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How does the presence of chromosome 1q21.2 and additional loci influence the risk of spontaneous coronary artery dissection (SCAD) and myocardial infarction (MI)?

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Final answer:

The presence of chromosome 1q21.2 and additional loci may influence the risk of SCAD and MI by contributing to genetic predisposition, which alongside other risk factors like high LDL levels, can lead to atherosclerosis and coronary artery occlusion.

Step-by-step explanation:

The presence of a gene locus such as chromosome 1q21.2 and additional loci can influence the risk of spontaneous coronary artery dissection (SCAD) and myocardial infarction (MI) by contributing to the genetic predisposition for these cardiovascular events. For example, certain mutations in these loci may lead to changes in the structure or function of blood vessels or may affect lipid metabolism, which can increase the risk of atherosclerosis—a primary underlying cause of heart disorders like SCAD and MI.

In this context, known risk factors such as high levels of low-density lipoprotein (LDL), low levels of high-density lipoprotein (HDL), hypertension, diabetes, obesity, and lack of exercise can exacerbate the predisposition caused by such genetic factors, leading to the formation of atherosclerotic plaques that occlude coronary arteries and result in ischemia and myocardial infarction.

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