AHA Releases a Scientific Statement for Spontaneous Coronary Artery Dissection

By Gerald Chi, M.D. on

Spontaneous coronary artery dissection (SCAD) has gained considerable recognition as an important cause of acute myocardial infarction (AMI), particularly among young females without conventional cardiovascular risk factors.  To facilitate dissemination of current knowledge on SCAD, a Scientific Statement from the American Heart Association was recently published in Circulation by Hayes et al. concerning the current knowledge of epidemiology, precipitants and triggers, pathophysiology, and associated comorbidities.  Furthermore, the document provides an overview of the advance in diagnostic imaging, management options, as well as the prognostic outlook for SCAD, in hopes of spurring a paradigm shift in the care of this under-diagnosed condition.

With respect to the epidemiology, Hayes et al. indicates that the prevalence of SCAD ranges from 0.2 to 4.0% among all ACS cases and from 8.7 to 35.0% among women less than 50 years of age with ACS according to contemporary angiographic registries.  Evidence from cohort series demonstrates that fibromuscular dysplasia is one the most common associated conditions and is observed in 25 to 86% of patients with SCAD.  The authors consider familiarity with the angiographic characteristics and appropriate utilization of intracoronary imaging as important steps to improve the diagnosis of SCAD.

The Scientific Statement acknowledges the lack of prospective comparative trials to offer evidence-based guidance on revascularization and medication.  Based upon observational data, an algorithm for the management of acute SCAD is proposed, supporting a conservative approach in hemodynamically stable patients without objective evidence of ongoing ischemia or high-risk anatomy such as left main or severe proximal two-vessel dissection.

In keeping with the current guideline-directed use of antiplatelet therapy after acute coronary syndrome, expert opinions generally recommend the administration of aspirin for at least one year after an acute SCAD attack in the absence of contraindications.  According to ACC/AHA guidelines for the management of AMI, the Scientific Statement confirms that angiotensin-converting enzyme inhibitors or angiotensin receptor blockers should be used when SCAD is complicated by left ventricular (LV) systolic dysfunction.  Beta-adrenergic blockers may be considered in SCAD patients who have LV dysfunction or arrhythmias and for management of hypertension.  Routine administration of statin therapy is not recommended and should be reserved for the prevention of atherosclerotic disease if indicated.

The authors also advise patients with SCAD to avoid precipitating factors such as prolonged high-intensity activities, highly competitive or contact sports, activities performed to exhaustion (racing, boot camp), abrupt increases in physical activity without a warm-up, exercise in extremes of temperature (hot yoga, cold weather) or terrain, or performance of Valsalva maneuver during lifting or exercise.  Regarding the assessment and management of post-SCAD chest pain, the current ACC/AHA guidelines for ACS are recommended, with additional consideration of SCAD extension or de novo recurrence in the differential diagnosis.  Finally, the Scientific Statement points to the research priorities in the realm of SCAD, and calls upon medical community to continue efforts to raise the awareness and educate fellow physicians.

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