Why the study?
Non-obstructive coronary artery disease and atrial fibrillation often coexist, yet their interrelation, underlying pathophysiological mechanisms, and clinical implications are not well understood.
This narrative review highlights the bidirectional pathophysiological interplay between non-obstructive coronary artery disease and atrial fibrillation, emphasizing that coronary microvascular ischemia promotes atrial arrhythmogenesis via inflammation and fibrosis while atrial fibrillation exacerbates myocardial oxygen supply-demand mismatch and endothelial dysfunction.
This article aims to analyze the relationship between non-obstructive coronary artery disease (NOCAD) and atrial fibrillation (AF), exploring the underlying pathophysiological mechanisms and implications for clinical management. NOCAD and AF are prevalent cardiovascular conditions that often coexist, yet their interrelation is not well understood. NOCAD can lead to ischemic necrosis of cardiomyocytes and their replacement with fibrous tissue, sustaining focal ectopic activity in atrial myocardium. Atrial fibrillation, on the other hand, the most common sustained cardiac arrhythmia, is able to accelerate atherosclerosis and increase oxygen consumption in the myocardium, creating a mismatch between supply and demand, and thus promoting the development or worsening of coronary ischemia. Therefore, NOCAD and AF seem to be a complex interplay with one begets another.
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Oancea et al. (2024) studied this question.
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