Spontaneous Subarachnoid Hemorrhage and the Heart: The Silent Threat to Atrial Electrical Activity

Spontaneous Subarachnoid Hemorrhage and the Heart: The Silent Threat to Atrial Electrical Activity | 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 Spontaneous Subarachnoid Hemorrhage and the Heart: The Silent Threat to Atrial Electrical Activity Caner Sarıkaya, Fatma Özge Salkın, Cansu Sarıkaya, Eyüp Varol, and 1 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-6270952/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 9 You are reading this latest preprint version Abstract Background: Spontaneous subarachnoid hemorrhage has been associated with significant cardiovascular changes, including alterations in atrial electrical activity. This study investigates the impact of SAH on atrial function using P wave dispersion (PWD) as an electrocardiographic marker. Methods: This retrospective study included 131 individuals (50 SAH patients and 81 healthy controls) admitted to Ümraniye Training and Research Hospital. Standard 12-lead electrocardiography (ECG) was used to measure P wave dispersion (PWD), defined as the difference between the maximum (Pmax) and minimum (Pmin) P wave durations. Statistical analyses were performed using SPSS version 25.0, with comparisons between groups made using the Mann-Whitney U test and Chi-Square test where applicable. Results: The mean P wave dispersion was significantly higher in the SAH group (1.03 ± 0.5) compared to the control group (0.63 ± 0.23, p < 0.001). Additionally, ST segment elevation was observed in 5 SAH patients, while 10 showed T wave inversions and 3 had prolonged QT intervals. However, no significant troponin elevation was noted, suggesting an SAH-induced ECG alteration rather than acute myocardial infarction. Postoperatively, 30 patients exhibited no cardiac complications, while 11 had hypertension, 2 had tachycardia, 1 had bradycardia, 1 had ST elevation, and 1 developed pericardial effusion. Transient atrial fibrillation was observed in four patients, and normal sinus rhythm was restored with medical treatment. Conclusion: The findings suggest that SAH is associated with significant disruptions in atrial electrical activity, as evidenced by increased P wave dispersion. Prolonged PWD may indicate an elevated risk of atrial fibrillation, contributing to further neurological deterioration. Understanding the cardiac implications of SAH is crucial for early intervention and improved patient outcomes. P wave dispersion autonomic nervous system electrocardiography aneurysm subarachnoid haemorrhage Introduction Subarachnoid hemorrhage is a severe neurological event associated with high morbidity and mortality. Although primarily recognized for its devastating effects on the brain, SAH also induces significant cardiovascular complications, including electrocardiographic (ECG) abnormalities, myocardial injury, and increased risk of arrhythmias [ 1 , 2 ]. The pathophysiology underlying these cardiac effects is complex, involving the autonomic nervous system, catecholamine surge, and direct myocardial injury [ 3 , 4 ]. Previous studies have suggested that hypothalamic stimulation and elevated intracranial pressure contribute to these cardiovascular changes, leading to alterations in heart rate variability and increased susceptibility to arrhythmias [ 5 , 6 ]. SAH-induced ECG abnormalities, such as ST-segment changes, QT prolongation, and T wave inversion, have been widely reported [ 7 , 8 ]. These findings have significant clinical implications, as they can mimic acute coronary syndromes, potentially leading to misdiagnosis and inappropriate treatment strategies [ 9 ]. Furthermore, studies have demonstrated that the extent of ECG abnormalities correlates with the severity of neurological damage and overall prognosis in SAH patients [ 10 , 11 ]. Given this strong association between neurological injury and cardiac dysfunction, investigating the electrophysiological changes in SAH patients is essential for optimizing management strategies and reducing adverse outcomes. One key electrocardiographic parameter affected by SAH is P wave dispersion (PWD), which reflects atrial conduction abnormalities and has been identified as a predictor of atrial fibrillation [ 9 , 12 ]. Increased PWD is indicative of heterogeneous atrial conduction, which may predispose patients to AF and other arrhythmias [ 13 ]. Since AF is a major risk factor for thromboembolic events, including stroke and delayed cerebral ischemia, recognizing early changes in PWD may provide valuable insight into the cardiac complications associated with SAH and help in risk stratification [ 14 ]. Although awareness of SAH-related cardiac changes has increased, their specific impact on atrial function remains insufficiently studied. This study highlights the importance of assessing P wave dispersion in aneurysmal SAH patients to better understand its role in arrhythmogenesis. Recognizing these electrophysiological changes may facilitate early identification of patients at risk for atrial fibrillation and other arrhythmias, ultimately contributing to more effective clinical management and improved outcomes. Materials and Methods This retrospective study was approved by the Ethics Committee of Ümraniye Training and Research Hospital (Approval No: B.10.1.TKH.4.34.H.GO.0.01/350) for the period 2022–2023. The study population consisted of patients diagnosed with aneurysmal subarachnoid hemorrhage admitted to Ümraniye Training and Research Hospital, alongside a control group of healthy individuals who presented to the cardiology outpatient clinic without any additional diseases. Informed consent was obtained from all patients. Study Design and Participants Patients included in this study were diagnosed with aneurysmal SAH within the first 24 hours of bleeding and underwent standard 12-lead electrocardiography (ECG) evaluation. The control group consisted of healthy individuals without known cardiovascular, neurological, or systemic diseases. A total of 131 participants were enrolled, comprising 50 SAH patients and 81 healthy controls. The patient group was selected based on hospital admission records, and the control group was chosen from individuals undergoing routine cardiac evaluations. Inclusion Criteria Patients were included in the study if they met the following conditions: Aged 18 years or older Diagnosed with aneurysmal SAH within the first 24 hours of bleeding, confirmed by computed tomography (CT) and angiography Underwent preoperative ECG evaluation No prior history of atrial fibrillation [9] or other chronic arrhythmias Provided informed consent or had consent obtained from family members Exclusion Criteria Patients were excluded from the study if they had any of the following conditions: History of malignancy, pregnancy, or chronic systemic diseases Presence of valvular heart disease, ventricular premature beats, or atrioventricular conduction abnormalities Diagnosed with congestive heart failure, thyroid diseases, or diabetes mellitus History of alcoholism, coronary artery disease (CAD), or collagen diseases Presence of chronic obstructive pulmonary disease (COPD) or electrolyte imbalances that could affect cardiovascular function Electrocardiographic Evaluation Standard 12-lead ECGs were obtained at a paper speed of 25 mm/sec and amplitude of 10 mm/mV. ECGs were reviewed by a cardiologist for abnormalities in heart rate, rhythm, ST-segment deviations, QT intervals, and T wave morphology. P wave dispersion (PWD) was calculated by measuring the difference between the maximum (Pmax) and minimum (Pmin) P wave durations recorded across the 12 ECG leads. Tachycardia was defined as a heart rate >100 bpm, while bradycardia was defined as 410 ms) and QRS durations <100 ms were considered abnormal. Statistical Analysis The sample size calculation was performed using G Power 3.1.9.7 software (Franz Faul, Germany), with an effect size (d) of 0.711. Based on a power of 95% and a 5% margin of error, a minimum of 88 participants was required. Statistical analyses were conducted using SPSS version 25.0. The normality of continuous variables was assessed using Kolmogorov-Smirnov tests and histogram evaluations. Descriptive analyses were presented as mean, standard deviation, median, interquartile range (IQR), and min-max values. Categorical variables were compared using the Chi-Square Test, while non-normally distributed variables were analyzed using the Mann-Whitney U Test. A p-value <0.05 was considered statistically significant. Results A total of 131 individuals participated in the study, including 50 patients with aneurysmal SAH and 81 healthy controls. The mean age of the SAH group was 53.48 ± 12.74 years, while the control group had a mean age of 56.94 ± 12.36 years. There was no statistically significant difference between the groups in terms of age (p = 0.071) or gender distribution (p = 0.919) (Table 1). Table 1 : ¹Mann Whitney U Testi. ²Ki-Kare Testi. There is no significant difference between the two groups in terms of age and gender. Patient Control Total p n % N % n % Age 53,48±12,74 51,5 (29-94) 56,94±12,36 55 (24-83) 55,62±12,57 53 (24-94) 0,071¹ Gender Male 23 (46,00) 38 (46,91) 61 (46,56) 0,919² Female 27 (54,00) 43 (53,09) 70 (53,44) Demographic and Clinical Characteristics In the SAH group, 6 patients (12.0%) had diabetes, 23 patients (46.0%) had hypertension, and 3 patients (6.0%) had coronary artery disease (CAD). In contrast, the control group had 9 patients (11.1%) with diabetes and 21 patients (25.9%) with hypertension, but no cases of CAD (Table 2). Table 2 : Diabetes, Hypertension, Coronary Artery Disease, of the Patient Group Patient Group n % Diabetes No 44 (88,00) Yes 6 (12,00) HT (Hypertension) No 27 (54,00) Yes 23 (46,00) KAH (Coronary Artery Disease) No 47 (94,00) Yes 3 (6,00) Electrocardiographic Findings Analysis of preoperative ECGs in SAH patients revealed several abnormalities. ST-segment elevation was observed in 5 patients (10%), while 10 patients (20%) showed T wave inversions. QT prolongation was detected in 3 patients (6%), but troponin levels remained within normal limits, suggesting that these ECG changes were related to SAH-induced neurogenic effects rather than acute myocardial infarction (MI). P wave dispersion (PWD) was significantly prolonged in SAH patients compared to the control group (Table 3). P Wave Dispersion Analysis The mean Pmax was significantly higher in SAH patients (1.58 ± 0.5 ms) compared to controls (1.31 ± 0.42 ms), p = 0.001. The mean Pmin was lower in SAH patients (0.55 ± 0.15 ms vs. 0.67 ± 0.24 ms, p = 0.003). The mean P wave dispersion (PWD) was markedly increased in the SAH group (1.03 ± 0.5 ms) compared to controls (0.63 ± 0.23 ms), p < 0.001 (Table 3). Table 3: Mann Whitney U Test. Pmin value is higher in the control group than in the patient group. Pdisp value is higher in the patient group than in the control group. Patient Control Total p n % n % n % Pmax 1,58±0,5 1,5 (1-2,5) 1,31±0,42 1 (1-2) 1,41±0,47 1,5 (1-2,5) 0,001 Pmin 0,55±0,15 0,5 (0,5-1) 0,67±0,24 0,5 (0,5-1) 0,62±0,22 0,5 (0,5-1) 0,003 Pdisp 1,03±0,5 1 (0,5-2) 0,63±0,23 0,5 (0,05-1) 0,78±0,41 0,5 (0,05-2) <0,001 These findings suggest that SAH leads to increased atrial electrical heterogeneity, potentially predisposing patients to arrhythmias such as atrial fibrillation [9]. Postoperative Cardiac Complications Postoperatively, 34 patients (68.0%) in the SAH group exhibited no cardiac abnormalities. However, 11 patients (22.0%) developed hypertension, while 2 patients (4.0%) had tachycardia and 1 patient (2.0%) developed bradycardia. Additionally, one patient (2.0%) exhibited persistent ST-segment elevation, and one patient (2.0%) developed pericardial effusion (Table 4). Transient atrial fibrillation was observed in four patients, and normal sinus rhythm was restored with medical treatment. Table 4: Post-op Cardiac Problem Post-op cardiac problem No 34 (60,00) Hypertension 11 (22,00) Transient Atrial Fibrillation 4 (8,00) Tachycardia 2 (4,00) Bradycardia 1 (2,00) ST elevation 1 (2,00) Pericardial effusion 1 (2,00) Discussion SAH-induced cardiac dysfunction has been extensively studied, with evidence supporting the role of sympathetic hyperactivity and catecholamine-mediated myocardial injury [ 15 , 16 ]. Animal models have demonstrated that stimulation of the hypothalamus and other autonomic centers results in significant ECG changes, including ST-segment deviations, QT prolongation, and arrhythmias [ 17 , 18 ]. Similar findings in human studies have shown that patients with aneurysmal SAH frequently develop these cardiac abnormalities, which can be mistaken for primary cardiac events such as myocardial infarction [ 7 , 8 ]. The present study confirms that P wave dispersion is significantly prolonged in SAH patients compared to healthy controls. This finding aligns with prior research suggesting that increased PWD serves as an independent risk factor for AF in patients with cerebrovascular disease [ 19 ]. Atrial conduction abnormalities in SAH patients may contribute to thromboembolic complications, delayed cerebral ischemia, and poor neurological outcomes [ 20 ]. Furthermore, patients experiencing vasospasm after SAH exhibit even greater PWD prolongation, supporting the hypothesis that atrial dysfunction plays a role in cerebral hypoperfusion [ 10 , 11 ]. Additionally, SAH-related cardiac dysfunction extends beyond electrophysiological disturbances, as studies have shown myocardial injury characterized by elevated cardiac biomarkers such as troponin and B-type natriuretic peptide (BNP) [ 3 , 4 ]. The combination of elevated intracranial pressure and catecholamine surge can lead to stress-induced cardiomyopathy, further exacerbating cardiovascular risk in these patients [ 14 ]. These findings emphasize the importance of a multidisciplinary approach to managing SAH patients, integrating neurology, cardiology, and intensive care to optimize outcomes. Postoperative monitoring of SAH patients revealed persistent cardiac abnormalities, including hypertension, tachycardia, and ST-segment elevation. These findings highlight the necessity of continuous ECG monitoring and early intervention strategies to mitigate potential complications [ 4 , 9 ]. Given the high prevalence of arrhythmias and myocardial injury in SAH patients, further studies should explore the long-term implications of these cardiac changes and their role in neurological recovery [ 3 ](Wu et al., 2011). This study has several limitations. First, it was a single-center retrospective study, which may limit the generalizability of the findings. A multi-center prospective study with a larger sample size would be necessary to confirm these results and further investigate the relationship between SAH and cardiac dysfunction. Second, long-term follow-up was not conducted, preventing an assessment of delayed-onset arrhythmias and their clinical impact. Future studies should include extended monitoring, such as continuous Holter ECG recordings, to determine the true burden of atrial fibrillation in SAH patients. Third, echocardiographic parameters were not evaluated, which could have provided additional insights into atrial structure and function in these patients. Lastly, while patients with known cardiovascular diseases were excluded, subclinical cardiovascular conditions or autonomic dysfunction may still have influenced the findings, highlighting the need for further in-depth evaluations. Conclusion The findings of this study demonstrate that