766):680-9. doi: 10.1016/S0140-6736(10)61506-1. Ismail SR, Mohammad MSF, Butterworth AS, et al. Risk factors of secondary cardiovascular events in a multi-ethnic Asian population with acute myocardial infarction: A retrospective cohort study from Malaysia. J Cardiovasc Dev Dis. 2023 Jun 9;10(6):250. doi: 10.3390/jcdd10060250. Korff S, Katus HA, Giannitsis E. Differential diagnosis of elevated troponins. Heart. 2006 Jul;92(7):987-93. doi: 10.1136/hrt.2005.071282. Ooi DS, Isotalo PA, Veinot JP. Correlation of antemortem serum creatine kinase, creatine kinase-MB, troponin I, and troponin T with cardiac pathology. Clin Chem. 2000 Mar;46(3):338-44. doi: https://doi.org/10.1093/clinchem/46.3.338 Bañón R, Hernández-Romero D, Navarro E, Pérez-Cárceles MD, Noguera-Velasco JA, Osuna E. Combined determination of B-type natriuretic peptide and high-sensitivity troponin I in the postmortem diagnosis of cardiac disease. Forensic Sci Med Pathol. 2019 Dec;15(4):528-535. doi: 10.1007/s12024-019-00150-1. Mair J, Lindahl B, Müller C, et al. What to do when you question cardiac troponin values. Eur Heart J Acute Cardiovasc Care. 2018 Sep;7(6):577-586. doi: 10.1177/2048872617708973. Wagh AV, Kulkarni K, Gadpal RR, Wagh RV. Histomorphological spectrum of various cardiac changes in sudden death: An autopsystudy. International Journal of Scientific Research. 2022.11(01),10–13. doi: https://doi.org/10.36106/ijsr/2000407 Waller BF, Catellier MJ, Clark MA, Hawley DA, Pless JE. Cardiac pathology in 2007 consecutive forensic autopsies. Clin Cardiol. 1992 Oct;15(10):760-5. doi: 10.1002/clc.4960151014. Shubhangi VA., Pragya VJain., Grace F. et al. An autopsy study of the histopathological spectrum of cardiac diseases in cases of sudden death [Internet]. 2022. [cited on 2024 July 28]. Available from: https://1library.net/document/zwk73m0z-autopsy-studyhistopathological-spectrum-cardiac-diseases-cases-sudden.html Nisha M, Bhawna S, Sumiti G, et al. Histomorphological spectrum of various cardiac changes in sudden death: An autopsy study. Iranian Journal of Pathology. 6(4), 179–186. [Internet]. 2011. [cited on 2024 July 24]. Available from: http://ijp.iranpath.org/article_8515_bafd03eba96f11265dba34b10feb68a6.pdf Khandekar DS, Mahadani J. Histomorphological analysis of various heart diseases: An autopsy study. Journal of Medical Science and Clinical Research. 2018;6(8). doi: https://doi.org/10.18535/jmscr/v6i8.192 Additional Declarations No competing interests reported. Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-8452675","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":567263888,"identity":"b99ab1fd-cddd-4cf1-8156-338c50253973","order_by":0,"name":"Oi Chia YAP","email":"","orcid":"","institution":"Hospital Sultanah Aminah, Ministry of Health, Jalan Persiaran Abu Bakar Sultan, 80100","correspondingAuthor":false,"prefix":"","firstName":"Oi","middleName":"Chia","lastName":"YAP","suffix":""},{"id":567263889,"identity":"4aad6f2f-8a93-4c97-9d8e-aed836f13511","order_by":1,"name":"Mohamad Aznool Haidy AHSORORI","email":"","orcid":"","institution":"Hospital Sultanah Aminah, Ministry of Health, Jalan Persiaran Abu Bakar Sultan, 80100","correspondingAuthor":false,"prefix":"","firstName":"Mohamad","middleName":"Aznool Haidy","lastName":"AHSORORI","suffix":""},{"id":567263890,"identity":"0e00c230-039f-4139-a8a3-e80149e03afe","order_by":2,"name":"Faridah MOHD NOR","email":"","orcid":"","institution":"Faculty of Medicine, Universiti Kebangsaan Malaysia, Jalan Yaacob Latif, Bandar Tun Razak, 56000","correspondingAuthor":false,"prefix":"","firstName":"Faridah","middleName":"MOHD","lastName":"NOR","suffix":""},{"id":567263891,"identity":"2ebad84e-3880-496f-baa8-798a2d242896","order_by":3,"name":"Mohd Swarhib SHAFEE","email":"","orcid":"","institution":"University Sultan Zainal Abidin, Jalan Tembila, 22200","correspondingAuthor":false,"prefix":"","firstName":"Mohd","middleName":"Swarhib","lastName":"SHAFEE","suffix":""},{"id":567263892,"identity":"574ac7d6-3800-4786-940d-c8ae27400178","order_by":4,"name":"Nadiawati ABDUL RAZAK","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA3UlEQVRIiWNgGAWjYDCCA0DMYwBiMTY+gHCJ1sLG2GxAghYQg42BTYIoLXy3zx788KbALrF/fnNbNU/NHTl+BuaHj27g0SJ5Li9Zco5BcuKMY4xtt3mOPTOWbGAzNs7Bo8XgDI+BNI8Bc24DWAvb4cQNB3jYpAloMf7NY1CfOx+opZjnH3FazIC2HM7dANTCzNtGhBZJoBbLOQbH6zceS2yWnNt32FiymYBf+IAOu/HmT7Wx3OHjDz+8+XZYjp+9+eFjfFpQABM4gpiJVQ4CjD9IUT0KRsEoGAUjBgAAVY1PdTulsvIAAAAASUVORK5CYII=","orcid":"","institution":"Faculty of Medicine and Defense Health, National Defense University of Malaysia, Kem Sungai Besi, 57000, m","correspondingAuthor":true,"prefix":"","firstName":"Nadiawati","middleName":"ABDUL","lastName":"RAZAK","suffix":""}],"badges":[],"createdAt":"2025-12-26 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06:17:44","extension":"xml","order_by":5,"title":"","display":"","copyAsset":false,"role":"acdc-reference","size":115171,"visible":true,"origin":"","legend":"","description":"","filename":"e596b8ad53e642e7aa4e6609b70610101structuring.xml","url":"https://assets-eu.researchsquare.com/files/rs-8452675/v1/3fc58e14eb36cac778144f7d.xml"},{"id":99341115,"identity":"2aa8b33d-75bd-490d-8ba7-61776c55e425","added_by":"auto","created_at":"2026-01-01 06:17:44","extension":"html","order_by":6,"title":"","display":"","copyAsset":false,"role":"acdc-reference","size":126519,"visible":true,"origin":"","legend":"","description":"","filename":"earlyproof.html","url":"https://assets-eu.researchsquare.com/files/rs-8452675/v1/445f1a1f13a64455b738c28c.html"},{"id":99341110,"identity":"6e6e1d66-80e4-405e-af5a-051d01a393f1","added_by":"auto","created_at":"2026-01-01 06:17:44","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":1440826,"visible":true,"origin":"","legend":"\u003cp\u003eGross and histopathological findings of coronary artery and heart. (A) Cross sections of left anterior descending artery: Significant occlusion of coronary artery by atheromatous plaque; (B) Acute and subacute myocardial infarction. Acute myocardial infarction: contraction band/coagulative necrosis and infiltration of acute inflammatory cells; Subacute myocardial infarction: granulation tissue on the top left (arrow) (Haematoxylin \u0026amp; eosin (H\u0026amp;E) stain, 400x magnification); (C) Subacute myocardial infarction: granulation tissue (H\u0026amp;E stain, 400x magnification); (D) Fibrofatty replacement of myocardium (H\u0026amp;E stain, 100x magnification)\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-8452675/v1/5159308c8a8779b2330de908.png"},{"id":106959124,"identity":"7ae582cd-05c7-4708-9078-a92278b8c40f","added_by":"auto","created_at":"2026-04-15 08:47:20","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":2793571,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8452675/v1/3ab6ae08-e51e-492c-b3b6-685d50ddc8cb.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"\u003cp\u003eTroponin Clues: An Academic Reappraisal of Cardiac and Coronary Artery Pathologies in Sudden Death among Medicolegal Autopsies\u003c/p\u003e","fulltext":[{"header":"BACKGROUND","content":"\u003cp\u003eSudden cardiac death (SCD) accounts for an estimated 15% to 20% of all deaths globally and is a leading cause of mortality worldwide.\u003csup\u003e\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e\u003c/sup\u003e The World Health Organization (WHO), according to the International Classification of Diseases, version 11 (ICD-11) defines sudden death as non-violent and not otherwise explained death occurring instantaneously or less than 24 hours from the onset of symptoms.\u003csup\u003e\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e\u003c/sup\u003e These cases generally refer to the death of apparently healthy individuals who are not under close medical care, although they may have an underlying medical illness which does not incapacitate them prior to this. \u003csup\u003e3,4\u003c/sup\u003e In this study, a temporal limitation between the onset of symptoms and the death, i.e. 24 hours, was not applied.\u003c/p\u003e \u003cp\u003eThe United States has an annual incidence of 60 per 100,000 cases of SCD, in which roughly 300,000\u0026ndash;400,000 SCD occur each year. Based on death certificate data, SCD accounts for up to 15% of deaths in Western nations.