Hypertensive patients often complain of angina pectoris in spite of a normal coronary angiogram. The aim of this study was to establish whether electrographical signs of transient myocardial ischaemia during 24-h ST Holter monitoring are associated with an increased left ventricular muscle mass. Thirty-five hypertensive patients were studied by 24-h Holter monitoring and M-mode and two-dimensional echocardiography. For control purposes nine normotensives were studied by the same protocol. Hypertensives with and without ST-segment depression did not differ in respect of blood pressure or left ventricular muscle mass (162.9 +/- 80 vs. 162.3 +/- 53 g m-2). Since both groups only showed a borderline left ventricular hypertrophy, the myocardial factor does not seem to be important for the occurrence of ST segment depression. Primary functional and structural alterations at the microcirculation level seem to be responsible for the occurrence of transient episodes of ST segment depression in the Holter electrocardiogram, indicating transient myocardial ischaemia.
Hypertensive left ventricular hypertrophy comprises myocyte hypertrophy, interstitial fibrosis and structural alterations in the coronary microcirculation. This leads to impairment of diastolic function in the left ventricle and coronary flow reserve despite normal epicardial arteries. Consequently, antihypertensive treatment should aim at (1) reversing myocyte hypertrophy, (2) restoring myocardial structure and (3) improving coronary flow reserve without lowering blood pressure. In recent years many clinical studies have shown that regression of hypertensive hypertrophy can be induced by long-term treatment with ACE inhibitors, calcium-channel blockers, beta-receptor blockers and antisympathonic drugs. However, vasodilators and diuretics, which stimulate adrenoceptor activity and increase angiotensin II levels, were found to be less effective in reversing left ventricular hypertrophy. The trophic influence of catecholamines and angiotensin II on the myocardium counteracts the effect of systolic wall stress reduction due to blood pressure lowering. As regards reversal of interstitial fibrosis, ACE inhibitors seem to be effective, because fibroblast growth was found to be stimulated by angiotensin II. Recently, clinical studies have confirmed previous experimental data that improvement in impaired coronary vasodilator reserve can be realized by long-term antihypertensive therapy. In adopting an antihypertensive treatment strategy prime consideration should be given to reversal of cardiac remodelling through restoration of myocardial structure and repair of the coronary microcirculation.
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