spontaneous SAH is associated with significant alterations in atrial electrical activity, as evidenced by increased P wave dispersion. These changes may predispose patients to atrial fibrillation and other arrhythmias, contributing to worse neurological and cardiovascular outcomes. The presence of ECG abnormalities, including ST-segment elevation and QT prolongation, underscores the importance of comprehensive cardiac monitoring in SAH patients. Given the potential risk of thromboembolic events and delayed cerebral ischemia, the early detection of atrial dysfunction using PWD could aid in identifying patients at high risk for adverse outcomes. Further research with larger, multi-center cohorts and long-term follow-up is necessary to establish the prognostic value of PWD in SAH patients and to develop targeted strategies for managing SAH-associated cardiac complications. Declarations Conflict of Interest The authors declare that they have no conflicts of interest related to this study. Funding No financial support or funding was received for this study. Ethical Approval This study was approved by the Istanbul Ümraniye Training and Research Hospital Ethics Committee (Decision no: B.10.1.TKH.4.34.H.GP.0.01/49). All procedures performed in this study involving human participants were in accordance with the ethical standards of the institutional and national research committee, as well as the 1964 Helsinki Declaration and its later amendments. Informed Consent Due to the retrospective nature of the study, formal informed consent was waived by the ethics committee. However, patient data confidentiality and privacy were strictly maintained throughout the study. Data Availability The datasets used and analyzed during the current study are available from the corresponding author upon reasonable request. References Abdalla MS, Smith BC, Kirchner A, et al.: Subarachnoid Hemorrhage From Cavernous Malformation Masquerading as Myocardial Infarction. J Med Cases. 2023, 14:105-110. 10.14740/jmc4064 Agrawal S, Nijs K, Subramaniam S, Englesakis M, Venkatraghavan L, Chowdhury T: Predictor role of heart rate variability in subarachnoid hemorrhage: A systematic review. J Clin Monit Comput. 2024, 38:177-185. 10.1007/s10877-023-01043-z Wu B, Wang X, Zhang JH: Cardiac damage after subarachnoid hemorrhage. Acta Neurochir Suppl. 2011, 110:215-218. 10.1007/978-3-7091-0353-1_37 Wang HP, Chen CC, Lee CC, et al.: Using a continuous electrocardiographic patch with heart rhythm analysis in the subacute stage of aneurysmal subarachnoid hemorrhage: The feasibility verification. Clin Neurol Neurosurg. 2023, 228:107687. 10.1016/j.clineuro.2023.107687 Jangra K, Grover VK, Bhagat H, et al.: Evaluation of the Effect of Aneurysmal Clipping on Electrocardiography and Echocardiographic Changes in Patients With Subarachnoid Hemorrhage: A Prospective Observational Study. J Neurosurg Anesthesiol. 2017, 29:335-340. 10.1097/ANA.0000000000000318 Nakagawa Y, Kusayama T, Tamai S, et al.: Association between skin sympathetic nerve activity and electrocardiogram alterations after subarachnoid hemorrhage. Physiol Rep. 2025, 13:e70202. 10.14814/phy2.70202 Aziz EMH, Alhatemi AQM, Hashim HT, Khaleel AS: Mimicking myocardial infarction: a subarachnoid haemorrhage case report. Oxf Med Case Reports. 2024, 2024:omae154. 10.1093/omcr/omae154 Cima K, Grams A, Metzler B: Subarachnoid haemorrhage mimicking a STEMI. Eur Heart J Acute Cardiovasc Care. 2017, 6:736-737. 10.1177/2048872616655942 Mustafa A, Hitt N, Smirlis E, Koranne K: ST Depression in the Setting of Subarachnoid Hemorrhage. Cureus. 2021, 13:e19030. 10.7759/cureus.19030 Kadooka K, Hadeishi H, Kadooka K: Delayed Normalization of Electrocardiograms in Patients with Takotsubo Cardiomyopathy due to Aneurysmal Subarachnoid Hemorrhage. World Neurosurg. 2017, 100:467-473. 10.1016/j.wneu.2017.01.051 Janus SE, Hoit BD: The three faces of takotsubo cardiomyopathy in a single patient. Echocardiography. 2020, 37:135-138. 10.1111/echo.14560 Ayaz M, Yanardag SB: SAH-Induced Electrophysiological Changes of Ventricular Myocytes and Role of N-acetylcysteine Protection. J Neurol Surg A Cent Eur Neurosurg. 2019, 80:72-80. 10.1055/s-0038-1655739 Komatsuzaki M, Takasusuki T, Kimura Y, Yamaguchi S: Assessment of the ECG T-Wave in Patients With Subarachnoid Hemorrhage. J Neurosurg Anesthesiol. 2021, 33:58-64. 10.1097/ANA.0000000000000624 Lang M, Jakob SM, Takala R, et al.: The prevalence of cardiac complications and their impact on outcomes in patients with non-traumatic subarachnoid hemorrhage. Sci Rep. 2022, 12:20109. 10.1038/s41598-022-24675-8 Norberg E, Odenstedt-Herges H, Rydenhag B, Oras J: Impact of Acute Cardiac Complications After Subarachnoid Hemorrhage on Long-Term Mortality and Cardiovascular Events. Neurocrit Care. 2018, 29:404-412. 10.1007/s12028-018-0558-0 Yaghmoor BE, Alotaibi SM, Enani MZ, et al.: Electrocardiographic changes following intracranial haemorrhage: a retrospective cohort study. Neurosciences (Riyadh). 2020, 25:104-111. 10.17712/nsj.2020.2.20190109 Tan G, Huguenard AL, Donovan KM, et al.: The effect of transcutaneous auricular vagus nerve stimulation on cardiovascular function in subarachnoid hemorrhage patients: A randomized trial. Elife. 2025, 13. 10.7554/eLife.100088 Lele A, Lakireddy V, Gorbachov S, Chaikittisilpa N, Krishnamoorthy V, Vavilala MS: A Narrative Review of Cardiovascular Abnormalities After Spontaneous Intracerebral Hemorrhage. J Neurosurg Anesthesiol. 2019, 31:199-211. 10.1097/ANA.0000000000000493 Longhitano Y, Bottinelli M, Pappalardo F, et al.: Electrocardiogram alterations in non-traumatic brain injury: a systematic review. J Clin Monit Comput. 2024, 38:407-414. 10.1007/s10877-023-01075-5 Lin XQ, Zheng LR: Myocardial ischemic changes of electrocardiogram in intracerebral hemorrhage: A case report and review of literature. World J Clin Cases. 2019, 7:3603-3614. 10.12998/wjcc.v7.i21.3603 Additional Declarations No competing interests reported. Cite Share Download PDF Status: Under Review Version 1 posted Reviews received at journal 07 May, 2025 Reviewers agreed at journal 07 May, 2025 Reviews received at journal 07 May, 2025 Reviewers agreed at journal 05 May, 2025 Reviewers invited by journal 05 May, 2025 Editor assigned by journal 29 Apr, 2025 Editor invited by journal 06 Apr, 2025 Submission checks completed at journal 02 Apr, 2025 First submitted to journal 02 Apr, 2025 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-6270952","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":453435405,"identity":"e6780e7f-bdd7-4b24-bd2e-f4f0830aac97","order_by":0,"name":"Caner Sarıkaya","email":"data:image/png;base64,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","orcid":"","institution":"Maltepe University","correspondingAuthor":true,"prefix":"","firstName":"Caner","middleName":"","lastName":"Sarıkaya","suffix":""},{"id":453435406,"identity":"58fde7f1-2509-408d-b346-7f1569d27c58","order_by":1,"name":"Fatma Özge Salkın","email":"","orcid":"","institution":"Seyhan State Hospital","correspondingAuthor":false,"prefix":"","firstName":"Fatma","middleName":"Özge","lastName":"Salkın","suffix":""},{"id":453435407,"identity":"6eaa4600-82d4-439d-9b26-ae8440526c78","order_by":2,"name":"Cansu Sarıkaya","email":"","orcid":"","institution":"Bahçeşehir University Medical Park Göztepe Hospital","correspondingAuthor":false,"prefix":"","firstName":"Cansu","middleName":"","lastName":"Sarıkaya","suffix":""},{"id":453435408,"identity":"d588ae5a-9fba-4172-91cb-c1aa8cf7be56","order_by":3,"name":"Eyüp Varol","email":"","orcid":"","institution":"Medicana Ataköy Hospital","correspondingAuthor":false,"prefix":"","firstName":"Eyüp","middleName":"","lastName":"Varol","suffix":""},{"id":453435409,"identity":"0f9de724-28fd-46ba-b9de-9bc05349c281","order_by":4,"name":"Cumhur Kaan Yaltırık","email":"","orcid":"","institution":"Maltepe University","correspondingAuthor":false,"prefix":"","firstName":"Cumhur","middleName":"Kaan","lastName":"Yaltırık","suffix":""}],"badges":[],"createdAt":"2025-03-20 15:23:20","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-6270952/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-6270952/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":82248128,"identity":"a63bfe85-a97f-4471-a0ce-9bd80cbaad4e","added_by":"auto","created_at":"2025-05-08 09:32:35","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":482710,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-6270952/v1/245b642f-70f4-452f-b9eb-73fe707ecd30.