\u003csup\u003e\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e\u003c/sup\u003e In Klang Valley, Malaysia, natural death constituted 37.8% of the medicolegal autopsies in the year 2014. Of all the natural causes of sudden death, cardiovascular diseases account for 75.8%. Coronary artery disease contributes for 60% of SCD, whereas the remaining SCD cases are attributed to ischaemic heart disease, acute myocardial infarction (MI), cardiomyopathy and hypertensive heart disease.\u003csup\u003e\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eOften, SCD is the first and only symptom a deceased person displays and is the most frequent cause of death from heart disease. The sudden, unexpected nature of SCD, as well as its high incidence and fatality, renders it a major unsolved issue in the fields of emergency medicine and public health. Forensic pathology examinations and detailed autopsies are essential for diagnosing SCD. A timely diagnosis and early intervention of coronary artery disease may potentially lower the mortality of SCD.\u003csup\u003e\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eAlthough troponin had been proposed by the European Society of Cardiology and the American College of Cardiology as a marker of choice for post-mortem diagnosis of MI, its use in forensic medical diagnosis had not been thoroughly demonstrated. Among the three isoforms of the troponin complex, namely, troponin I, T and C, troponin I and T isoforms are exclusive to myocardial cells, and these differences have enabled the development of highly sensitive in-vivo diagnostic methods.\u003csup\u003e\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e\u003c/sup\u003e The results of Rahimi \u003cem\u003eet al.\u003c/em\u003e\u0026rsquo;s 2018 study in Malaysia indicated that troponin T is neither specific nor useful as a cardiac biomarker. Consequently, it may not serve as a useful post-mortem diagnostic tool.\u003csup\u003e\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eAs earlier studies on troponin skewed towards laboratory settings, this research project focused on the point-of-care setting of troponin I, which gives the advantage of shorter turnaround time and does not require advanced training for the operating personnel.\u003c/p\u003e"},{"header":"METHODS","content":"\u003cp\u003eThis study aims to compare the troponin I level between MI and non-MI in cardiac death, to demonstrate the epidemiology of SCD in Johor Bahru and provide a database on the frequency of morphological observations on the heart and coronary artery among cardiac death cases, hence aiding in the prompt diagnosis and prevention of SCD.\u003c/p\u003e \u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003ch2\u003eStudy population\u003c/h2\u003e \u003cp\u003eA cross-sectional study was conducted over one year, from January 2023 to December 2023, on medicolegal autopsy cases in the Department of Forensic Medicine at Hospital Sultanah Aminah Johor Bahru (HSAJB). A Police 61 order was issued by investigating police officers to government medical officers to perform medicolegal post-mortem examinations. Informed consent was obtained from the next of kin or guardians of the subjects by the doctors.\u003c/p\u003e \u003cp\u003eThe inclusion criteria were all medicolegal autopsies conducted during the study period for individuals aged 18 years and above, with samples selected through simple random sampling. One exclusion criterion was cases of SCD or suspected cardiac death without troponin I results or gross or histopathological findings of the heart and coronary arteries, such as bodies in advanced decomposition, skeletonized remains, charred bodies, or haemolyzed/clotted blood samples for troponin I. Other exclusion criteria included post-mortem cases with incomplete reports or data, unidentified bodies, and bodies with no next of kin or guardian to provide informed consent.\u003c/p\u003e \u003cp\u003eSudden cardiac death (SCD) is defined as natural, unexpected death in apparently well individuals. \u003csup\u003e2\u0026ndash;4\u003c/sup\u003e In this study, a temporal limitation between the onset of symptoms and the death, i.e. 24 hours, was not applied. In this study, cardiac death refers to natural death cases where the death is due to heart disease/pathology, for example, MI. Non-cardiac death refers to natural death cases where the death is not attributed to heart pathology/disease, but to other organs, for instance, pneumonia. Unnatural death indicates death that is not brought upon by natural disease, for instance, head injury due to a road traffic collision and hanging.\u003c/p\u003e \u003cp\u003eFor every decedent, the following data, which consisted of age, sex, ethnicity, cause and manner of death, were collected. For cardiac death or death that was suspected to be due to heart disease, data regarding troponin I level, gross and histopathological findings of the heart and coronary artery and toxicology result were gathered.\u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003eBiochemical analysis\u003c/h3\u003e\n\u003cp\u003eAbout 3\u0026ndash;5 ml of blood was routinely drawn from femoral/subclavian/jugular veins during post-mortem examination of every subject that was suspected of having cardiac pathology. The blood was put into an ethylenediaminetetraacetic acid (EDTA) tube. The blood sample was then processed on an analyzer, Quidel Triage Meter Pro, which used a point-of-care fluorescence immunoassay method immediately. The analyzer gave exact numerical values for results of \u0026le;\u0026thinsp;10 ng/ml, while for results above 10 ng/ml, the results were issued as a range, which was \u0026gt;\u0026thinsp;10 ng/ml. The cut-off value of post-mortem troponin I is at 9.5 ng/mL.\u003csup\u003e10\u003c/sup\u003e The test had fulfilled the quality control (QC) recommendation from the manufacturer of the device and also the current Clinical Laboratory Improvement Amendments (CLIA) guidelines.\u003csup\u003e\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e\n\u003ch3\u003eGross and histopathological examination of the heart and the coronary artery\u003c/h3\u003e\n\u003cp\u003eFor gross examination of the heart, the significant coronary artery occlusion by atheromatous plaques and/or thrombus is defined as \u0026ge;\u0026thinsp;75% luminal occlusion on cross-sectioning. Heart weight exceeding 500 g in a male and 400 g in a female is regarded as cardiomegaly. The weight of the subjects was not taken into consideration in determining cardiomegaly in this study. The thickness of the left and right ventricles is measured at the midventricular level, without taking into account the trabeculae and papillary muscles. Normal range for the thickness of the ventricles is 12\u0026ndash;15 mm for the left ventricular wall and 3\u0026ndash;5 mm for the right ventricular wall.\u003csup\u003e\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eWith respect to the histopathological examination of the heart, a minimum two representative sections were taken from the heart, where a sample was obtained from the left ventricle/interventricular septum and right ventricle, respectively. A minimum of one representative section from the main coronary artery was taken. Tissue processing was done after the samples were fixed in 10% formalin. After the tissue blocks were sectioned, they were adhered to the slides and stained with hematoxylin and eosin (H\u0026amp;E) stain. All histological sections were examined under a microscope for any pathology by the medical officer and forensic pathologist in charge.\u003c/p\u003e \u003cp\u003eMyocardial infarction (MI) is defined as the death of myocardial tissue that is caused by ischaemia, which is the reduction or cessation of blood flow to myocytes to a degree that oxygen delivery is not adequate to meet the metabolic demands of the cells.