[Coronary microangiopathy in hypertensive heart disease: pathogenesis, diagnosis and therapy]

Abstract

Coronary reserve plays an important role in myocardial oxygen supply. During rest, oxygen consumption is near to maximal. An increase in myocardial oxygen demand can only be covered by an increase in coronary flow by dilation of coronary vessels. The maximal achievable rise in coronary blood flow is called coronary reserve. Coronary reserve is not only enhanced in patients with coronary artery disease but also in patients with disorders of coronary microcirculation for example in arterial hypertension. The following review will deal especially with disorders of the microcirculation in arterial hypertension. The impairment of coronary reserve is a result of structural and functional alterations. Structural alterations include an increase in media wall thickness of the small coronary arteries and a reduction of coronary capillaries. Extravascular myocardial forces which determine coronary resistance include myocardial hypertrophy and qualitative changes of myocardium like interstitial and perivascular fibrosis. The role of functional alterations like endothelial related vasomotion is discussed. The renin-angiotensin system modulates the growth of the small muscle cells of the vessels and induces protooncogenes and other growth factors. Therefore the renin-angiotensin system may also play an important role in hypertensive remodeling. Hypertensive coronary microangiopathy is diagnosed by exercise stress test and ST-segment-monitoring over 24 hours to show myocardial ischemia. Also nuclear medicine technics can be used if conventional methods of showing ischemia don't work. The diagnosis is definite if the determination of coronary reserve shows that the maximal coronary blood flow is not achieved. Coronary flow can be measured by the argon-gas-method, the thermodulation-technic or by the doppler-method. Also by nuclear medicine technics (PET) the coronary flow reserve can be determined. The advantages of these methods are discussed. In experimental studies calcium-channel-blockers, ACE-inhibitors and moxonidine showed an increase in density of capillaries and also a reduction of myocardial hypertrophy, which both result in an improvement of coronary reserve. Clinical studies of our group demonstrate that coronary microangiopathy in hypertensives can be improved by calcium-channel-blockers and ACE-inhibitors after one year treatment. Beta-receptor-blockers show no clear improvement of coronary reserve. It has to be shown by further studies whether the improvement of coronary reserve is more important for prognosis than the regression of myocardial hypertrophy.