Abstract

Coronary heart disease (CHD) remains the leading cause of mortality in developed nations. With age, fatty deposits accumulate in the walls of the coronary arteries and other blood vessels supplying the heart. This buildup restricts blood flow, leading to angina, shortness of breath, and, in some cases, fatal myocardial infarction. While there are several modifiable risk factors for CHD, elevated levels of the amino acid homocysteine (HCY) have emerged as a significant contributor. Experimental and epidemiological studies consistently demonstrate a strong correlation between hyperhomocysteinemia and cardiovascular disease (CVD), and clinical data confirm that HCY functions as an independent risk factor. This article explores the molecular mechanisms underlying HCY’s contribution to CVD risk, offering deeper insights into the pathophysiology of CHD and its associations with elevated homocysteine levels.