\u003csup\u003e\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e\u003c/sup\u003e Acute MI is characterized by the presence of contraction band necrosis and pyknosis of nuclei with or without interstitial oedema, hypereosinophilia of cytoplasm and waviness of myocyte fiber in the earliest stage; and polymorphonuclear leukocytes infiltration and coagulative necrosis in the inflammatory stage. Subacute or healing MI is depicted by well-established granulation tissues with new blood vessels and collagen deposition, and/or increased collagen deposition with decreased cellularity. A healed MI demonstrates dense collagenous scar without cellular infiltration \u003csup\u003e\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e \u003cdiv id=\"Sec6\" class=\"Section2\"\u003e \u003ch2\u003eStatistical analysis\u003c/h2\u003e \u003cp\u003eThe data were analyzed using the Statistical Package for the Social Sciences (SPSS) software (version 29.0), with parameters tabulated using frequencies and percentages. The association between age, sex, and ethnicity with SCD was analyzed using the Pearson Chi-Square test. The Pearson Chi-Square test was also used to interpret the association between MI and non-MI cases with troponin I levels, as well as the association between acute MI and subacute and healed (non-acute) MI. A p-value of less than 0.05 was considered statistically significant.\u003c/p\u003e \u003c/div\u003e"},{"header":"RESULTS","content":"\u003cp\u003eA total of 157 medicolegal autopsy cases from HSAJB were recruited in the study. Fourteen cases were excluded due to the unavailability of troponin I results, mostly due to haemolysis and decomposition of the blood samples, or the lack of histopathological findings of the heart and coronary arteries in cardiac death cases. This resulted in a final sample of 143 cases. The medicolegal autopsy cases were classified into two main groups: SCD (cardiac death and non-cardiac death) and non-SCD (unnatural death). Cardiac deaths were further subdivided into MI (acute, subacute, and healed MI) and non-MI groups, and into acute MI and non-acute MI (subacute and healed infarction) based on histopathological findings.\u003c/p\u003e\n\u003cdiv id=\"Sec8\" class=\"Section2\"\u003e\n \u003ch2\u003ePrevalence of sudden cardiac death and cardiac death\u003c/h2\u003e\n \u003cp\u003eAmong the 143 medicolegal autopsy cases, the prevalence of SCD was 54.6%, while the prevalence of cardiac death was 42.7%. Cardiac death accounted for 78.2% of all SCD cases.\u003c/p\u003e\n\u003c/div\u003e\n\u003ch3\u003eCause and manner of death\u003c/h3\u003e\n\u003cp\u003eSCD (54.6%) accounted for the majority of medicolegal autopsy cases, compared to unnatural deaths (45.5%) (Table \u003cspan class=\"InternalRef\"\u003e1\u003c/span\u003e). Among the three subgroups, unnatural death was the most prevalent at 45.5%, followed by cardiac death at 42.7%, and non-cardiac death at 11.9%.\u003c/p\u003e\n\u003cdiv class=\"gridtable\"\u003e\u0026nbsp;\u003ctable id=\"Tab1\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e\n \u003cdiv class=\"CaptionContent\"\u003e\n \u003cp\u003eCause of death for medicolegal autopsies in the year 2023\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003ccolgroup cols=\"2\"\u003e\u003c/colgroup\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eCause of death\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eNo. (%)\u003c/p\u003e\n \u003cp\u003e(n\u0026thinsp;=\u0026thinsp;143)\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eNatural death (Sudden cardiac death (SCD))\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e78 (54.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eCardiac death\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e\u003cem\u003e61 (42.7)\u003c/em\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eNon-cardiac death\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e\u003cem\u003e17 (11.9)\u003c/em\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eOthers\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e8 (5.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCentral nervous system disorder\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e6 (4.2)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eRespiratory disease\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e3 (2.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eUnnatural death (Non-sudden cardiac death)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e65 (45.5)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eRoad traffic collision\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e50 (35.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHanging\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e5 (3.5)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003ePoisoning/drug-related death\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e5 (3.5)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eBlunt injury\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e2 (1.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eStab/slash injury\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e2 (1.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eFall from height\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e1 (0.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003c/table\u003e\n\u003c/div\u003e\n\u003ch3\u003eInsert Table 1\u003c/h3\u003e\n\u003cp\u003eThe most common cause of death in the cardiac death subgroup was coronary atherosclerosis (31.1%), with no histopathological evidence of acute MI (Table \u003cspan class=\"InternalRef\"\u003e2\u003c/span\u003e). This was followed by acute MI due to coronary atherosclerosis (24.6%) and acute MI due to coronary artery thrombosis or complicated coronary atherosclerosis (14.8%). Overall, coronary atherosclerosis and its complications were the leading causes of cardiac death, accounting for 85.2% of cases.\u003c/p\u003e\n\u003cdiv class=\"gridtable\"\u003e\u0026nbsp;\u003ctable id=\"Tab2\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv class=\"CaptionNumber\"\u003eTable 2\u003c/div\u003e\n \u003cdiv class=\"CaptionContent\"\u003e\n \u003cp\u003eCause of death among cardiac death\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003ccolgroup cols=\"2\"\u003e\u003c/colgroup\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eCause of death for cardiac death cases\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eN (%)\u003c/p\u003e\n \u003cp\u003e(n\u0026thinsp;=\u0026thinsp;61)\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCoronary atherosclerosis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e19 (31.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAcute myocardial infarction due to coronary atherosclerosis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e15 (24.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAcute myocardial infarction due to coronary artery thrombosis or complicated coronary atherosclerosis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e9 (14.8)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCoronary artery thrombosis or complicated coronary atherosclerosis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e4 (6.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCardiac tamponade due to ruptured aortic dissection\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e3 (4.9)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAcute myocardial infarction with non-obstructive coronary arteries\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e2 (3.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eIschaemic heart disease\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e2 (3.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eSudden arrhythmic death syndrome\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e2 (3.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCardiac tamponade due to ruptured acute myocardial infarction due to coronary atherosclerosis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e1 (1.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCoronary artery anomaly\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e1 (1.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMyocarditis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e1 (1.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCardiomyopathy\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e1 (1.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCardiac sarcoidosis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e1 (1.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003c/table\u003e\n\u003c/div\u003e\n\u003cdiv id=\"Sec11\" class=\"Section2\"\u003e\n \u003ch2\u003eInsert Table\u0026nbsp;\u003cspan class=\"InternalRef\"\u003e2\u003c/span\u003e\u003c/h2\u003e\n \u003cp\u003eFollowing natural death (54.6%), the second most common manner of death in medicolegal autopsy cases at HSAJB was accidental death (37.1%), followed by suicide (4.9%), misadventure (2.1%), homicide (0.7%), and unascertained causes (0.7%).