Spontaneous Coronary Artery Dissection: JACC State-of-the-Art Review

Sharonne N. Hayes, MD; Marysia S. Tweet, MD; David Adlam, DPHIL; Esther S.H. Kim, MD; Rajiv Gulati, MD; Joel E. Price, MD, MPH; Carl H. Rose, MD

Disclosures

J Am Coll Cardiol. 2020;76(8):961-984. 

In This Article

Abstract and Introduction

Abstract

Over the past decade, spontaneous coronary artery dissection (SCAD) has emerged as an important cause of myocardial infarction, particularly among younger women. The pace of knowledge acquisition has been rapid, but ongoing challenges include accurately diagnosing SCAD and improving outcomes. Many SCAD patients experience substantial post-SCAD symptoms, recurrent SCAD, and psychosocial distress. Considerable uncertainty remains about optimal management of associated conditions, risk stratification and prevention of complications, recommendations for physical activity, reproductive planning, and the role of genetic evaluations. This review provides a clinical update on the diagnosis and management of patients with SCAD, including pregnancy-associated SCAD and pregnancy after SCAD, and highlight high-priority knowledge gaps that must be addressed.

Introduction

Over the past decade, there has been a paradigm shift in clinical appreciation of spontaneous coronary artery dissection (SCAD), a nonatherosclerotic, nontraumatic cause of acute coronary syndrome and sudden cardiac death. Recent practice-changing data have informed how this condition is diagnosed and managed. Consensus statements from the United States and Europe[1,2] affirm that SCAD is no longer so "rare" such that it cannot be studied; however, despite improved recognition of SCAD, high-level evidence-based guidance for optimal acute and long-term care are lacking. Available data to guide diagnostic and patient management decisions are still mostly retrospective, observational, and often confounded by selection, survival, and reporting biases. However, recent collaborative multicenter and multinational investigations promise to provide more evidence to inform clinical care.

This review aims to build upon prior consensus statements, incorporate recent evidence to advance understanding of the pathophysiology of SCAD, highlight the importance of and optimal means to accurately diagnose acute SCAD, and discuss controversies and current practice in early post-SCAD management. Developments in our understanding of genetic predilections for SCAD highlight the need for development of molecular, cellular, and whole animal model systems to gain further mechanistic insight into the pathobiology of SCAD. Finally, top priority topics are highlighted to address the pressing clinical and research questions in the care of patients with SCAD.

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