Pathophysiology of hypertensive heart disease Cardiac hypertrophy occurs in response to an overload. When the working load increases, myocytes enlarge until the stress per cell returns to normal [4]. Hypertrophy is commonly considered to be a useful mechanism to preserve myocardial function. However, epidemiological studies have shown that left ventricular hypertrophy itself is a major cardiovascular risk factor and independent of height in both systolic and diastolic pressures [5]. Thus, cardiac hypertrophy cannot be considered a physiological process and seems to contain maladaptive changes which affect the prognosis.

As well as myocardial hypertrophy, media hypertrophy of the arterioles develops, resulting in increased wall thickness-to-radius ratio. In consequence, coronary microangiopathy occurs [1, 6], as illustrated in animal studies and humans. Due to media hypertrophy, the ability of regulation of coronary resistance vessels decreases and results in a reduction of the coronary flow reserve [6, 7]. This reduction of the coronary reserve can be quantified by the argon method in patients with hypertensive heart disease [6], by determination of the coronary blood flow before and after maximal vasodilation induced by dipyridamol. Strauer [6] showed, that the coronary flow reserve in essential hypertension is reduced by up to 30%. Patients with such a reduced coronary reserve often suffer from stenocardia and dyspnoea. Frequent ischemic periods must be discussed as a trigger, already proved by ST-segment Holter monitoring [8, 9]. This reduced coronary flow reserve in patients with left ventricular hypertrophy can be demonstrated relatively early in the asymptomatic