\u003c/p\u003e\n\u003c/div\u003e\n\u003cdiv id=\"Sec12\" class=\"Section2\"\u003e\n \u003ch2\u003eSociodemographic data and their association with sudden cardiac death\u003c/h2\u003e\n \u003cp\u003eAmong the 143 cases, male subjects comprised the majority, with 123 cases (86.0%), while female subjects accounted for 20 cases (14.0%). Both SCD and unnatural deaths (non-SCD) predominantly involved males (85.9\u0026ndash;86.2%) compared to females. However, there was no significant association between SCD and sex (p\u0026thinsp;=\u0026thinsp;0.965). SCD (54.5%) and unnatural deaths (45.5%) were equally represented among male subjects.\u003c/p\u003e\n \u003cp\u003eThe largest proportion of medicolegal autopsy cases were from the age group of 36\u0026ndash;59 years (54.5%), followed by 18\u0026ndash;35 years (37.1%) and those aged 60 years and above (8.4%). There was a significant association between SCD and age (p\u0026thinsp;\u0026lt;\u0026thinsp;0.001), with the 36\u0026ndash;59 years age group (69.2%) being the most prevalent in SCD cases. Conversely, the most common age group for unnatural deaths was 18\u0026ndash;35 years (53.8%).\u003c/p\u003e\n \u003cp\u003eThe majority of subjects were Malay (37.8%), with the remainder comprising Chinese (29.3%), Indian (23.1%), and other ethnicities (10.5%). Malays were the predominant ethnicity in SCD cases (42.3%), followed by Chinese (29.5%), and both Indian and other ethnicities (14.1% each). There was a significant association between SCD and ethnicity (p\u0026thinsp;=\u0026thinsp;0.017), with SCD being most common among Malays.\u003c/p\u003e\n\u003c/div\u003e\n\u003cdiv id=\"Sec13\" class=\"Section2\"\u003e\n \u003ch2\u003eTroponin I level in cardiac death cases\u003c/h2\u003e\n \u003cdiv id=\"Sec14\" class=\"Section3\"\u003e\n \u003ch2\u003eAssociation between myocardial infarction and non-myocardial infarction with troponin I level\u003c/h2\u003e\n \u003cp\u003eAmong the 61 cases of cardiac death, elevated troponin I (\u0026ge;\u0026thinsp;9.5 ng/ml) was observed in 39 cases (63.9%), while 22 cases (36.1%) had normal troponin I levels (\u0026lt;\u0026thinsp;9.5 ng/ml) (Table \u003cspan class=\"InternalRef\"\u003e3\u003c/span\u003e). A significant difference in troponin I levels was found between MI and non-MI cases (p\u0026thinsp;=\u0026thinsp;0.004). Most MI cases (71.7%) exhibited elevated troponin I levels, whereas a majority of non-MI cases (87.5%) had normal troponin I levels. The MI subgroup was the primary contributor to elevated troponin I cases (97.4%; 38 cases).\u003c/p\u003e\n \u003cdiv class=\"gridtable\"\u003e\u0026nbsp;\u003ctable id=\"Tab3\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv class=\"CaptionNumber\"\u003eTable 3\u003c/div\u003e\n \u003cdiv class=\"CaptionContent\"\u003e\n \u003cp\u003eRelationship between myocardial infarction and non-myocardial infarction with troponin I\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003ccolgroup cols=\"6\"\u003e\u003c/colgroup\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\" rowspan=\"2\"\u003e\n \u003cp\u003eHistopathological findings of heart\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\" colspan=\"2\"\u003e\n \u003cp\u003eTroponin I level (ng/ml)\u003c/p\u003e\n \u003cp\u003eNo. (%)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\" rowspan=\"2\"\u003e\n \u003cp\u003eNo. (%)\u003c/p\u003e\n \u003cp\u003e(n\u0026thinsp;=\u0026thinsp;61)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\" rowspan=\"2\"\u003e\n \u003cp\u003eChi-square value (\u0026chi;\u003csup\u003e2\u003c/sup\u003e)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\" rowspan=\"2\"\u003e\n \u003cp\u003ep-value\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003e\u0026lt;\u0026thinsp;9.5\u003c/p\u003e\n \u003cp\u003e(n\u0026thinsp;=\u0026thinsp;22)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003e\u0026ge;\u0026thinsp;9.5\u003c/p\u003e\n \u003cp\u003e(n\u0026thinsp;=\u0026thinsp;39)\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMyocardial infarction\u003csup\u003ea\u003c/sup\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e15\u003c/p\u003e\n \u003cp\u003e(28.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e38\u003c/p\u003e\n \u003cp\u003e(71.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e53\u003c/p\u003e\n \u003cp\u003e(86.9)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e10.564\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.004\u003csup\u003eb,\u003c/sup\u003e*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNon-myocardial infarction\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e7\u003c/p\u003e\n \u003cp\u003e(87.5)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003cp\u003e(12.5)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e8\u003c/p\u003e\n \u003cp\u003e(13.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003ctfoot\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"6\"\u003e\u003csup\u003ea\u003c/sup\u003eMyocardial infarction subgroup consisted of acute, subacute and healed myocardial infarction. \u003csup\u003eb\u003c/sup\u003ePearson Chi-square with continuous correction. *p\u0026thinsp;\u0026lt;\u0026thinsp;0.05\u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tfoot\u003e\n \u003c/table\u003e\n \u003c/div\u003e\n \u003c/div\u003e\n\u003c/div\u003e\n\u003cdiv id=\"Sec15\" class=\"Section2\"\u003e\n \u003ch2\u003eInsert Table\u0026nbsp;\u003cspan class=\"InternalRef\"\u003e3\u003c/span\u003e\u003c/h2\u003e\n \u003cp\u003e\u003cem\u003eAssociation between acute myocardial infarction and subacute and healed (non-acute) myocardial infarction with troponin I level\u003c/em\u003e\u003c/p\u003e\n \u003cp\u003eAmong the 53 cases of MI, elevated troponin I was observed in 38 cases (71.7%) (Table \u003cspan class=\"InternalRef\"\u003e4\u003c/span\u003e). A minority of MI cases (28.3%) had normal troponin I levels despite histopathological evidence of MI. No significant difference was found between acute and subacute and healed (non-acute) MI regarding troponin I levels (p\u0026thinsp;=\u0026thinsp;0.763). Both acute (73.3%) and subacute and healed MI (69.6%) showed a tendency for elevated troponin I.\u003c/p\u003e\n \u003cdiv class=\"gridtable\"\u003e\u0026nbsp;\u003ctable id=\"Tab4\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv class=\"CaptionNumber\"\u003eTable 4\u003c/div\u003e\n \u003cdiv class=\"CaptionContent\"\u003e\n \u003cp\u003eRelationship between acute myocardial infarction and subacute and healed (non-acute) myocardial infarction with troponin I\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003ccolgroup cols=\"6\"\u003e\u003c/colgroup\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\" rowspan=\"2\"\u003e\n \u003cp\u003eHistopathological findings of heart\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\" colspan=\"2\"\u003e\n \u003cp\u003eTroponin I level (ng/ml)\u003c/p\u003e\n \u003cp\u003eNo. (%)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\" rowspan=\"2\"\u003e\n \u003cp\u003eNo. (%)\u003c/p\u003e\n \u003cp\u003e(n\u0026thinsp;=\u0026thinsp;53)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\" rowspan=\"2\"\u003e\n \u003cp\u003eChi-square value (\u0026chi;\u003csup\u003e2\u003c/sup\u003e)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\" rowspan=\"2\"\u003e\n \u003cp\u003ep-value\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003e\u0026lt;\u0026thinsp;9.5\u003c/p\u003e\n \u003cp\u003e(n\u0026thinsp;=\u0026thinsp;15)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003e\u0026ge;\u0026thinsp;9.5\u003c/p\u003e\n \u003cp\u003e(n\u0026thinsp;=\u0026thinsp;38)\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAcute myocardial infarction\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e8\u003c/p\u003e\n \u003cp\u003e(26.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e22\u003c/p\u003e\n \u003cp\u003e(73.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e30\u003c/p\u003e\n \u003cp\u003e(56.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.091\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.763\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eSubacute and healed myocardial infarction\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e7\u003c/p\u003e\n \u003cp\u003e(30.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e16\u003c/p\u003e\n \u003cp\u003e(69.