Spontaneous coronary artery dissection (SCAD): recent findings

A recent review was published in Heart, Lung and Circulation.

From the review:

Previously considered rare, SCAD is now recognised to be the cause of 2–4% of all cases of ACS, 24–36% of myocardial infarcts (MI) in women less than 50 years, and the commonest cause of an MI associated with pregnancy. SCAD predominantly affects women (92–98% of cases), who are relatively young (42–52 yrs) and have a low incidence of traditional risk factors.

In addition to primary or isolated SCAD, spontaneous dissection of coronary arteries can occur in association with connective tissue disorders [10] [e.g., Marfan's syndrome (fibrillin, FBN1, gene defect), Ehlers Danlos, type 4 (collagen, COL3A1, gene), cystic medial necrosis, Loeys-Dietz syndrome (LDS), type II (transforming growth factor B receptor, TGFBR2, or SMAD3 genes); atherosclerotic coronary artery disease; aortic dissection with coronary artery extension, or inflammatory disorders (e.g., systemic lupus erythematosus (SLE), Crohn's disease, ulcerative colitis).

These cases might be termed syndromic (as opposed to primary) SCAD.

More from the review:

There is no single unifying disease process leading to SCAD, although, based on the finding of familial clustering of SCAD cases with involvement of mother-daughter, identical twin sisters, sister-sister, aunt-niece, and first-cousin pairs [14] , and strong association of SCAD with fibromuscular dysplasia (FMD)…

Risk factors for SCAD include intense physical exercise (isometric or aerobic), Valsalva manoeuvre (e.g., retching, vomiting, bowel movement, coughing), pregnancy (most commonly in the peripartum period)…

Conservative medical management is recommended in patients without ongoing chest pain or ECG changes and usually is associated with spontaneous healing of the affected segment on subsequent angiography [18] . Long-term aspirin and β-blockers are commonly prescribed, although the rationale for using anti-platelet or anti-coagulant therapy, including aspirin, in patients with an IMH without an intimal tear, is tenuous, given that such therapy may increase bleeding within the vessel wall. Intravenous heparin should not be given or should be stopped in such patients once the diagnosis has been made. Thrombolytic therapy, dual antiplatelet therapy and glycoprotein IIb/IIIa inhibitors should be typically avoided. There is also little rationale for the use of statins unless the patient is dyslipidaemic. Angiotensin converting enzyme inhibitors or angiotensin receptor blockers may be administered to patients with a large MI providing they are not hypotensive.

Percutaneous coronary interventions (PCI) ± stenting should be avoided as outcomes are poor. Moreover, the affected vessel is prone to iatrogenic dissection and extension...