Spontaneous multivessel coronary artery dissection in a female without connective tissue disease: An acute myocardial infarction in a young patient.

A 38-year-old woman presented with a 1-hour history of acute pleuritic chest pain, radiating to the arms and back, associated with diaphoresis. This episode followed 3 days of continuous, clear vomiting and diarrhoea, initially thought to be gastroenteritis. Her past medical history included anxiety, endometriosis with multiple laparoscopic surgeries and a uterine rupture during her second pregnancy resulting in Caesarean delivery. Cardiovascular and respiratory examination were unremarkable. Initial bedside investigations included an electrocardiogram (ECG), which showed minor T-wave inversion in lead III. Laboratory tests revealed elevated high-sensitivity troponin levels peaking at 1000 ng/L, suggesting a myocardial injury. Coronary angiography on day 3 revealed a probable intramural haematoma and dissection flap of the left anterior descending (LAD) artery ( Fig. 1D ). Unfortunately, the procedure was complicated by an iatrogenic, catheter-induced dissection of the right coronary artery (RCA) ( Fig. 1A - C ), resulting in acute vessel occlusion and an inferior ST-elevation myocardial infarction (STEMI). The patient was promptly treated with percutaneous coronary intervention (PCI), involving extensive stenting of the RCA, which successfully restored vessel patency ( Fig. 2 ). Fig. 1 Initial invasive coronary angiography. (A) First diagnostic coronary angiogram of the RCA performed using a 5Fr Judkins right catheter, showing contrast flow into the RCA. (B and C) highlighting the linear radiolucency within the RCA lumen (white arrows) indicative of an intimal flap—a hallmark of coronary artery dissection. (D) A possible linear radiolucency along the LAD artery (red arrow) suggesting an additional dissection, not initially identified during the initial procedure. RCA, right coronary artery; LAD, left anterior descending. Fig 1 Fig. 2 Immediate percutaneous coronary intervention for catheter-induced dissection. Angiographic image showed immediate percutaneous coronary intervention (PCI) of the right coronary artery (RCA) following identification of iatrogenic dissection. Overlapping Onyx Frontier drug-eluting stents (3.0 × 38 mm, 3.0 × 38 mm and 3.5 × 15 mm) were deployed to 12 atmospheres from distal to ostial RCA. Poststenting showed angiography demonstrated restored vessel patency. RCA, right coronary artery. Fig 2 Initial invasive coronary angiography. (A) First diagnostic coronary angiogram of the RCA performed using a 5Fr Judkins right catheter, showing contrast flow into the RCA. (B and C) highlighting the linear radiolucency within the RCA lumen (white arrows) indicative of an intimal flap—a hallmark of coronary artery dissection. (D) A possible linear radiolucency along the LAD artery (red arrow) suggesting an additional dissection, not initially identified during the initial procedure. RCA, right coronary artery; LAD, left anterior descending. Immediate percutaneous coronary intervention for catheter-induced dissection. Angiographic image showed immediate percutaneous coronary intervention (PCI) of the right coronary artery (RCA) following identification of iatrogenic dissection. Overlapping Onyx Frontier drug-eluting stents (3.0 × 38 mm, 3.0 × 38 mm and 3.5 × 15 mm) were deployed to 12 atmospheres from distal to ostial RCA. Poststenting showed angiography demonstrated restored vessel patency. RCA, right coronary artery. Echocardiography revealed a normal left ventricular (LV) ejection fraction (>55%) with no evidence of regional wall motion abnormalities. Continuous telemetry revealed normal sinus rhythm throughout. Cardiac magnetic resonance imaging (CMRI) revealed no evidence of myocardial infarction or myocarditis. On day 6, the patient experienced recurrent chest discomfort, similar to her initial presentation, accompanied by a new troponin rise to 2,344 ng/L. ECG showed no ischaemic changes. Repeat coronary angiography and intravascular ultrasound (IVUS) of the RCA demonstrated an improved appearance of the distal right coronary artery ( Fig. 3 ). There was residual haematoma, but no dissection. Mild stent malapposition was identified in the mid-vessel and this was subsequently