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e23\u003c/p\u003e\n \u003cp\u003e(43.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003c/table\u003e\n \u003c/div\u003e\n\u003c/div\u003e\n\u003cdiv id=\"Sec16\" class=\"Section2\"\u003e\n \u003ch2\u003eInsert Table\u0026nbsp;\u003cspan class=\"InternalRef\"\u003e4\u003c/span\u003e\u003c/h2\u003e\n \u003cdiv id=\"Sec17\" class=\"Section3\"\u003e\n \u003ch2\u003eGross and histopathological findings of coronary arteries\u003c/h2\u003e\n \u003cp\u003eThe majority of coronary arteries (53.8%) exhibited no pathology. The most common gross pathology found in the coronary arteries was uncomplicated coronary atherosclerosis (Fig. \u003cspan class=\"InternalRef\"\u003e1\u003c/span\u003e), present in 41.3% of specimens, followed by coronary artery thrombosis (3.3%) and intraplaque hemorrhage (0.9%). A significant proportion of cardiac death cases with coronary atherosclerosis exhibited critical coronary artery occlusion (61.2%). This significant occlusion was most frequently observed in the left anterior descending artery (LAD) (48.2%), followed by the right coronary artery (RCA) (23.5%) and the left circumflex artery (LCX) (22.4%).\u003c/p\u003e\n \u003c/div\u003e\n\u003c/div\u003e\n\u003cdiv id=\"Sec18\" class=\"Section2\"\u003e\n \u003ch2\u003eInsert Fig.\u0026nbsp;\u003cspan class=\"InternalRef\"\u003e1\u003c/span\u003e\u003c/h2\u003e\n \u003cp\u003eNo microscopic pathology was found in 6.3% of the sampled coronary arteries. The predominant histopathological finding in coronary arteries was uncomplicated coronary atherosclerosis, present in 70.0% of specimens, followed by intraplaque hemorrhage (12.5%) and coronary artery thrombosis (3.8%).\u003c/p\u003e\n\u003c/div\u003e\n\u003cdiv id=\"Sec19\" class=\"Section2\"\u003e\n \u003ch2\u003eGross and histopathological findings of heart\u003c/h2\u003e\n \u003cp\u003eAmong the examined hearts, 70.5% exhibited gross pathology, while 29.5% showed no gross pathology. Fibrosis was the most common gross finding, observed in 50.8% of samples, followed by cardiomegaly (19.7%) and hemorrhage (16.4%) (Table \u003cspan class=\"InternalRef\"\u003e5\u003c/span\u003e).\u003c/p\u003e\n \u003cdiv class=\"gridtable\"\u003e\u0026nbsp;\u003ctable id=\"Tab5\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv class=\"CaptionNumber\"\u003eTable 5\u003c/div\u003e\n \u003cdiv class=\"CaptionContent\"\u003e\n \u003cp\u003ePrevalence of gross heart findings in adults aged 18 years and above\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003ccolgroup cols=\"2\"\u003e\u003c/colgroup\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eGross findings of the heart\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eTotal\u003c/p\u003e\n \u003cp\u003eNo. (%) (n\u0026thinsp;=\u0026thinsp;61)\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003e\u003cem\u003ePresence of gross finding of the heart\u003c/em\u003e\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003e\u003cem\u003e43 (70.5)\u003c/em\u003e\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eFibrosis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e31 (50.8)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCardiomegaly\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e12 (19.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHaemorrhage\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e10 (16.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eThinning of ventricular wall\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e8 (13.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eThickened left ventricular wall\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e7 (11.5)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eDilated appearance of the heart chamber\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e7 (11.5)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eThickened interventricular septum\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e5 (8.2)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eOthers\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e5 (8.2)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCardiac tamponade\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e4 (6.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003ePale myocardium\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e4 (6.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMottled appearance\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e4 (6.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eThickened right ventricular wall\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e2 (3.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eYellow-tan discolouration\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e2 (3.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eRuptured myocardium\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e1 (1.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eReplacement/infiltration of myocardium by fats\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e1 (1.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eNo gross finding of the heart\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e\u003cstrong\u003e18 (29.5)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003c/table\u003e\n \u003c/div\u003e\n\u003c/div\u003e\n\u003cdiv id=\"Sec20\" class=\"Section2\"\u003e\n \u003ch2\u003eInsert Table \u003cspan class=\"InternalRef\"\u003e5\u003c/span\u003e\u003c/h2\u003e\n \u003cp\u003eHistopathological findings were present in 91.8% of the examined hearts, with only 8.2% showing no microscopic findings (Table \u003cspan class=\"InternalRef\"\u003e6\u003c/span\u003e). Interstitial/replacement fibrosis was the most frequently observed microscopic finding, noted in 82.0% of cases, followed by contraction band/coagulative necrosis (34.4%), and infiltration by inflammatory cells (26.3%) (Fig. \u003cspan class=\"InternalRef\"\u003e1\u003c/span\u003e).\u003c/p\u003e\n \u003cdiv class=\"gridtable\"\u003e\u0026nbsp;\u003ctable id=\"Tab6\" border=\"1\" class=\"fr-table-selection-hover\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv class=\"CaptionNumber\"\u003eTable 6\u003c/div\u003e\n \u003cdiv class=\"CaptionContent\"\u003e\n \u003cp\u003eHistopathological findings of the heart\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003ccolgroup cols=\"2\"\u003e\u003c/colgroup\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eHistopathological findings of the heart\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eTotal\u003c/p\u003e\n \u003cp\u003eNo. (%) (n\u0026thinsp;=\u0026thinsp;61)\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003e\u003cem\u003ePresence of histopathological finding of the heart\u003c/em\u003e\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003e\u003cem\u003e56 (91.8)\u003c/em\u003e\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eInterstitial/replacement fibrosis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e50 (82.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eContraction band/coagulative necrosis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e21 (34.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eInfiltration by inflammatory cells\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e16 (26.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHypertrophy of myocytes\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e15 (24.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003ePerivascular fibrosis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e14 (23.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHaemorrhage\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e13 (21.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eGranulation tissue\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e12 (19.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eInterstitial oedema\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e9 (14.8)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMyocyte hypereosinophilia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e8 (13.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eWaviness of myocytes\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e4 (6.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eReplacement/infiltration of myocardium by fats\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e4 (6.