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Spontaneous Subarachnoid Hemorrhage and the Heart: The Silent Threat to Atrial Electrical Activity","fulltext":[{"header":"Introduction","content":"\u003cp\u003eSubarachnoid hemorrhage is a severe neurological event associated with high morbidity and mortality. Although primarily recognized for its devastating effects on the brain, SAH also induces significant cardiovascular complications, including electrocardiographic (ECG) abnormalities, myocardial injury, and increased risk of arrhythmias [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e, \u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. The pathophysiology underlying these cardiac effects is complex, involving the autonomic nervous system, catecholamine surge, and direct myocardial injury [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]. Previous studies have suggested that hypothalamic stimulation and elevated intracranial pressure contribute to these cardiovascular changes, leading to alterations in heart rate variability and increased susceptibility to arrhythmias [\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e, \u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eSAH-induced ECG abnormalities, such as ST-segment changes, QT prolongation, and T wave inversion, have been widely reported [\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e, \u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]. These findings have significant clinical implications, as they can mimic acute coronary syndromes, potentially leading to misdiagnosis and inappropriate treatment strategies [\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e]. Furthermore, studies have demonstrated that the extent of ECG abnormalities correlates with the severity of neurological damage and overall prognosis in SAH patients [\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e, \u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e]. Given this strong association between neurological injury and cardiac dysfunction, investigating the electrophysiological changes in SAH patients is essential for optimizing management strategies and reducing adverse outcomes.\u003c/p\u003e \u003cp\u003eOne key electrocardiographic parameter affected by SAH is P wave dispersion (PWD), which reflects atrial conduction abnormalities and has been identified as a predictor of atrial fibrillation [\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e, \u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e]. Increased PWD is indicative of heterogeneous atrial conduction, which may predispose patients to AF and other arrhythmias [\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e]. Since AF is a major risk factor for thromboembolic events, including stroke and delayed cerebral ischemia, recognizing early changes in PWD may provide valuable insight into the cardiac complications associated with SAH and help in risk stratification [\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eAlthough awareness of SAH-related cardiac changes has increased, their specific impact on atrial function remains insufficiently studied. This study highlights the importance of assessing P wave dispersion in aneurysmal SAH patients to better understand its role in arrhythmogenesis. Recognizing these electrophysiological changes may facilitate early identification of patients at risk for atrial fibrillation and other arrhythmias, ultimately contributing to more effective clinical management and improved outcomes.\u003c/p\u003e"},{"header":"Materials and Methods","content":"\u003cp\u003eThis retrospective study was approved by the Ethics Committee of \u0026Uuml;mraniye Training and Research Hospital (Approval No: B.10.1.TKH.4.34.H.GO.0.01/350) for the period 2022\u0026ndash;2023. The study population consisted of patients diagnosed with aneurysmal subarachnoid hemorrhage admitted to\u0026nbsp;\u0026Uuml;mraniye Training and Research Hospital, alongside a control group of healthy individuals who presented to the cardiology outpatient clinic without any additional diseases. Informed consent was obtained from all patients.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eStudy Design and Participants\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003ePatients included in this study were diagnosed with\u0026nbsp;aneurysmal SAH within the first 24 hours of bleeding\u0026nbsp;and underwent standard 12-lead electrocardiography (ECG) evaluation. The control group consisted of healthy individuals without known cardiovascular, neurological, or systemic diseases. A total of\u0026nbsp;131 participants\u0026nbsp;were enrolled, comprising\u0026nbsp;50 SAH patients and 81 healthy controls. The patient group was selected based on hospital admission records, and the control group was chosen from individuals undergoing routine cardiac evaluations.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eInclusion Criteria\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003ePatients were included in the study if they met the following conditions:\u003c/p\u003e\n\u003cul type=\"disc\"\u003e\n \u003cli\u003eAged\u0026nbsp;18 years or older\u003c/li\u003e\n \u003cli\u003eDiagnosed with\u0026nbsp;aneurysmal SAH within the first 24 hours of bleeding, confirmed by\u0026nbsp;computed tomography (CT) and angiography\u003c/li\u003e\n \u003cli\u003eUnderwent\u0026nbsp;preoperative ECG\u0026nbsp;evaluation\u003c/li\u003e\n \u003cli\u003eNo prior history of atrial fibrillation [9] or other chronic arrhythmias\u003c/li\u003e\n \u003cli\u003eProvided informed consent or had consent obtained from family members\u003c/li\u003e\n\u003c/ul\u003e\n\u003cp\u003e\u003cstrong\u003eExclusion Criteria\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003ePatients were excluded from the study if they had any of the following conditions:\u003c/p\u003e\n\u003cul type=\"disc\"\u003e\n \u003cli\u003eHistory of\u0026nbsp;malignancy, pregnancy, or chronic systemic diseases\u003c/li\u003e\n \u003cli\u003ePresence of\u0026nbsp;valvular heart disease, ventricular premature beats, or atrioventricular conduction abnormalities\u003c/li\u003e\n \u003cli\u003eDiagnosed with\u0026nbsp;congestive heart failure, thyroid diseases, or diabetes mellitus\u003c/li\u003e\n \u003cli\u003eHistory of\u0026nbsp;alcoholism, coronary artery disease (CAD), or collagen diseases\u003c/li\u003e\n \u003cli\u003ePresence of\u0026nbsp;chronic obstructive pulmonary disease (COPD) or electrolyte imbalances\u0026nbsp;that could affect cardiovascular function\u003c/li\u003e\n\u003c/ul\u003e\n\u003cp\u003e\u003cstrong\u003eElectrocardiographic Evaluation\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eStandard\u0026nbsp;12-lead ECGs\u0026nbsp;were obtained at a\u0026nbsp;paper speed of 25 mm/sec and amplitude of 10 mm/mV. ECGs were reviewed by a cardiologist for abnormalities in\u0026nbsp;heart rate, rhythm, ST-segment deviations, QT intervals, and T wave morphology. P wave dispersion (PWD) was calculated by measuring the\u0026nbsp;difference between the maximum (Pmax) and minimum (Pmin) P wave durations\u0026nbsp;recorded across the 12 ECG leads. Tachycardia was defined as a heart rate\u0026nbsp;\u0026gt;100 bpm, while bradycardia was defined as\u0026nbsp;\u0026lt;60 bpm. Prolonged\u0026nbsp;QT intervals (\u0026gt;410 ms)\u0026nbsp;and\u0026nbsp;QRS durations \u0026lt;100 ms\u0026nbsp;were considered abnormal.