Case Presentation: A 40-year-old woman with a history of asthma presented with progressive shortness of breath and acute onset chest pain. Following a severe asthma exacerbation, she reported increasing dyspnea on exertion that slowly worsened over the subsequent 2 weeks, which she attributed to her asthma. On the day of presentation, she reported mild, asthma related coughing throughout the day. Following one coughing episode, she developed pronounced shortness of breath followed by severe, sudden onset, non-radiating, left-sided chest pain that persisted for approximately 40 minutes. Review of systems was negative for orthopnea, paroxysmal nocturnal dyspnea, recent emotional stressors, or sick contacts. Her family history was significant only for mixed connective tissue disease in her mother. Vitals and exam were within normal limits. An ECG showed T-wave inversions in leads II, III, AVF, and V3-V6. High sensitivity troponins and CK-MB were elevated and peaked at 402 ng/L and 22 ng/mL, respectively. A transthoracic echocardiogram (TTE) showed an ejection fraction of 45% with apical and inferior wall akinesis. A CT coronary angiogram showed abrupt tapering of the mid to distal left anterior descending artery resulting in moderate to severe luminal narrowing over a 4 cm segment. A diagnosis of spontaneous coronary artery dissection (SCAD) was made. The patient was managed conservatively with metoprolol, aspirin, clopidogrel and anti-anginal therapy including nitrates and amlodipine. She was referred to cardiac rehabilitation therapy and her anti-anginals were up-titrated as an outpatient. On follow up, a repeat TTE showed recovered ejection fraction at 64% with only mild apical hypokinesis.
Discussion: SCAD is a rare cause of acute coronary syndrome (ACS), comprising 0.1 to 4 percent of cases. It is thought to be caused by hemodynamic stresses or hormonal fluctuations, occurring most commonly in young females. It is often seen in the peri-partum setting or in those with a personal or family history of connective tissue disease, especially fibromuscular dysplasia, although 20% of cases are estimated to be idiopathic. SCAD most commonly occurs in the mid and distal coronary arteries and most often in the left anterior descending artery. They are categorized into 3 types based on the angiographic appearance and characteristics of the dissection. The most common, Type II, is characterized by diffuse stenosis extending length-wise along the coronary artery. Cardiac CT angiography is the modality of choice to diagnosis SCAD, but for patients with equivocal results, intracoronary imaging can be considered to confirm the diagnosis. In hemodynamically stable patients, conservative management is preferred given that SCAD is usually self-resolving. In particular, beta blockers have been shown to decrease the recurrence of SCAD. Conversely, percutaneous coronary intervention (PCI) or other more invasive strategies have been shown to be technically difficult and are associated with a risk of further coronary artery dissection.
Conclusions: In young, otherwise healthy women with minimal cardiovascular risk factors presenting with ACS, a diagnosis of SCAD should be considered. Conservative management is recommended in hemodynamically stable patients due to the self-limiting nature of SCAD, and there may be an increased risk of harm with more aggressive therapies such as PCI. Anti-anginal and beta blocker therapy are the cornerstones of medical management of SCAD.