Disrupting circadian control of peripheral myogenic reactivity mitigates cardiac injury following myocardial infarction.

A portion of peripheral vascular tone and hence, total peripheral resistance, is under circadian control. Myocardial infarction preferentially augments vascular tone in the active phase, when the heart works hardest to provide adequate tissue perfusion. Disrupting the circadian clock reduces peripheral resistance and is associated with improved cardiac function and reduced infarct expansion post-myocardial infarction. The intersection between the circadian clock and myogenic signaling could be a potential therapeutic target to manage peripheral resistance and improve cardiac outcome following an infarction. This mechanism may be safer than current vasodilators, since the therapeutic maximum does not threaten essential hemodynamic control.