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eOthers\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e4 (6.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMyocardial bridging\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e2 (3.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMural thrombus\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e1 (1.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eRuptured myocardium\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e1 (1.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eNo histopathological finding of the heart\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e\u003cstrong\u003e5 (8.2)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003c/table\u003e\n \u003c/div\u003e\n\u003c/div\u003e\n\u003cdiv id=\"Sec21\" class=\"Section2\"\u003e\n \u003ch2\u003eInsert Table\u0026nbsp;\u003cspan class=\"InternalRef\"\u003e6\u003c/span\u003e\u003c/h2\u003e\n\u003c/div\u003e"},{"header":"DISCUSSION","content":"\u003cp\u003eSudden cardiac death (SCD) remains a significant issue in public health and emergency medicine and is a major contributor to medicolegal autopsy cases globally. The Department of Forensic Medicine at HSAJB, one of only two autopsy centers in Johor Bahru with a population of approximately 1.71\u0026nbsp;million, reported a SCD prevalence of 54.6%.\u003csup\u003e14\u003c/sup\u003e This is notably higher compared to other studies, which have reported prevalence rates ranging from 30% to 37.8%. \u003csup\u003e6,15\u003c/sup\u003e Additionally, cardiac diseases were the leading cause of SCD, accounting for 78.2% of cases in this study. This finding aligns with previous studies by Kumar \u003cem\u003eet al.\u003c/em\u003e (2007) and Rahimi \u003cem\u003eet al.\u003c/em\u003e (2018), which reported cardiac diseases as responsible for 64.9% to 75.8% of SCDs.\u003csup\u003e\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e,\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e\u003c/sup\u003e Our study revealed that the most common cause of cardiac death was ischaemic heart disease/coronary atherosclerosis, accounting for 85.2% of cases, which was consistent with findings from previous studies, which reported rates between 75% and 80%.\u003csup\u003e17,18\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eOne factor contributing to the high prevalence of SCD in this study is the increase in obesity and diabetes rates globally during the early 2000s, which are key risk factors for coronary atherosclerosis.\u003csup\u003e\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e\u003c/sup\u003e The low health screening rates among Malaysians, ranging from 10% to 49.7%, may also contribute to the high prevalence of cardiac death.\u003csup\u003e\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e,\u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e\u003c/sup\u003e Additionally, the majority of cardiac death cases in this study were individuals aged 36\u0026ndash;59 years (73.8%), a group where ischaemic heart disease/coronary atherosclerosis is more prevalent compared to congenital heart anomalies, cardiomyopathy, myocarditis, and arrhythmic disorders.\u003csup\u003e\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e,\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eThe study's findings align with those observed in Western societies, where approximately 15% of overall SCD is attributed to non-ischemic structural heart diseases, such as cardiomyopathy and infiltrative diseases like sarcoidosis and amyloidosis.\u003csup\u003e\u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e,\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e\u003c/sup\u003e In this study, 3.3% of cardiac death cases had negative autopsies with a presumptive cause of sudden arrhythmic death syndrome, though genetic studies were not performed. This percentage is lower than reported by Murakoshi \u003cem\u003eet al.\u003c/em\u003e and Winkel \u003cem\u003eet al.\u003c/em\u003e (10\u0026ndash;29%).\u003csup\u003e25,26\u003c/sup\u003e The difference may be because individuals under 35 years old, who are commonly affected by sudden arrhythmic death syndrome, represented only 18.0% of cardiac death cases in this study. Notably, all cases of sudden arrhythmic death syndrome in this study involved two men under 35 years old.\u003c/p\u003e \u003cp\u003eThis study found a male predominance in SCD cases; however, no significant association between SCD and sex was established. The male-to-female ratio in SCD cases ranged from 4.8 to 5, as reported by Ding \u003cem\u003eet al.\u003c/em\u003e and Eckart \u003cem\u003eet al\u003c/em\u003e.\u003csup\u003e7,27\u003c/sup\u003e. A Malaysian study from 2020 reported an even greater male predominance, with a 39-fold difference.\u003csup\u003e\u003cspan citationid=\"CR28\" class=\"CitationRef\"\u003e28\u003c/span\u003e\u003c/sup\u003e Researchers suggest that this male predominance may be attributed to the protective effects of oestrogen, which has both immediate and long-term impacts, including athero-protective effects on serum lipid concentrations and direct effects on blood vessels.\u003csup\u003e\u003cspan citationid=\"CR29\" class=\"CitationRef\"\u003e29\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eA significant association between SCD and age was observed, with the majority of cases occurring in individuals aged 36\u0026ndash;59 years. This contrasts with other studies that report an increased incidence of SCD with advancing age.\u003csup\u003e\u003cspan citationid=\"CR28\" class=\"CitationRef\"\u003e28\u003c/span\u003e,\u003cspan citationid=\"CR30\" class=\"CitationRef\"\u003e30\u003c/span\u003e\u003c/sup\u003e This discrepancy may be due to the lower rate of medicolegal autopsies for SCD cases among individuals aged 60 years and above at our center.\u003c/p\u003e \u003cp\u003eOur study also found a significant association between SCD and ethnicity, with SCD being more prevalent among Malays. This finding differs from studies by Kumar \u003cem\u003eet al.\u003c/em\u003e and Ly \u003cem\u003eet al.\u003c/em\u003e, which reported higher SCD prevalence among Indians and Chinese in Malaysia.\u003csup\u003e\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e,\u003cspan citationid=\"CR28\" class=\"CitationRef\"\u003e28\u003c/span\u003e\u003c/sup\u003e INTERHEART research suggests that Indians in Asia face a higher risk of developing cardiac disease earlier in life compared to other races due to a shared history of diabetes, which is closely linked to cardiac disease.\u003csup\u003e\u003cspan citationid=\"CR31\" class=\"CitationRef\"\u003e31\u003c/span\u003e,\u003cspan citationid=\"CR32\" class=\"CitationRef\"\u003e32\u003c/span\u003e\u003c/sup\u003e The cultural and genetic diversity among Malaysia's multi-ethnic population may contribute to unique cardiovascular morbidity and mortality risks that differ from those observed in Western populations.\u003csup\u003e\u003cspan citationid=\"CR33\" class=\"CitationRef\"\u003e33\u003c/span\u003e\u003c/sup\u003e Ismail \u003cem\u003eet al.\u003c/em\u003e found higher associations of hypertension and left bundle branch block in Malays and aborigines, while Indians showed a higher association with left ventricular ejection fraction\u0026thinsp;\u0026le;\u0026thinsp;40%.\u003csup\u003e34\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eCardiac troponin is released swiftly from myocytes following myocardial damage and can be detected in the blood within 3\u0026ndash;4 hours. It typically peaks after 16\u0026ndash;18 hours and remains detectable for up to 10\u0026ndash;21 days, which aids in diagnosis.\u003csup\u003e\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e,\u003cspan citationid=\"CR35\" class=\"CitationRef\"\u003e35\u003c/span\u003e\u003c/sup\u003e Our study found a significant difference between MI and non-MI cases in terms of troponin I levels, with a majority of MI cases (71.7%) exhibiting elevated levels. This finding aligns with Ooi \u003cem\u003eet al.\u003c/em\u003e, who found that the troponin I levels in MI group differed significantly from those of the no-pathology group.\u003csup\u003e\u003cspan citationid=\"CR36\" class=\"CitationRef\"\u003e36\u003c/span\u003e\u003c/sup\u003e However, our result is in contrast with the finding of preceding study by Banon \u003cem\u003eet al.