Article Text

other Versions

PDF
Acute coronary syndromes
Spontaneous coronary artery dissection
  1. Abtehale Al-Hussaini,
  2. David Adlam
  1. Department of Cardiovascular Sciences, University of Leicester, Glenfield Hospital, Leicester, UK
  1. Correspondence to Dr David Adlam, Department of Cardiovascular Sciences, University of Leicester, Glenfield Hospital, Groby Road, Leicester LE3 9QP, UK; da134{at}leicester.ac.uk

Statistics from Altmetric.com

Learning objectives

  • To recognise spontaneous coronary artery dissection (SCAD) as a cause of myocardial infarction in low-risk, predominantly female, patients and to understand that although SCAD is an important cause of peripartum myocardial infarction, ~90% of incident cases are not pregnant.

  • To be aware that a visible dissection flap at angiography is absent in the majority of cases.

  • To understand the rationale for an ‘as conservative as possible’ approach to revascularisation and key challenges in medical treatment.

Introduction

Spontaneous coronary artery dissection (SCAD) is an increasingly recognised cause of non-atherosclerotic acute coronary syndromes leading to myocardial infarction. It is characterised by the presence of blood entering and separating the layers of the coronary arterial wall to form a false lumen. This leads to external compression of the true coronary lumen restricting coronary blood flow and leading to coronary insufficiency (figure 1). SCAD should be distinguished from atherosclerotic dissections arising from plaque rupture events or erosions allowing blood to enter the intimal space and from iatrogenic dissections arising during coronary procedures.

Figure 1

Pathophysiology of SCAD. A spontaneous haematoma forms in the outer media of a coronary artery forming an FL. This then compresses the artery from the outside restricting blood flow in the TL with typical histological and angiographic appearances. FL, false lumen; SCAD, spontaneous coronary artery dissection; TL, true lumen.

Epidemiology

The true incidence of SCAD is unknown, largely because most patients fall into the lowest risk categories for conventional atherosclerotic disease leading to underdiagnosis and probably lower rates of presentation by patients.1 Historically thought to be very rare, increasing use of high-sensitivity troponin with early angiography for the assessment of acute chest pain presentations has led to a greater recognition of SCAD. However, accurate angiographic diagnosis can be challenging and reported rates of SCAD diagnosis from angiographic registries (0.2%–0.7% of angiograms; 2.0% of ACS angiograms) …

View Full Text

Request permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.