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eStatistical Analysis\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe sample size calculation was performed using G Power 3.1.9.7 software (Franz Faul, Germany), with an effect size (d) of 0.711. Based on a power of 95% and a 5% margin of error, a minimum of 88 participants was required. Statistical analyses were conducted using SPSS version 25.0. The normality of continuous variables was assessed using Kolmogorov-Smirnov tests and histogram evaluations. Descriptive analyses were presented as mean, standard deviation, median, interquartile range (IQR), and min-max values. Categorical variables were compared using the Chi-Square Test, while non-normally distributed variables were analyzed using the Mann-Whitney U Test. A p-value \u0026lt;0.05 was considered statistically significant.\u003c/p\u003e"},{"header":"Results","content":"\u003cp\u003eA total of\u0026nbsp;131 individuals\u0026nbsp;participated in the study, including\u0026nbsp;50 patients with aneurysmal SAH\u0026nbsp;and\u0026nbsp;81 healthy controls. The\u0026nbsp;mean age of the SAH group was 53.48 \u0026plusmn; 12.74 years, while the control group had a mean age of\u0026nbsp;56.94 \u0026plusmn; 12.36 years. There was no statistically significant difference between the groups in terms of\u0026nbsp;age (p = 0.071)\u0026nbsp;or\u0026nbsp;gender distribution (p = 0.919)\u0026nbsp;(Table 1).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTable 1\u003c/strong\u003e: \u0026sup1;Mann Whitney U Testi. \u0026sup2;Ki-Kare Testi. There is no significant difference between the two groups in terms of age and gender.\u0026nbsp;\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"100%\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"2\" rowspan=\"2\" style=\"width: 15px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd colspan=\"2\" style=\"width: 26px;\"\u003e\n \u003cp\u003ePatient\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd colspan=\"2\" style=\"width: 25px;\"\u003e\n \u003cp\u003eControl\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd colspan=\"2\" style=\"width: 25px;\"\u003e\n \u003cp\u003eTotal\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" style=\"width: 7px;\"\u003e\n \u003cp\u003ep\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003en\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003eN\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12px;\"\u003e\n \u003cp\u003e%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003en\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12px;\"\u003e\n \u003cp\u003e%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"2\" style=\"width: 15px;\"\u003e\n \u003cp\u003eAge\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e53,48\u0026plusmn;12,74\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e51,5 (29-94)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e56,94\u0026plusmn;12,36\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12px;\"\u003e\n \u003cp\u003e55 (24-83)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e55,62\u0026plusmn;12,57\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12px;\"\u003e\n \u003cp\u003e53 (24-94)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 7px;\"\u003e\n \u003cp\u003e0,071\u0026sup1;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"2\" style=\"width: 8px;\"\u003e\n \u003cp\u003eGender\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 6px;\"\u003e\n \u003cp\u003eMale\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e23\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e(46,00)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e38\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12px;\"\u003e\n \u003cp\u003e(46,91)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e61\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12px;\"\u003e\n \u003cp\u003e(46,56)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" style=\"width: 7px;\"\u003e\n \u003cp\u003e0,919\u0026sup2;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 6px;\"\u003e\n \u003cp\u003eFemale\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e27\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e(54,00)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e43\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12px;\"\u003e\n \u003cp\u003e(53,09)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e70\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12px;\"\u003e\n \u003cp\u003e(53,44)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003eDemographic and Clinical Characteristics\u003c/p\u003e\n\u003cp\u003eIn the SAH group, 6 patients (12.0%) had diabetes, 23 patients (46.0%) had hypertension, and 3 patients (6.0%) had coronary artery disease (CAD). In contrast, the control group had 9 patients (11.1%) with diabetes and 21 patients (25.9%) with hypertension, but no cases of CAD (Table 2).\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTable 2\u003c/strong\u003e:\u0026nbsp;Diabetes, Hypertension, Coronary Artery Disease, of the Patient Group\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"100%\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"2\" style=\"width: 69px;\"\u003e\n \u003cp\u003ePatient Group\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 16px;\"\u003e\n \u003cp\u003en\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"2\" style=\"width: 34px;\"\u003e\n \u003cp\u003eDiabetes\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 34px;\"\u003e\n \u003cp\u003eNo\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 16px;\"\u003e\n \u003cp\u003e44\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e(88,00)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 34px;\"\u003e\n \u003cp\u003eYes\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 16px;\"\u003e\n \u003cp\u003e6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e(12,00)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"2\" style=\"width: 34px;\"\u003e\n \u003cp\u003eHT (Hypertension)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 34px;\"\u003e\n \u003cp\u003eNo\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 16px;\"\u003e\n \u003cp\u003e27\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e(54,00)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 34px;\"\u003e\n \u003cp\u003eYes\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 16px;\"\u003e\n \u003cp\u003e23\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e(46,00)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"2\" style=\"width: 34px;\"\u003e\n \u003cp\u003eKAH (Coronary Artery Disease)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 34px;\"\u003e\n \u003cp\u003eNo\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 16px;\"\u003e\n \u003cp\u003e47\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e(94,00)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 34px;\"\u003e\n \u003cp\u003eYes\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 16px;\"\u003e\n \u003cp\u003e3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e(6,00)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003eElectrocardiographic Findings\u003c/p\u003e\n\u003cp\u003eAnalysis of preoperative ECGs in SAH patients revealed several abnormalities.\u003c/p\u003e\n\u003cul type=\"disc\"\u003e\n \u003cli\u003eST-segment elevation\u0026nbsp;was observed in\u0026nbsp;5 patients (10%), while\u0026nbsp;10 patients (20%) showed T wave inversions.