Pulse Pressure in der Therapiesteuerung der Hypertonie?

Abstract

Data from the Framingham and several other studies have demonstrated a relatively consistent increase of systolic blood pressure over lifetime but a decrease of diastolic blood pressure after the age of 50-60 years-resulting in an increase of pulse pressure (PP). Epidemiologic studies in the past 10-15 years have stressed the importance of PP as an independent risk factor for cardiovascular morbidity and mortality, especially myocardial infarction and congestive heart failure.A wide clinic PP (60-65 mmHg) has been shown to be a marker of increased arterial stiffness and an elevated cardiovascular morbidity. PP is determined by combined hemodynamic cardiac (ventricular ejection) and arterial factors, like arterial stiffness as well as the timing and intensity of wave reflections. Recent careful measurements have suggested that PP is transmitted much deeper into the microcirculation, which is strongly influenced by aging, hypertension, diabetes, and renal insufficiency (endothelial dysfunction, eutrophic and hypertrophic remodeling, progressive loss of microvessels). Antihypertensive drugs may improve vascular compliance and the alterations of microvascular architecture by reducing blood pressure, relaxing vascular smooth muscle, or promoting long-term effects on extracellular matrix, collagen, vascular smooth muscle, and cardiomyocyte growth and remodeling.Diuretics, beta blockers, long-acting calcium channel blockers, angiotensin-converting enzyme (ACE) inhibitors and angiotensin I (AT(1)) receptor antagonists were critically discussed in relation to their influence on vascular compliance, endothelial dysfunction, the remodeling process, PP, and cardiovascular morbidity and mortality. The vascular protective action of some (especially AT(1) antagonists, ACE inhibitors, calcium channel blockers) but not all (beta blockers) may contribute to improve the outcome of hypertensive patients, although this is presently unproven.