Key result
FMD and SCAD share significant clinical and genetic pleiotropy, including high prevalence of extracoronary vascular abnormalities and shared genetic risk loci such as PHACTR1.
Why the study?
Multifocal FMD and spontaneous coronary artery dissection share clinical associations, extracoronary vascular abnormalities, and genetic links, motivating a review of their shared biology and relationship.
Highlights the shared systemic arteriopathy and genetic susceptibility underlying both FMD and SCAD, supporting the rationale for comprehensive vascular screening in affected patients.
Answers are grounded in this paper and cite their sources.
Shared pleiotropy may support vascular screening consideration in FMD/SCAD; leaves open prospective validation of genetic risk stratification.
Multifocal fibromuscular dysplasia (FMD) and spontaneous coronary artery dissection are both sex-biased diseases disproportionately affecting women over men in a 9:1 ratio. Traditionally known in the context of renovascular hypertension, recent advances in knowledge about FMD have demonstrated that FMD is a systemic arteriopathy presenting as arterial stenosis, aneurysm, and dissection in virtually any arterial bed. FMD is also characterized by major cardiovascular presentations including hypertension, stroke, and myocardial infarction. Similar to FMD, spontaneous coronary artery dissection is associated with a high prevalence of extracoronary vascular abnormalities, including FMD, aneurysm, and extracoronary dissection, and recent studies have also found genetic associations between the two diseases. This review will summarize the relationship between FMD and spontaneous coronary artery dissection with a focus on common clinical associations, histopathologic mechanisms, genetic susceptibilities, and the biology of these diseases. The current status of disease models and critical future research directions will also be addressed.
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Kim et al. (2021) conducted a review in Fibromuscular dysplasia (FMD) and spontaneous coronary artery dissection (SCAD). FMD and SCAD was evaluated. FMD and SCAD share significant clinical and genetic pleiotropy, including high prevalence of extracoronary vascular abnormalities and shared genetic risk loci such as PHACTR1.
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