\u003c/li\u003e\n \u003cli\u003eQT prolongation\u0026nbsp;was detected in\u0026nbsp;3 patients (6%), but troponin levels remained within normal limits, suggesting that these ECG changes were related to\u0026nbsp;SAH-induced neurogenic effects rather than acute myocardial infarction (MI).\u003c/li\u003e\n \u003cli\u003eP wave dispersion (PWD) was\u0026nbsp;significantly prolonged in SAH patients\u0026nbsp;compared to the control group (Table 3).\u003c/li\u003e\n\u003c/ul\u003e\n\u003cp\u003eP Wave Dispersion Analysis\u003c/p\u003e\n\u003cul type=\"disc\"\u003e\n \u003cli\u003eThe\u0026nbsp;mean Pmax\u0026nbsp;was significantly\u0026nbsp;higher in SAH patients (1.58 \u0026plusmn; 0.5 ms) compared to controls (1.31 \u0026plusmn; 0.42 ms), p = 0.001.\u003c/li\u003e\n \u003cli\u003eThe\u0026nbsp;mean Pmin\u0026nbsp;was lower in SAH patients (0.55 \u0026plusmn; 0.15 ms vs. 0.67 \u0026plusmn; 0.24 ms, p = 0.003).\u003c/li\u003e\n \u003cli\u003eThe mean P wave dispersion (PWD) was markedly increased in the SAH group (1.03 \u0026plusmn; 0.5 ms) compared to controls (0.63 \u0026plusmn; 0.23 ms), p \u0026lt; 0.001 (Table 3).\u003c/li\u003e\n\u003c/ul\u003e\n\u003cp\u003e\u003cstrong\u003eTable 3:\u003c/strong\u003e Mann Whitney U Test. Pmin value is higher in the control group than in the patient group. Pdisp value is higher in the patient group than in the control group.\u0026nbsp;\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"100%\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"2\" style=\"width: 15px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd colspan=\"2\" style=\"width: 26px;\"\u003e\n \u003cp\u003ePatient\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd colspan=\"2\" style=\"width: 25px;\"\u003e\n \u003cp\u003eControl\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd colspan=\"2\" style=\"width: 25px;\"\u003e\n \u003cp\u003eTotal\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" style=\"width: 7px;\"\u003e\n \u003cp\u003ep\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003en\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003en\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12px;\"\u003e\n \u003cp\u003e%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003en\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12px;\"\u003e\n \u003cp\u003e%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 15px;\"\u003e\n \u003cp\u003ePmax\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e1,58\u0026plusmn;0,5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e1,5 (1-2,5)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e1,31\u0026plusmn;0,42\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12px;\"\u003e\n \u003cp\u003e1 (1-2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e1,41\u0026plusmn;0,47\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12px;\"\u003e\n \u003cp\u003e1,5 (1-2,5)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 7px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e0,001\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 15px;\"\u003e\n \u003cp\u003ePmin\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e0,55\u0026plusmn;0,15\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e0,5 (0,5-1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e0,67\u0026plusmn;0,24\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12px;\"\u003e\n \u003cp\u003e0,5 (0,5-1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e0,62\u0026plusmn;0,22\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12px;\"\u003e\n \u003cp\u003e0,5 (0,5-1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 7px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e0,003\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 15px;\"\u003e\n \u003cp\u003ePdisp\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e1,03\u0026plusmn;0,5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e1 (0,5-2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e0,63\u0026plusmn;0,23\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12px;\"\u003e\n \u003cp\u003e0,5 (0,05-1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e0,78\u0026plusmn;0,41\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12px;\"\u003e\n \u003cp\u003e0,5 (0,05-2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 7px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e\u0026lt;0,001\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003eThese findings suggest that SAH leads to increased atrial electrical heterogeneity, potentially predisposing patients to arrhythmias such as atrial fibrillation [9].\u003c/p\u003e\n\u003cp\u003ePostoperative Cardiac Complications\u003c/p\u003e\n\u003cul type=\"disc\"\u003e\n \u003cli\u003ePostoperatively,\u0026nbsp;34 patients (68.0%) in the SAH group exhibited no cardiac abnormalities.\u003c/li\u003e\n \u003cli\u003eHowever,\u0026nbsp;11 patients (22.0%) developed hypertension, while\u0026nbsp;2 patients (4.0%) had tachycardia\u0026nbsp;and\u0026nbsp;1 patient (2.0%) developed bradycardia.\u003c/li\u003e\n \u003cli\u003eAdditionally,\u0026nbsp;one patient (2.0%) exhibited persistent ST-segment elevation, and\u0026nbsp;one patient (2.0%) developed pericardial effusion\u0026nbsp;(Table 4).\u003c/li\u003e\n \u003cli\u003eTransient atrial fibrillation \u0026nbsp;was observed in four patients, and normal sinus rhythm was restored with medical treatment.\u003c/li\u003e\n\u003c/ul\u003e\n\u003cp\u003e\u003cstrong\u003eTable 4:\u003c/strong\u003e Post-op Cardiac Problem\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"100%\" class=\"fr-table-selection-hover\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"7\" style=\"width: 34px;\"\u003e\n \u003cp\u003ePost-op cardiac problem\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 34px;\"\u003e\n \u003cp\u003eNo\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 16px;\"\u003e\n \u003cp\u003e34\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e(60,00)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 34px;\"\u003e\n \u003cp\u003eHypertension\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 16px;\"\u003e\n \u003cp\u003e11\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e(22,00)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 34px;\"\u003e\n \u003cp\u003eTransient Atrial Fibrillation \u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 16px;\"\u003e\n \u003cp\u003e4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e(8,00)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 34px;\"\u003e\n \u003cp\u003eTachycardia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 16px;\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e(4,00)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 34px;\"\u003e\n \u003cp\u003eBradycardia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 16px;\"\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e(2,00)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 34px;\"\u003e\n \u003cp\u003eST elevation\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 16px;\"\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e(2,00)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 34px;\"\u003e\n \u003cp\u003ePericardial effusion\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 16px;\"\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 13px;\"\u003e\n \u003cp\u003e(2,00)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u0026nbsp;\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eSAH-induced cardiac dysfunction has been extensively studied, with evidence supporting the role of sympathetic hyperactivity and catecholamine-mediated myocardial injury [\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e, \u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e]. Animal