Do we need to lower coronary resistances?

The coronary blood flow (CBF) and thus coronary resistances are controlled by several factors including intramyocardial resistances related to systolic compression. Because left ventricular systole exerts a striking effect on left CBF, it is obvious that CBF will be reduced by factors such as tachycardia, or enhancement of left ventricular contractile force. Coronary resistances are under metabolic, endothelial, myogenic, and neurohumoral control. The vegetative nervous system has both vasoconstriction (α-adrenergic and parasympathetic cholinergic) and vasodilatation (β-adrenergic) effects. Actually, under vasodilatation conditions, the major part of the coronary resistance is located at the capillary level. Therefore, the low myocardial capillary density observed in experimental models of hypertension and in patients is a major component of increased coronary resistance. Exercise training is associated with adaptations in the coronary microvasculature, including increased arteriolar densities and/or diameters and increased capillary density providing a morphometric basis for the observed decrease in coronary resistance in exercise-trained animals and patients. Several antihypertensive drugs have shown evidence of beneficial effects on myocardial microvascular densities and thus on coronary resistances. A combination of perindopril and indapamide has been tested in several experimental models and in hypertensive patients. Microvascular remodeling and resulting decreased coronary resistance were clearly evidenced in animals and in patients treated with a combination of perindopril/indapamide.