\u003c/em\u003e which demonstrated that there were no statistically significant differences between ischaemic deaths and non-ischaemic death for high-sensitivity troponin I.\u003csup\u003e37\u003c/sup\u003e Factors contributing to false-negative results in our study included autolysis, microbial degradation, and the natural metabolic processes that occur post-mortem, despite troponin I typically increasing in a time-dependent manner, particularly if the post-mortem interval exceeds 48 hours.\u003csup\u003e\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eOur study did not find a significant difference between acute and subacute and healed (non-acute) MI in relation to troponin I levels. Both acute (73.3%) and subacute and healed MI (69.6%) cases showed elevated troponin I levels. We have been unable to find similar preceding research for this parameter to compare our results. However, Ooi \u003cem\u003eet al.\u003c/em\u003e found a significant difference between the troponin I level and the odds ratios for acute and subacute MI with healed MI, which was in contrast with our study.\u003csup\u003e\u003cspan citationid=\"CR36\" class=\"CitationRef\"\u003e36\u003c/span\u003e\u003c/sup\u003e The false-positive result in our study could be due to post-mortem time-dependent increases in troponin levels. Additionally, cardiac troponin can be detected in the blood earlier (about 3 hours) compared to the earliest histopathological changes, such as coagulative necrosis, which are detectable within the first 6 to 12 hours.\u003csup\u003e\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e,\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e\u003c/sup\u003e Furthermore, troponin I can persist in the blood for up to 10\u0026ndash;21 days, which may result in false positives as the MI progresses from the acute to subacute phase. Other potential sources of analytical interference, such as heterophilic antibodies, fibrin clots, and haemolysis, should also be considered when interpreting post-mortem troponin I results \u003csup\u003e\u003cspan citationid=\"CR35\" class=\"CitationRef\"\u003e35\u003c/span\u003e,\u003cspan citationid=\"CR38\" class=\"CitationRef\"\u003e38\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eIn this study, the most prevalent coronary artery pathology was uncomplicated coronary atherosclerosis, observed in 41.3% of cases. Complications of this condition, including intraplaque hemorrhage and coronary artery thrombosis, were the next most frequent pathologies. These results align with findings from Wagh \u003cem\u003eet al\u003c/em\u003e.\u003csup\u003e39\u003c/sup\u003e However, our results differ from those of Waller \u003cem\u003eet al.\u003c/em\u003e, who reported tunneled coronary arteries (myocardial bridging) (23.1%) as the most common cardiac pathology, as opposed to atherosclerotic coronary heart disease (20.6%).\u003csup\u003e40\u003c/sup\u003e This discrepancy may be attributed to differences in study populations.\u003c/p\u003e \u003cp\u003eOur study found that the left anterior descending artery (LAD) was the most commonly affected artery (37.6%), which is consistent with findings from Shubhangi \u003cem\u003eet al.\u003c/em\u003e and Wagh \u003cem\u003eet al\u003c/em\u003e.\u003csup\u003e39,41\u003c/sup\u003e Fibrosis was notably the most frequent finding in our study, present in 50.8% of gross specimens and 82.0% of histopathological specimens. This was followed by acute MI changes. These results are consistent with studies by Nisha \u003cem\u003eet al.\u003c/em\u003e and Wagh \u003cem\u003eet al.\u003c/em\u003e, where fibrosis was more commonly observed than acute MI.\u003csup\u003e39,42\u003c/sup\u003e In contrast, a 2018 study in India found cardiac adiposity (23.0%) to be the most common cardiac morphology, followed by atherosclerotic coronary heart disease (21.1%) and left ventricular hypertrophy (19.0%).\u003csup\u003e43\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eThe high prevalence of fibrosis in cardiac death cases in our study suggests that many subjects had a history of previous MI, regardless of the cause and whether they were symptomatic, before their deaths. This finding highlights the chronic nature of their cardiac pathology, which could have been identified through regular health screenings or medical consultations during the progression of their diseases.\u003c/p\u003e \u003cdiv id=\"Sec23\" class=\"Section2\"\u003e \u003ch2\u003eLIMITATION OF STUDY\u003c/h2\u003e \u003cp\u003eDifference in the post-mortem interval and haemolysis of the post-mortem blood samples were among the factors and interferences that pose limitation in this study. There remains the issue of clinically validated cut-off concentrations in post-mortem samples of point-of-care troponin I, thus further work is necessary to establish appropriate diagnostic cut-off values in the respective forensic laboratory. The statistical interpretation of the study could be limited by the small sample size of female participants.\u003c/p\u003e \u003c/div\u003e"},{"header":"CONCLUSION","content":"\u003cp\u003eCoronary atherosclerosis and its complications were the most common causes of cardiac death, predominantly affecting individuals aged 36\u0026ndash;59 years and those of Malay ethnicity. Therefore, annual health screenings and awareness campaigns should be specifically targeted towards Malay individuals aged 36 and older to help prevent SCD.\u003c/p\u003e \u003cp\u003eThis study demonstrated that although there was a significant difference in troponin I levels between MI and non-MI cases, however, no significant difference was found between acute with subacute and healed (non-acute) MI in relation to troponin I levels. Consequently, it is plausible to consider using troponin I as an auxiliary investigation rather than as a sole diagnostic tool for MI while exercising caution during interpretation of result.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cdiv class=\"DefinitionList\"\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eSCD\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eSudden cardiac death\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eMI\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003emyocardial infarction\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eWHO\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eWorld Health Organization\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eEDTA\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eethylenediaminetetraacetic acid\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eCLIA\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eClinical Laboratory Improvement Amendments\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eLAD\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eleft anterior descending artery\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eRCA\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eright coronary artery\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eLCX\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eleft circumflex artery\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003c/div\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cem\u003eEthical approval and consent to participate\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003eThe data were obtained from the post-mortem reports. Ethical clearance had been obtained from the Medical Research \u0026amp; Ethics Committee, Ministry of Health Malaysia (Reference number: 22-02449-F23) and Research Ethics Committee of the Faculty Medicine, Universiti Kebangsaan Malaysia (Reference number: UKM PPI/111/8/JEP-2022-653).\u0026nbsp;Informed consent was obtained from the next of kin or guardian of all the studied subjects in the study.\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eConsent for publication\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003eWe would also like to thank the Director General of Health Malaysia for his permission to publish this article.\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eFunding\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003eNone\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eHayashi M, Shimizu W, Albert CM. The spectrum of epidemiology underlying sudden cardiac death. 