Key result
Optimal cardioprotective therapies and reversal of cardiac dysfunction require concomitant targeting and amelioration of coronary microvascular dysfunction.
This review emphasizes the complex regulation of coronary microcirculation and the necessity of targeting microvascular dysfunction alongside myocardial dysfunction in cardiac disease.
May inform trial design for microvascular-targeted therapies; leaves open clinical efficacy pending prospective validation.
Coronary blood flow is closely regulated to meet the changing metabolic demands of the working myocardium. Resistance of the coronary vasculature is determined by metabolic, myogenic, endothelial, and neural mechanisms. The influence of these control mechanisms varies throughout the coronary circulation, as they have dominant sites of action in vessels of different caliber. Coronary vascular resistance depends upon the coordinated response to these influences. Within a segment of the coronary circulation, resistance may be determined, for example, by competitive interaction between neural vasoconstriction and metabolic vasodilation. Such a system in which control occurs through multiple mechanisms with varying effects allows for precise control of coronary blood flow. This system also provides protection against dysfunction of a single control mechanism. If one fails, other control mechanisms can compensate for that loss of function. Thus, adequate delivery of oxygen and nutrients can be maintained despite potential dysfunction and large fluctuations in metabolic demands of the myocardium. In disease states, these regulatory mechanisms may also fail, and endothelial dysfunction is commonly seen in the setting of cardiac disease. Optimal cardioprotective therapies must target the coronary microcirculation and cardiac myocytes in tandem. Similarly, reversal of cardiac dysfunction requires concomitant amelioration of coronary microvascular dysfunction.
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Judy M. Muller‐Delp (2013) conducted a review in Cardiac disease. Optimal cardioprotective therapies and reversal of cardiac dysfunction require concomitant targeting and amelioration of coronary microvascular dysfunction.
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