addressed with postdilatation using a noncompliant balloon ( Fig. 4A and B ). The patient had no further chest discomfort and was discharged home on day 8 with dual-antiplatelet therapy (aspirin 75 mg once daily and clopidogrel 75 mg once daily) with a low-dose beta-blocker (bisoprolol 1.25 mg once daily). Fig. 3 Follow-up invasive coronary angiography demonstrating stent patency. Re-look invasive coronary angiography 6 days post-stenting later showed improved angiographic appearance of the previously-stented RCA. RCA, right coronary artery. Fig 3 Fig. 4 Intravascular ultrasound (IVUS) evaluation 6 days post-percutaneous coronary intervention. IVUS imaging was performed to access stent apposition and vessel wall integrity. (A and B) Cross sectional IVUS images reveal an echo-free space (white asterisks), indicative of a false lumen caused by dissection. (C) A segment with mixed echogenic stagnant blood (red arrow), confirmed intramural haematoma. Additionally, minor stent malapposition is noted in the mid-vessel (A and B) which was addressed with a 3.25 mm noncompliant (NC) balloon inflated to 14 atmospheres, improving stent expansion and wall apposition. Fig 4 Follow-up invasive coronary angiography demonstrating stent patency. Re-look invasive coronary angiography 6 days post-stenting later showed improved angiographic appearance of the previously-stented RCA. RCA, right coronary artery. Intravascular ultrasound (IVUS) evaluation 6 days post-percutaneous coronary intervention. IVUS imaging was performed to access stent apposition and vessel wall integrity. (A and B) Cross sectional IVUS images reveal an echo-free space (white asterisks), indicative of a false lumen caused by dissection. (C) A segment with mixed echogenic stagnant blood (red arrow), confirmed intramural haematoma. Additionally, minor stent malapposition is noted in the mid-vessel (A and B) which was addressed with a 3.25 mm noncompliant (NC) balloon inflated to 14 atmospheres, improving stent expansion and wall apposition. However, 1 month following her discharge, the patient represented to the hospital with symptoms reminiscent of her initial episode—recurrent central chest pain at rest, radiating to her back and down her left arm. The episode occurred while she was watching television after dinner. Laboratory investigations revealed a mildly elevated troponin levels, peaking at 236 ng/L, without significant ischaemic changes on ECG. Repeat coronary angiography demonstrated a stable appearance of the right coronary artery ( Fig. 5A ). Nonselective angiography of the left coronary artery revealed severe narrowing of the proximal left anterior descending (LAD) artery, along with a dissection flap and intramural contrast staining in the proximal left circumflex (LCx) artery ( Fig. 5 , Fig. 5 ). These findings were subsequently confirmed on CT coronary angiography (CTCA) ( Fig. 6A and B , Fig 7A ). The patient had a prolonged hospital admission in the cardiac coronary care for observation and continuous cardiac monitoring where her cardiac rhythm was normal throughout. Fig. 5 Diagnostic coronary angiography (third procedure). (A) Repeat coronary angiogram demonstrated a stable appearance of previously stented RCA. (B and C) Nonselective contrast injection showed a dissection flap in LCx artery (red arrows); visible as a linear radiolucency and severe narrowing of proximal LAD artery. RCA, right coronary artery; LCx, left circumflex; LAD, left anterior descending. Fig 5 Fig. 6 CT coronary angiography demonstrating LAD dissection with thrombosed false lumen. (A) Unenhanced low-dose CT scan performed for coronary calcium scoring revealed high attenuation within the proximal LAD coronary artery wall, suggesting an intramural thrombus (white arrow). (B) Contrast-enhanced CT coronary angiogram shows soft tissue density within the wall of the proximal LAD with luminal narrowing, suggestive of coronary dissection and a thrombosed false lumen (dashed arrow). CT, computed tomography; LAD, left anterior descending. Fig 6 Fig. 7 Multimodality follow-up demonstrating LAD dissection and spontaneous healing. (A) CMR with cross-sectional views of the proximal LAD coronary artery revealed severe stenosis of the contrast-opacified true lumen of proximal LAD (arrowheads). (B) Follow-up CT