| Summary: | The coronary vascular system has a unique structure and function that is adaptive to myocardial demand. It is composed of a continuous network of vessels receding in size from epicardial arteries to the microvascular circulation. Failure to meet myocardial demand results in ischemia, angina, and adverse myocardial outcomes. It is evident that 50 % of patients with angina have a non-obstructive coronary disease and 66 % of these patients have coronary microvascular dysfunction (CMD). The impact of CMD on the atria and ventricles is exhibited through its association with atrial fibrillation and distortion of ventricular repolarization. Ultimately, this influence increases the risk of mortality, morbidity, and sudden cardiac arrest. CMD serves as an independent risk for atrial fibrillation, increases ventricular electrical inhomogeneity, and contributes to the progression of cardiac disease. The underlying pathogenesis may be attributed to oxidative stress evident through reactive oxygen species, impaired vasoactive function, and structural disorders such as fibrotic changes. Myocardial ischemia, brought about by a demand-supply mismatch in CMD, may create a milieu for ventricular arrythmia and sudden cardiac arrest through distortion of ventricular repolarization parameters such as QT dispersion and corrected QT dispersion.
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