The cause of myocardial ischaemia without major coronary artery disease is microvascular coronary artery disease. The pathophysiological basis of microvascular ischaemia is impaired coronary flow reserve (CFR). Microvascular ischaemia is most frequently associated to hypertension. It is a syndrome of typical chest pain, positive ECG or thallium stress test and normal coronary angiogram. The diagnostic technique of choice is the measurement of CFR reduction at iv. dipyridamole or adenosine infusion. Two main mechanisms account for abnormalities of the coronary microcirculation: myocardial and vascular. Myocardial hypertrophy in combination with increased wall stress may contribute to the reduction of CFR. Interstitial fibrosis including perivascular fibrosis was proposed to be another etiologic factor of impaired coronary microcirculation. Hypertensive remodelling of the coronary microcirculation includes the reduction of vascular density and the increase of the wall/lumen ratio of the small intramyocardial vessels. These alterations can be measured in humans using endomyocardial biopsy. The most important functional factor responsible for microvascular coronary artery disease is endothelial dysfunction, assessed by intracoronary acetilcholin infusion. Microvascular coronary artery disease may be associated with hypertensive heart failure. Hypertensive microvascular coronary artery disease can be reversible, therefore the goals of antihypertensive therapy include not only blood pressure control, regression of hypertrophy and prevention of interstitial fibrosis but also the regression of microvascular abnormalities. Such combined effect can be expected from ACE inhibitors, calcium antagonists and moxonidine.
|Translated title of the contribution||Microvascular coronary artery disease in hypertension|
|Number of pages||6|
|Journal||Lege Artis Medicinae|
|Publication status||Published - Nov 20 1997|
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