coronary angiogram with CMR after 50 days revealed significant interval improvement in luminal patency of the left proximal LAD (arrowheads) and resolution of the previously identified thrombosed false lumen. These findings indicate progressive vessel wall healing and patency without further invasive intervention. CMR, curved multiplanar reformats; CT, computed tomography; LAD, left anterior descending. Fig 7 Diagnostic coronary angiography (third procedure). (A) Repeat coronary angiogram demonstrated a stable appearance of previously stented RCA. (B and C) Nonselective contrast injection showed a dissection flap in LCx artery (red arrows); visible as a linear radiolucency and severe narrowing of proximal LAD artery. RCA, right coronary artery; LCx, left circumflex; LAD, left anterior descending. CT coronary angiography demonstrating LAD dissection with thrombosed false lumen. (A) Unenhanced low-dose CT scan performed for coronary calcium scoring revealed high attenuation within the proximal LAD coronary artery wall, suggesting an intramural thrombus (white arrow). (B) Contrast-enhanced CT coronary angiogram shows soft tissue density within the wall of the proximal LAD with luminal narrowing, suggestive of coronary dissection and a thrombosed false lumen (dashed arrow). CT, computed tomography; LAD, left anterior descending. Multimodality follow-up demonstrating LAD dissection and spontaneous healing. (A) CMR with cross-sectional views of the proximal LAD coronary artery revealed severe stenosis of the contrast-opacified true lumen of proximal LAD (arrowheads). (B) Follow-up CT coronary angiogram with CMR after 50 days revealed significant interval improvement in luminal patency of the left proximal LAD (arrowheads) and resolution of the previously identified thrombosed false lumen. These findings indicate progressive vessel wall healing and patency without further invasive intervention. CMR, curved multiplanar reformats; CT, computed tomography; LAD, left anterior descending. Given the background of recurrent coronary artery dissections, joint hypermobility and a history of uterine rupture at term during her second pregnancy requiring emergency Caesarean delivery, an underlying connective tissue disorder was suspected. Clinical examination by a rheumatologist revealed joint hypermobility in the hands, elbows and knees. Genetic screening was performed to evaluate for connective tissue disorders, including Cutis Laxa, Ehlers-Danlos Syndrome, Marfan Syndrome, Loeys-Dietz Syndrome and familial aortic aneurysm syndromes. The results were negative, with no pathogenic variants identified to confirm a hereditary connective tissue disease. Additionally, CT angiography of the abdominal aorta and its major branches revealed no abnormalities. Surveillance CT coronary angiography (CTCA) demonstrated gradual improvement in the coronary dissections involving the LAD and LCx. Following extensive multidisciplinary discussions, a decision was made to continue with conservative treatment. The patient was discharged home after 23 days in the hospital on a single antiplatelet (clopidogrel 75 mg once daily) and low-dose beta-blocker (bisoprolol 1.25 mg once daily). She was advised to avoid any physical activity such as heavy lifting and strenuous activities. Unfortunately, 1 month later, the patient was re-referred by her general practitioner for cardiac evaluation due to an ongoing 3-week history of chest tightness on mild exertion. On this occasion, troponin levels were within normal limits (<5 ng/L) and serial ECGs were normal. Cardiovascular examination remained unremarkable. A repeat CT coronary angiography (CTCA) showed significant improvement of the coronary dissections; with increased patency and calibre of the LAD and proximal LCx segments ( Fig. 7B ). There were short residual dissections at the origins of the first and second obtuse marginal branches associated with mild to moderate luminal narrowing. Stents in the right coronary artery (RCA) appeared widely patent with good distal flow. She was initially trialled on a selective sinus node I(f) channel inhibitor (ivabradine 5mg twice daily) which did not relieve her symptoms. However, the introduction of a long-acting nitrate (imdur 30 mg once daily) resulted in a marked improvement in symptom burden.