models have demonstrated that stimulation of the hypothalamus and other autonomic centers results in significant ECG changes, including ST-segment deviations, QT prolongation, and arrhythmias [\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e, \u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e]. Similar findings in human studies have shown that patients with aneurysmal SAH frequently develop these cardiac abnormalities, which can be mistaken for primary cardiac events such as myocardial infarction [\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e, \u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eThe present study confirms that P wave dispersion is significantly prolonged in SAH patients compared to healthy controls. This finding aligns with prior research suggesting that increased PWD serves as an independent risk factor for AF in patients with cerebrovascular disease [\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e]. Atrial conduction abnormalities in SAH patients may contribute to thromboembolic complications, delayed cerebral ischemia, and poor neurological outcomes [\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e]. Furthermore, patients experiencing vasospasm after SAH exhibit even greater PWD prolongation, supporting the hypothesis that atrial dysfunction plays a role in cerebral hypoperfusion [\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e, \u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eAdditionally, SAH-related cardiac dysfunction extends beyond electrophysiological disturbances, as studies have shown myocardial injury characterized by elevated cardiac biomarkers such as troponin and B-type natriuretic peptide (BNP) [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]. The combination of elevated intracranial pressure and catecholamine surge can lead to stress-induced cardiomyopathy, further exacerbating cardiovascular risk in these patients [\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e]. These findings emphasize the importance of a multidisciplinary approach to managing SAH patients, integrating neurology, cardiology, and intensive care to optimize outcomes.\u003c/p\u003e \u003cp\u003ePostoperative monitoring of SAH patients revealed persistent cardiac abnormalities, including hypertension, tachycardia, and ST-segment elevation. These findings highlight the necessity of continuous ECG monitoring and early intervention strategies to mitigate potential complications [\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e, \u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e]. Given the high prevalence of arrhythmias and myocardial injury in SAH patients, further studies should explore the long-term implications of these cardiac changes and their role in neurological recovery [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e](Wu et al., 2011).\u003c/p\u003e \u003cp\u003eThis study has several limitations. First, it was a single-center retrospective study, which may limit the generalizability of the findings. A multi-center prospective study with a larger sample size would be necessary to confirm these results and further investigate the relationship between SAH and cardiac dysfunction. Second, long-term follow-up was not conducted, preventing an assessment of delayed-onset arrhythmias and their clinical impact. Future studies should include extended monitoring, such as continuous Holter ECG recordings, to determine the true burden of atrial fibrillation in SAH patients. Third, echocardiographic parameters were not evaluated, which could have provided additional insights into atrial structure and function in these patients. Lastly, while patients with known cardiovascular diseases were excluded, subclinical cardiovascular conditions or autonomic dysfunction may still have influenced the findings, highlighting the need for further in-depth evaluations.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eThe findings of this study demonstrate that spontaneous SAH is associated with significant alterations in atrial electrical activity, as evidenced by increased P wave dispersion. These changes may predispose patients to atrial fibrillation and other arrhythmias, contributing to worse neurological and cardiovascular outcomes. The presence of ECG abnormalities, including ST-segment elevation and QT prolongation, underscores the importance of comprehensive cardiac monitoring in SAH patients. Given the potential risk of thromboembolic events and delayed cerebral ischemia, the early detection of atrial dysfunction using PWD could aid in identifying patients at high risk for adverse outcomes. Further research with larger, multi-center cohorts and long-term follow-up is necessary to establish the prognostic value of PWD in SAH patients and to develop targeted strategies for managing SAH-associated cardiac complications.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eConflict of Interest\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare that they have no conflicts of interest related to this study.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNo financial support or funding was received for this study.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eEthical Approval\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis study was approved by the Istanbul \u0026Uuml;mraniye Training and Research Hospital Ethics Committee (Decision no: B.10.1.TKH.4.34.H.GP.0.01/49). All procedures performed in this study involving human participants were in accordance with the ethical standards of the institutional and national research committee, as well as the 1964 Helsinki Declaration and its later amendments.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eInformed Consent\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eDue to the retrospective nature of the study, formal informed consent was waived by the ethics committee. However, patient data confidentiality and privacy were strictly maintained throughout the study.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eData Availability\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe datasets used and analyzed during the current study are available from the corresponding author upon reasonable request.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eAbdalla MS, Smith BC, Kirchner A, et al.: Subarachnoid Hemorrhage From Cavernous Malformation Masquerading as Myocardial Infarction. J Med Cases. 2023, 14:105-110. 10.14740/jmc4064\u003c/li\u003e\n\u003cli\u003eAgrawal S, Nijs K, Subramaniam S, Englesakis M, Venkatraghavan L, Chowdhury T: Predictor role of heart rate variability in subarachnoid hemorrhage: A systematic review. J Clin Monit Comput. 2024, 38:177-185. 10.1007/s10877-023-01043-z\u003c/li\u003e\n\u003cli\u003eWu B, Wang X, Zhang JH: Cardiac damage after subarachnoid hemorrhage. Acta Neurochir Suppl. 2011, 110:215-218. 10.1007/978-3-7091-0353-1_37\u003c/li\u003e\n\u003cli\u003eWang HP, Chen CC, Lee CC, et al.: Using a continuous electrocardiographic patch with heart rhythm analysis in the subacute stage of aneurysmal subarachnoid hemorrhage: The feasibility verification. Clin Neurol Neurosurg. 2023, 228:107687. 10.1016/j.clineuro.2023.107687\u003c/li\u003e\n\u003cli\u003eJangra K, Grover VK, Bhagat H, et al.: Evaluation of the Effect of Aneurysmal Clipping on Electrocardiography and Echocardiographic Changes in Patients With Subarachnoid Hemorrhage: A Prospective Observational Study. J Neurosurg Anesthesiol. 2017, 29:335-340. 10.1097/ANA.0000000000000318\u003c/li\u003e\n\u003cli\u003eNakagawa Y, Kusayama T, Tamai S, et al.: Association between skin sympathetic nerve activity and electrocardiogram alterations after subarachnoid hemorrhage. Physiol Rep. 2025, 13:e70202. 