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New genetic research finds spontaneous coronary artery dissection, or SCAD, heart attacks may be more similar to different diseases than to other heart attacks.
SCAD is poorly understood, and it's so far impossible to predict which combination of genes and environmental triggers will lead coronary arteries to spontaneously tear, or dissect, leading to a heart attack that requires emergency, life-saving medical care.

Researchers have now uncovered additional genetic clues to better understand SCAD, which are desperately needed, says senior author Santhi Ganesh, M.D., from the Michigan Medicine Frankel Cardiovascular Center. The genes Ganesh and colleagues have identified further illustrate the difference between SCAD and the more common heart attack, when plaque builds up in the artery and limits blood flow, called atherosclerosis.

"The SCAD risk alleles were inversely associated with coronary disease and myocardial infarction due to atherosclerotic disease, suggesting very different underlying biology in the artery causing each type of heart attack," Ganesh says.

"It is especially intriguing that many of the same genetic markers are involved, but in different ways, in both SCAD-induced heart attack and atherosclerotic heart attack."

The researchers performed a genome-wide association study, analyzing millions of genetic markers in patients with SCAD and healthy controls. They found a significant association of several specific genetic regions associated with SCAD, which further implicated specific genes influenced by the identified genetic variants, Ganesh says.

Finally, the SCAD risk alleles were positively associated with migraine headache, which highlights a shared genetic basis for migraine headache and SCAD. Ganesh says more research is needed to precisely define the biological relationship of SCAD to vascular diseases such as FMD and migraine headache, as well as its implications for clinical care.

"Identifying these genetic risk alleles helps further advance our understanding of risks of SCAD.