Written informed consent was obtained from the patient for publication of this case report, including relevant clinical details and accompanying images. This patient was made aware that identifiable information may be included in the publication.

A high index of suspicion for SCAD is warranted in young women presenting with ACS. Conservative and medical management remain the cornerstone of treatment with regular follow-up CT coronary angiograms (CTCA) for stable patients with SCAD as the majority of dissections tend to heal spontaneously. However, coronary revascularisation is indicated in cases involving the left main stem, complete vessel occlusion, ongoing chest pains or haemodynamic instability. PCI remains technically challenging and should be undertaken by experienced operators, utilising intravascular imaging and ideally with onsite surgical back-up due to increased risk of procedural complications.

Spontaneous coronary artery dissection (SCAD) in young women is relatively uncommon and presents with unique clinical challenges in management. With SCAD predominantly affecting young females, it is hypothesised that physical and emotional stressors contribute to its occurrence. In our case, the patient likely experienced gastroenteritis prior to hospital presentation, which may have acted as a trigger, with stress-induced catecholamine surges potentially contributing to shear stress in the coronary arteries. One study found that extreme physical stressors and emotional stress contributes to 40% and 24% of SCAD respectively [ 4 ]. This case underscores the potential risks of coronary angiography in patients with SCAD. The initial coronary angiogram was complicated by a probable iatrogenic catheter-induced dissection of the right coronary artery (RCA). Computed tomography coronary angiography (CTCA) is the preferred initial and follow-up noninvasive imaging modality for suspected SCAD, when available. However, the sensitivity of CTCA for distal or branch vessel dissection is limited [ 5 ]. In the acute management of SCAD, current guidelines generally recommend a conservative approach where feasible. This includes consideration for coronary revascularization in cases of ongoing ischemia or haemodynamic instability and coronary artery bypass grafting (CABG) for severe dissections involving the left main coronary artery or proximal segments [ 6 ]. In this particular case, a conservative management approach was adopted for the left coronary artery dissections, allowing for the possibility of spontaneous arterial healing. This strategy was supported by serial monitoring with CT coronary angiography (CTCA) supplemented with medical therapy. Dual antiplatelet therapy (DAPT) was de-escalated to single antiplatelet therapy (SAPT) after 4 weeks. This decision was guided by current consensus on the management of iatrogenic dissections post-PCI. While DAPT can be effective, it has been associated with a 2-to-4 fold increased risk of major adverse cardiovascular events (MACE) in this setting [ 7 ]. Additionally, beta-blocker therapy is recommended due to its association with a significantly lower risk of recurrent SCAD. Evidence suggest that beta-blockers may lower the likelihood of recurrence by approximately two-thirds. This remains an area of active research, with ongoing randomized controlled trials such as the BA-SCAD study, which is designed to further evaluate the efficacy of beta-blockers and antiplatelet agents in SCAD management [ 8 ]. These individualised therapeutic strategies reflect a growing understanding of the underlying pathophysiological of SCAD, with the goal of optimising patient outcomes while minimizing the risks associated with invasive interventions [ 9 ].

Spontaneous coronary artery dissection (SCAD) refers to a nontraumatic, nonatherosclerotic tear in an epicardial coronary artery which may range from an intimal rupture to the formation of an intramural hematoma and false lumen. SCAD is the leading cause of acute coronary syndrome (ACS) in young women [ 1 ]. It accounts for approximately 0.1%-4% of all ACS presentations. In women under the age of 50, SCAD is implicated in up to one-third of ACS cases [ 2 ]. This condition most commonly affects middle-aged women, typically in the absence of traditional cardiovascular risk factors [ 3 , 4 ]