Coronary Artery Spasm—Risk Factors and Pathophysiological Mechanisms | ||||
Records of Pharmaceutical and Biomedical Sciences | ||||
Volume 8, Issue 1, 2024, Page 191-198 PDF (859.6 K) | ||||
Document Type: Mini-reviews | ||||
DOI: 10.21608/rpbs.2024.327931.1332 | ||||
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Authors | ||||
Farah El-Sabbagh ![]() ![]() ![]() | ||||
1department of Biochemistry, faculty of Pharmacy, Sinai University (Kantra campus), El-Arish, Egypt | ||||
2Department of Biochemistry, Faculty of Pharmacy, Suez Canal University, Ismailia, Egypt | ||||
3Faculty of Pharmacy - Suez Canal University | ||||
4Department of Cardiology, Faculty of Medicine, Zagazig University, Zagazig, Egypt | ||||
Abstract | ||||
Coronary artery spasm (CAS) is a common complication associated with transradial access (TRA) for coronary interventions, particularly affecting elderly patients. Coronary artery spasm (CAS), an intense vasoconstriction of coronary arteries that causes total or subtotal vessel occlusion, plays an important role in myocardial ischemic syndromes including stable and unstable angina, acute myocardial infarction, and sudden cardiac death. Coronary angiography and provocative testing usually are required to establish a definitive diagnosis. While the mechanisms underlying the development of CAS are still poorly understood, risk factors include sex, age, smoking, hypertension, and diabetes. Physical and/or mental stress, alcohol consumption and administration of pharmacological agents are precipitation factors. Moreover, polymorphisms in genes encoding for ALDH2, endothelial NO synthase, paraoxonase 1, NADH/NADPH oxidase, and interleukin-6 are linked with occurrence of CAS. Accordingly, oxidative stress, endothelial dysfunction, and low-grade chronic inflammation play an important role in the pathogenesis of CAS, leading to increased coronary smooth muscle Ca2+ sensitivity through RhoA/ROCK activation and hypercontraction. | ||||
Keywords | ||||
Coronary artery spasm; pathophysiology; paraoxanase; nitric oxide | ||||
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