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J Am Coll Cardiol. 2004 Sep 15;44(6):1268-75. doi: 10.1016/j.jacc.2004.06.029.\u003c/li\u003e\n\u003cli\u003eZheng ZJ, Croft JB, Giles WH, Mensah GA. Sudden cardiac death in the United States, 1989 to 1998. Circulation. 2001 Oct 30;104(18):2158-63. doi: 10.1161/hc4301.098254.\u003c/li\u003e\n\u003cli\u003eMurakoshi N, Aonuma K. Epidemiology of arrhythmias and sudden cardiac death in Asia. Circ J. 2013;77(10):2419-31. doi: 10.1253/circj.cj-13-1129.\u003c/li\u003e\n\u003cli\u003eWinkel BG, Holst AG, Theilade J, \u003cem\u003eet al\u003c/em\u003e. Nationwide study of sudden cardiac death in persons aged 1-35 years. Eur Heart J. 2011 Apr;32(8):983-90. doi: 10.1093/eurheartj/ehq428.\u003c/li\u003e\n\u003cli\u003eEckart RE, Shry EA, Burke AP \u003cem\u003eet al.\u003c/em\u003e Sudden death in young adults: An autopsy-based series of a population undergoing active surveillance. J Am Coll Cardiol. 2011 Sep 13;58(12):1254-61. doi: 10.1016/j.jacc.2011.01.049.\u003c/li\u003e\n\u003cli\u003eLy CK, Nadesan K, Samberkar SP, Byard RW, Samberkar PN. Ethnic variability in mortality from ischaemic heart disease/cardiomegaly in Malaysia. Med Leg J. 2021 Mar;89(1):37-39. doi: 10.1177/0025817220960597.\u003c/li\u003e\n\u003cli\u003eWinkel BG, Risgaard B, Bjune T, \u003cem\u003eet al.\u003c/em\u003e Gender differences in sudden cardiac death in the young-a nationwide study. BMC Cardiovasc Disord. 2017 Jan 7;17(1):19. doi: 10.1186/s12872-016-0446-5.\u003c/li\u003e\n\u003cli\u003eShuvy M, Qiu F, Lau G, \u003cem\u003eet al\u003c/em\u003e. Temporal trends in sudden cardiac death in Ontario, Canada. Resuscitation. 2019 Mar;136:1-7. doi: 10.1016/j.resuscitation.2019.01.010.\u003c/li\u003e\n\u003cli\u003eJha AK, Varosy PD, Kanaya AM, \u003cem\u003eet al.\u003c/em\u003e Differences in medical care and disease outcomes among black and white women with heart disease. Circulation. 2003 Sep 2;108(9):1089-94. doi: 10.1161/01.CIR.0000085994.38132.E5.\u003c/li\u003e\n\u003cli\u003eRodriguez CJ, Allison M, Daviglus ML, \u003cem\u003eet al.\u003c/em\u003e Status of cardiovascular disease and stroke in Hispanics/Latinos in the United States: a science advisory from the American Heart Association. Circulation. 2014 Aug 12;130(7):593-625. doi: 10.1161/CIR.0000000000000071.\u003c/li\u003e\n\u003cli\u003eDans A, Ng N, Varghese C, Tai ES, Firestone R, Bonita R. The rise of chronic non-communicable diseases in Southeast Asia: Time for action. Lancet. 2011 Feb 19;377(9766):680-9. doi: 10.1016/S0140-6736(10)61506-1.\u003c/li\u003e\n\u003cli\u003eIsmail SR, Mohammad MSF, Butterworth AS, \u003cem\u003eet al.\u003c/em\u003e Risk factors of secondary cardiovascular events in a multi-ethnic Asian population with acute myocardial infarction: A retrospective cohort study from Malaysia. J Cardiovasc Dev Dis. 2023 Jun 9;10(6):250. doi: 10.3390/jcdd10060250.\u003c/li\u003e\n\u003cli\u003eKorff S, Katus HA, Giannitsis E. Differential diagnosis of elevated troponins. Heart. 2006 Jul;92(7):987-93. doi: 10.1136/hrt.2005.071282.\u003c/li\u003e\n\u003cli\u003eOoi DS, Isotalo PA, Veinot JP. Correlation of antemortem serum creatine kinase, creatine kinase-MB, troponin I, and troponin T with cardiac pathology. Clin Chem. 2000 Mar;46(3):338-44. doi: https://doi.org/10.1093/clinchem/46.3.338\u003c/li\u003e\n\u003cli\u003eBa\u0026ntilde;\u0026oacute;n R, Hern\u0026aacute;ndez-Romero D, Navarro E, P\u0026eacute;rez-C\u0026aacute;rceles MD, Noguera-Velasco JA, Osuna E. Combined determination of B-type natriuretic peptide and high-sensitivity troponin I in the postmortem diagnosis of cardiac disease. Forensic Sci Med Pathol. 2019 Dec;15(4):528-535. doi: 10.1007/s12024-019-00150-1.\u003c/li\u003e\n\u003cli\u003eMair J, Lindahl B, M\u0026uuml;ller C, \u003cem\u003eet al.\u003c/em\u003e What to do when you question cardiac troponin values. Eur Heart J Acute Cardiovasc Care. 2018 Sep;7(6):577-586. doi: 10.1177/2048872617708973.\u003c/li\u003e\n\u003cli\u003eWagh AV, Kulkarni K, Gadpal RR, Wagh RV. Histomorphological spectrum of various cardiac changes in sudden death: An autopsystudy. International Journal of Scientific Research. 2022.11(01),10\u0026ndash;13. doi: https://doi.org/10.36106/ijsr/2000407\u003c/li\u003e\n\u003cli\u003eWaller BF, Catellier MJ, Clark MA, Hawley DA, Pless JE. Cardiac pathology in 2007 consecutive forensic autopsies. Clin Cardiol. 1992 Oct;15(10):760-5. doi: 10.1002/clc.4960151014.\u003c/li\u003e\n\u003cli\u003eShubhangi VA., Pragya VJain., Grace F. \u003cem\u003eet al.\u003c/em\u003e An autopsy study of the histopathological spectrum of cardiac diseases in cases of sudden death [Internet]. 2022. [cited on 2024 July 28]. Available from: https://1library.net/document/zwk73m0z-autopsy-studyhistopathological-spectrum-cardiac-diseases-cases-sudden.html \u003c/li\u003e\n\u003cli\u003eNisha M, Bhawna S, Sumiti G, et al. Histomorphological spectrum of various cardiac changes in sudden death: An autopsy study. Iranian Journal of Pathology. 6(4), 179\u0026ndash;186. [Internet]. 2011. [cited on 2024 July 24]. Available from: http://ijp.iranpath.org/article_8515_bafd03eba96f11265dba34b10feb68a6.pdf \u003c/li\u003e\n\u003cli\u003eKhandekar DS, Mahadani J. Histomorphological analysis of various heart diseases: An autopsy study. Journal of Medical Science and Clinical Research. 2018;6(8). doi: https://doi.org/10.18535/jmscr/v6i8.192\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"coronary artery, forensic, heart, sudden cardiac death, Troponin I","lastPublishedDoi":"10.21203/rs.3.rs-8452675/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8452675/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cstrong\u003eIntroduction: \u003c/strong\u003eSudden cardiac death (SCD) accounts for an estimated 15% to 20% of all deaths globally and is a leading cause of mortality.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eMethods:\u003c/strong\u003e A cross-sectional study over 1-year (2023) recruiting medicolegal autopsy cases that were conducted in the Department of Forensic Medicine, Hospital Sultanah Aminah Johor Bahru (HSAJB), Malaysia. The relationship between point-of-care troponin I level and myocardial infarction (MI) was analysed. The morphology of the heart and coronary artery in cardiac death was also recorded.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eResults:\u003c/strong\u003e A total of 143 cases were analyzed. Cardiac death was responsible for 78.2% of SCD. The leading cause of cardiac death was coronary atherosclerosis (31.1%). Significant association was demonstrated between SCD and the age group of 36–59 years old (p\u0026lt;0.001) and Malay ethnicity (p=0.017). No significant association between SCD and sex. Notably, a significant difference in troponin I levels between MI and non-MI cases (p=0.004), with the majority of MI cases (71.7%) showing elevated troponin I levels. No significant difference was observed in troponin I levels between acute and subacute and healed MI (p=0.763). The most common gross and histopathological finding in the coronary arteries was uncomplicated coronary atherosclerosis (41.3% gross; 70.0% histopathology). Fibrosis was the predominant macroscopic (50.8%) and microscopic (82.0%) finding in the heart.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConclusion: \u003c/strong\u003eCoronary atherosclerosis and its complications were identified as the most common causes of cardiac death. It is plausible to consider using troponin I as an auxiliary investigation rather than as a sole diagnostic tool for MI, while exercising caution during the interpretation of results.\u003c/p\u003e","manuscriptTitle":"Troponin Clues: An Academic Reappraisal of Cardiac and Coronary Artery Pathologies in Sudden Death among Medicolegal Autopsies","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-01-01 06:17:39","doi":"10.21203/rs.3.rs-8452675/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"17a8b0ec-d6fa-4160-9c32-73a04bb390e9","owner":[],"postedDate":"January 1st, 2026","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2026-04-12T08:40:01+00:00","versionOfRecord":[],"versionCreatedAt":"2026-01-01 06:17:39","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-8452675","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-8452675","identity":"rs-8452675","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}