10.14814/phy2.70202\u003c/li\u003e\n\u003cli\u003eAziz EMH, Alhatemi AQM, Hashim HT, Khaleel AS: Mimicking myocardial infarction: a subarachnoid haemorrhage case report. Oxf Med Case Reports. 2024, 2024:omae154. 10.1093/omcr/omae154\u003c/li\u003e\n\u003cli\u003eCima K, Grams A, Metzler B: Subarachnoid haemorrhage mimicking a STEMI. Eur Heart J Acute Cardiovasc Care. 2017, 6:736-737. 10.1177/2048872616655942\u003c/li\u003e\n\u003cli\u003eMustafa A, Hitt N, Smirlis E, Koranne K: ST Depression in the Setting of Subarachnoid Hemorrhage. Cureus. 2021, 13:e19030. 10.7759/cureus.19030\u003c/li\u003e\n\u003cli\u003eKadooka K, Hadeishi H, Kadooka K: Delayed Normalization of Electrocardiograms in Patients with Takotsubo Cardiomyopathy due to Aneurysmal Subarachnoid Hemorrhage. World Neurosurg. 2017, 100:467-473. 10.1016/j.wneu.2017.01.051\u003c/li\u003e\n\u003cli\u003eJanus SE, Hoit BD: The three faces of takotsubo cardiomyopathy in a single patient. Echocardiography. 2020, 37:135-138. 10.1111/echo.14560\u003c/li\u003e\n\u003cli\u003eAyaz M, Yanardag SB: SAH-Induced Electrophysiological Changes of Ventricular Myocytes and Role of N-acetylcysteine Protection. J Neurol Surg A Cent Eur Neurosurg. 2019, 80:72-80. 10.1055/s-0038-1655739\u003c/li\u003e\n\u003cli\u003eKomatsuzaki M, Takasusuki T, Kimura Y, Yamaguchi S: Assessment of the ECG T-Wave in Patients With Subarachnoid Hemorrhage. J Neurosurg Anesthesiol. 2021, 33:58-64. 10.1097/ANA.0000000000000624\u003c/li\u003e\n\u003cli\u003eLang M, Jakob SM, Takala R, et al.: The prevalence of cardiac complications and their impact on outcomes in patients with non-traumatic subarachnoid hemorrhage. Sci Rep. 2022, 12:20109. 10.1038/s41598-022-24675-8\u003c/li\u003e\n\u003cli\u003eNorberg E, Odenstedt-Herges H, Rydenhag B, Oras J: Impact of Acute Cardiac Complications After Subarachnoid Hemorrhage on Long-Term Mortality and Cardiovascular Events. Neurocrit Care. 2018, 29:404-412. 10.1007/s12028-018-0558-0\u003c/li\u003e\n\u003cli\u003eYaghmoor BE, Alotaibi SM, Enani MZ, et al.: Electrocardiographic changes following intracranial haemorrhage: a retrospective cohort study. Neurosciences (Riyadh). 2020, 25:104-111. 10.17712/nsj.2020.2.20190109\u003c/li\u003e\n\u003cli\u003eTan G, Huguenard AL, Donovan KM, et al.: The effect of transcutaneous auricular vagus nerve stimulation on cardiovascular function in subarachnoid hemorrhage patients: A randomized trial. Elife. 2025, 13. 10.7554/eLife.100088\u003c/li\u003e\n\u003cli\u003eLele A, Lakireddy V, Gorbachov S, Chaikittisilpa N, Krishnamoorthy V, Vavilala MS: A Narrative Review of Cardiovascular Abnormalities After Spontaneous Intracerebral Hemorrhage. J Neurosurg Anesthesiol. 2019, 31:199-211. 10.1097/ANA.0000000000000493\u003c/li\u003e\n\u003cli\u003eLonghitano Y, Bottinelli M, Pappalardo F, et al.: Electrocardiogram alterations in non-traumatic brain injury: a systematic review. J Clin Monit Comput. 2024, 38:407-414. 10.1007/s10877-023-01075-5\u003c/li\u003e\n\u003cli\u003eLin XQ, Zheng LR: Myocardial ischemic changes of electrocardiogram in intracerebral hemorrhage: A case report and review of literature. World J Clin Cases. 2019, 7:3603-3614. 10.12998/wjcc.v7.i21.3603\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"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":"bmc-neurology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"nurl","sideBox":"Learn more about [BMC Neurology](http://bmcneurol.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/nurl","title":"BMC Neurology","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"P wave dispersion, autonomic nervous system, electrocardiography, aneurysm, subarachnoid haemorrhage","lastPublishedDoi":"10.21203/rs.3.rs-6270952/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-6270952/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cstrong\u003eBackground:\u003c/strong\u003e Spontaneous subarachnoid hemorrhage has been associated with significant cardiovascular changes, including alterations in atrial electrical activity. This study investigates the impact of SAH on atrial function using P wave dispersion (PWD) as an electrocardiographic marker.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eMethods:\u003c/strong\u003e This retrospective study included 131 individuals (50 SAH patients and 81 healthy controls) admitted to Ümraniye Training and Research Hospital. Standard 12-lead electrocardiography (ECG) was used to measure P wave dispersion (PWD), defined as the difference between the maximum (Pmax) and minimum (Pmin) P wave durations. Statistical analyses were performed using SPSS version 25.0, with comparisons between groups made using the Mann-Whitney U test and Chi-Square test where applicable.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eResults:\u003c/strong\u003e The mean P wave dispersion was significantly higher in the SAH group (1.03 ± 0.5) compared to the control group (0.63 ± 0.23, p \u0026lt; 0.001). Additionally, ST segment elevation was observed in 5 SAH patients, while 10 showed T wave inversions and 3 had prolonged QT intervals. However, no significant troponin elevation was noted, suggesting an SAH-induced ECG alteration rather than acute myocardial infarction. Postoperatively, 30 patients exhibited no cardiac complications, while 11 had hypertension, 2 had tachycardia, 1 had bradycardia, 1 had ST elevation, and 1 developed pericardial effusion. Transient atrial fibrillation \u0026nbsp;was observed in four patients, and normal sinus rhythm was restored with medical treatment.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConclusion:\u003c/strong\u003e The findings suggest that SAH is associated with significant disruptions in atrial electrical activity, as evidenced by increased P wave dispersion. Prolonged PWD may indicate an elevated risk of atrial fibrillation, contributing to further neurological deterioration. Understanding the cardiac implications of SAH is crucial for early intervention and improved patient outcomes.\u003c/p\u003e","manuscriptTitle":"Spontaneous Subarachnoid Hemorrhage and the Heart: The Silent Threat to Atrial Electrical Activity","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-05-08 09:24:30","doi":"10.21203/rs.3.rs-6270952/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"editorInvitedReview","content":"","date":"2025-05-07T19:23:02+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"288036643901801773313513235579065121572","date":"2025-05-07T18:57:55+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-05-07T14:22:50+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"307804715693766574362680504021718938688","date":"2025-05-05T09:05:56+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2025-05-05T08:38:30+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2025-04-29T14:43:20+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2025-04-07T02:53:49+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2025-04-02T10:24:29+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Neurology","date":"2025-04-02T10:23:20+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"bmc-neurology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"nurl","sideBox":"Learn more about [BMC Neurology](http://bmcneurol.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/nurl","title":"BMC Neurology","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"c1e9549b-8329-4018-81e5-7a60aef4a165","owner":[],"postedDate":"May 8th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[],"tags":[],"updatedAt":"2025-05-08T09:24:30+00:00","versionOfRecord":[],"versionCreatedAt":"2025-05-08 09:24:30","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-6270952","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-6270952","identity":"rs-6270952","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}