A new review highlights the potential role of single nucleotide polymorphisms (SNPs) in improving the early diagnosis and targeted intervention of coronary microvascular dysfunction (CMD)—a condition linked to myocardial ischemia despite the absence of major artery blockages.
CMD affects a significant proportion of patients with chest pain, particularly women, and is associated with poor cardiovascular prognosis. However, current diagnostic approaches remain cumbersome, and effective treatments are limited. The review explores how genetic markers, particularly SNPs, could aid in risk prediction, disease prognosis, and personalized therapy for CMD.
The study compiles existing findings on CMD-related SNPs, detailing their impact on vascular function, inflammation, and endothelial dysfunction. It also investigates potential genetic links between CMD and other cardiovascular conditions such as coronary artery disease (CAD) and atherosclerosis, identifying shared risk factors that could guide further research.
Notably, the review underscores the pathogenic mechanisms of CMD, emphasizing how SNPs may influence vasoconstriction, endothelial function, and microvascular remodeling. Additionally, the paper identifies SNPs related to key risk factors such as diabetes, hypertension, and hyperlipidemia, further expanding the scope of genetic insights into CMD.
The findings suggest that a genetics-driven approach could revolutionize CMD diagnosis and treatment, offering a pathway toward precision medicine in cardiovascular health. Future research is expected to focus on validating these genetic markers and integrating them into clinical practice to improve patient outcomes.
This comprehensive review sets the stage for advancing genetic research in CMD, with implications for early detection and novel therapeutic strategies targeting microvascular dysfunction.
Source:
Journal reference:
Tian, D., et al. (2024). Single nucleotide polymorphisms: Implications in the early diagnosis and targeted intervention of coronary microvascular dysfunction. Genes & Diseases. doi.org/10.1016/j.gendis.2024.101249.