Key result
Coronary artery spasm stems from endothelial dysfunction, chronic inflammation, oxidative stress, hypercontractility, and ALDH2 deficiency.
Why the study?
Coronary artery spasm is a reversible multifactorial condition causing coronary closure and angina-like symptoms, but its underlying cellular mechanisms remain unclear.
This review highlights the multifactorial pathophysiologic mechanisms underlying coronary artery spasm, identifying potential diagnostic and therapeutic targets.
May inform coronary spasm evaluation; extends mechanistic framework but leaves therapeutic targets open for trials.
Coronary artery spasm (CAS) is a reversible phenomenon caused by spontaneous excessive vascular smooth muscle contractility and vascular wall hypertonicity, which results in partial or complete closure of the lumen of normal or atherosclerotic coronary arteries. The clinical picture of CAS includes chest discomfort which is similar in quality to that of stable effort angina. Mechanisms underlying the development of CAS are still unclear. CAS certainly is a multifactorial disease. In this review, we paid attention to the role of the main pathophysiologic mechanisms in CAS: endothelial dysfunction, chronic inflammation, oxidative stress, smooth muscle hypercontractility, atherosclerosis and thrombosis, and mutations leading to deficient aldehyde dehydrogenase 2 (ALDH2) activity. These findings might shed novel insight on the underlying mechanisms and identify potential diagnostic and therapeutic targets for cardiovascular diseases in the future.
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Franczyk et al. (2022) conducted a review in Coronary artery spasm. Coronary artery spasm is a multifactorial disease driven by endothelial dysfunction, chronic inflammation, oxidative stress, smooth muscle hypercontractility, and ALDH2 deficiency.
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