A review of the risk and precipitating factors for spontaneous coronary artery dissection

Abstract

IntroductionSpontaneous coronary artery dissection (SCAD) accounts for 1%–4% of cases of acute coronary syndrome (ACS). SCAD is caused by separation occurring within or between any of the three tunics of the coronary artery wall. This leads to intramural hematoma and/or formation of false lumen in the artery, which leads to ischemic changes or infarction of the myocardium. The incidence of SCAD is higher in women than in men, with a ratio of approximately 9:1. It is estimated that SCAD is responsible for 35% of ACS cases in women under the age of 60. The high frequency is particularly observed during pregnancy and in the peripartum period (first week). Traditional risk factors are rare in patients with SCAD, except for hypertension. Patients diagnosed with SCAD have different combinations of risk factors compared with patients who have atherosclerotic changes in their coronary arteries. We presented the most common so-called “non-traditional” risk factors associated with SCAD patients.Risk factors and precipitating disorders which are associated with SCADIn the literature, there are few diseases frequently associated with SCAD, and they are identified as predisposing factors. The predominant cause is fibromuscular dysplasia, followed by inherited connective tissue disorders, systemic inflammatory diseases, pregnancy, use of sex hormones or steroids, use of cocaine or amphetamines, thyroid disorders, migraine, and tinnitus. In recent years, the genetic predisposition for SCAD is also recognized as a predisposing factor. The precipitating factors are also different in women (emotional stress) compared with those in men (physical stress). Women experiencing SCAD frequently describe symptoms of anxiety and depression. These conditions could increase shear stress on the arterial wall and dissection of the coronary artery wall. Despite the advancement of SCAD, we can find significant differences in the clinical presentation between women and men.ConclusionWhen evaluating patients with chest pain or other ACS symptoms who have a low cardiovascular risk, particularly female patients, it is important to consider the possibility of ACS due to SCAD, particularly in conditions often associated with SCAD. This will increase the recognition of SCAD and the timely treatment of affected patients.

Spontaneous Coronary Artery Dissection in Clinical Practice: Pathophysiology and Therapeutic Approaches

“…The genetic substrate in SCAD pathogenesis is complex, polygenic, and not yet completely understood. Both rare and common disease-associated variants have been found in several genes, which are commonly caused by single nucleotide polymorphisms (SNPs), insertions or deletions, structural variants, intronic variants, and/or short tandem repeat expansions [31][32][33][34][35][36]. Most patients show multigenic rather than monogenic heritage contributing to the pathogenesis of both sporadic and familial SCAD [31][32][33][34].…”

“…Both rare and common disease-associated variants have been found in several genes, which are commonly caused by single nucleotide polymorphisms (SNPs), insertions or deletions, structural variants, intronic variants, and/or short tandem repeat expansions [31][32][33][34][35][36]. Most patients show multigenic rather than monogenic heritage contributing to the pathogenesis of both sporadic and familial SCAD [31][32][33][34]. According to the data, the frequency of genetic variants detected in SCAD patients is almost 8-10%, but it may be underreported [31,36].…”

“…Most common CTD are linked to genes encoding for extracellular matrix proteins in syndromic patterns, like vascular Ehlers-Danlos syndrome with collagen type III alpha 1 chain (COL3A1) gene, Marfan syndrome with fibrillin-1 (FBN1) gene, or Loeys-Dietz syndrome with transforming growth factor beta receptor I and II (TGFBR1 and TGFBR2), or mothers against decapentaplegic homolog 3 (SMAD3) genes. SCAD can be seen as a component of a complex spectrum in these disorders caused by arterial fragility, even in subclinical cases [31][32][33][36][37][38]. Henkin et al [39] estimated a 5.1% overlap of SCAD patients with CTD; common physical findings were non-specific joint hypermobility, translucent skin, myopia, and arachnodactyly.…”

Spontaneous coronary artery dissection: a focus on post-dissection care for the vascular medicine clinician

“…1/3 of P-SCAD cases occur in late pregnancy and 2/3 in the early postpartum period ( 16 , 32 ), and P-SCAD accounts for <5%–17% of SCAD cases overall and 14.5%–43% of pregnancy-associated AMI ( 2 , 14 , 18 , 33 , 34 ). SCAD has also been associated with multiparity ( 35 – 37 ), clomiphene ( 35 ), oral contraceptives ( 7 , 37 , 38 ), and hormone replacement therapy ( 7 , 37 , 38 ). Why it presents often in the peripartum period is unclear, but it could be linked to the hemodynamic changes of pregnancy such as increased cardiac output and blood volume, and reduced systemic vascular resistance ( 39 ).…”

“…It causes less than 1% of MI in some cohorts although it is likely underdiagnosed despite recent efforts at increasing awareness ( 2 ). SCAD occurs primarily in women who may not have traditional risk factors for atherosclerotic coronary artery disease and causes 25%–30% of MI in women younger than 50 years of age, as well as 15%–20% of peripartum and pregnancy-associated MI ( 3 – 7 ). Its pathophysiology is incompletely understood, but it probably results from dissection of the tunica media or rupture of the vasavasorum, causing intramural hemorrhage and hematoma and resultant luminal obstruction by the dissection flap or the hematoma itself.…”