Abstract
Microcirculation conduit, distribution, exchange and reception vessels usually retain a demand‐dependent vascular–tissue match as well as a nutrient friendly capillary–matrix tissue match. Various stimuli can initiate a vascular–capillary matrix‐tissue mismatch. Counter‐regulatory mechanisms result in hyperplasia or apoptosis. Microvascular disease (MVD) as a consequence or outcome of supply–demand mismatch has clinical therapeutic and prognostic implications in the hypertensive syndrome and coronary artery disease (CAD) cases. Recognition of the role of apoptosis and MVD may initiate a paradigm shift in clinical practice. Digitalis and other anti‐hypertensive agents have anti‐apoptotic action and MVD blunting effects that can control LVH development to reduce congestive heart failure (CHF) progression.
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