A heart attack induced by spontaneous coronary artery dissection occurs suddenly, rather than overtime, and commonly in younger people who did not appear to be at risk for a cardiac attack.

SCAD is poorly understood, and it’s currently difficult to predict which combo of genes and environmental factors will cause coronary arteries to tear or dissect spontaneously, resulting in a heart attack that necessitates immediate, life-saving medical attention.

The cause of SCAD is still unknown, but factors that increase the risk include women, recent childbirth, abnormal cell growth in artery walls (fibromuscular dysplasia), a history of migraine headaches, depression/anxiety, and the use of hormones in oral contraceptives or infertility treatments.

Now, a team of scientists from Massachusetts General Hospital (MGH) has found a possible genetic basis for SCAD: mutations in the genes controlling the development of fibrillar collagen, one of the most abundant proteins in the extracellular matrix or “scaffolding” that provides blood vessels with their shape, strength, and stability.

“This shows us that the extracellular matrix, the structural part of the blood vessel, is important in this disorder, specifically the collagenous part of that matrix,” said Mark E. Lindsay.

Although no medicines exist to either create or rebuild collagen in blood vessels, the discovery serves as a roadmap for researchers studying SCAD and could contribute to the emergence of new therapies or tactics for preventing spontaneous arterial dissection in at-risk individuals.

Lindsay and colleagues employed the genetic technology known as whole-exome sequencing, which looks at the portion of the human genome involved in the creation and regulation of proteins. The exomes of 130 women and men with SCAD were compared to those of 46,468 people who did not have SCAD.

They discovered uncommon genetic variants in fibrillar collagen genes that were 17 times more common than a background of 2506 other genes detected in coronary arteries.

Furthermore, they discovered that people with SCAD were more likely than people without SCAD to have these so-called “disruptive” (abnormal) uncommon variations within fibrillar collagen genes.

The conclusion was further corroborated by evidence that animals with inactive copies of the most prevalent SCAD gene variations had a higher risk of arterial dissection and enlargement than wild-type mice, with resulting changes in blood vessel collagen. This impact was particularly noticeable in female mice.

“Our findings have implications for genetic testing of patients with SCAD and other arterial dissections, suggesting that it may be helpful to add genes for some additional collagen isoforms to current test panels,” Lindsay added.

Source: 10.1001/jamacardio.2022.0001

Image Credit: Getty

You were reading: Don’t blame diet: a common cause of heart attacks in healthy, young adults – study finds