An increasing amount of evidence suggests that the development of myocardial ischemia in hypertensive patients without angiographically demonstrable coronary artery disease, may at least in part be due to anatomic and functional abnormalities of the coronary microvasculature. Studies employing cardiac imaging techniques, in particular positron emission tomography (PET), have demonstrated that the coronary flow reserve (CFR), i.e. the ratio of myocardial blood flow (MBF) during near maximal vasodilatation (pharmacologically-induced) to resting MBF, is significantly impaired in hypertensive patients with or without left ventricular hypertrophy (LVH). In the absence of significant coronary stenoses, an abnormal CFR is suggestive of dysfunction of the coronary microcirculation. In parallel, mechanistic studies have suggested that microvascular dysfunction can be a result of several interacting mechanisms, including myocyte remodeling, vascular (intramyocardial coronary arteriole) remodeling, and decreased vasodilatory capacity of the coronary microcirculatory endothelium. Furthermore, PET studies of patients with hypertrophic cardiomyopathy have demonstrated that the severity of CFR impairment is an independent predictor of clinical deterioration and death in these patients and may precede clinical deterioration by years. Similarly, preliminary studies in hypertensive patients with or without LVH have suggested that long-term therapy with the combination of the ACE inhibitor, perindopril 2 mg, and the diuretic, indapamide 0.625 mg, may improve the status of coronary microcirculation in these patients, although these findings need to be substantiated in larger studies.
ASJC Scopus subject areas
- Pharmacology (medical)