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Showing papers by "Roland E. Schmieder published in 1992"


Journal ArticleDOI
TL;DR: The data indicate that the frequency and severity of ventricular ectopy in patients with essential hypertension is determined by age, severity of left ventricular hypertrophy, chamber volume, and indices of contractility and pump function.

23 citations


Journal ArticleDOI
TL;DR: Antihypertensive therapy reduced excretion of total protein, albumin, and NAG activity in hypertensive patients with elevated pretreatment values, potentially indicating reversal of early hypertensive nephropathy.

18 citations


Journal ArticleDOI
TL;DR: An analysis of the underlying pathogenic mechanisms suggests the presence of multiple interacting pathogenic factors in the development of left ventricular hypertrophy and disparate rates of reduction with various antihypertensive drugs point to the existence of blood pressure-independent factors influencing reduction of LVH.

17 citations



Journal Article
TL;DR: A growing body of evidence from human trials supports the inverse correlation between blood pressure and decrease in GFR, even below a level of 140/90 mmHg.
Abstract: There is a clear, inverse association between the level of blood pressure and the progression of renal disease. This association appears to extend well within the «normotensive» blood pressure range. Currently, there are no absolutely incontrovertible data from prospective, randomized trials in humans documenting that high blood pressure is the cause of an accelerated loss of GFR, or that the loss in renal function can be prevented by lowering blood pressure below 140/90 mmHg. Nevertheless, an aggressive lowering of blood pressure in patients with hypertension and renal disease seems reasonable and desirable. First, the control of blood pressure lowers the «all causes» risk of cardiovascular morbidity and mortality in all patients with elevated blood pressure

5 citations


01 Jan 1992
TL;DR: The increasing evidence that identifies left ventricular hypertrophy (LVH) as a powerful prognostic factor leads to the question whether or not reduction of LVH is a desirable goal of antihypertensive therapy and moreover, whether a decrease in arterial pressure per se is the only or the main determinant for reduction ofLVH as discussed by the authors.
Abstract: The increasing evidence that identifies left ventricular hypertrophy (LVH) as a powerful prognostic factor leads to the question whether or not reduction of LVH is a desirable goal of antihypertensive therapy and, moreover, whether a decrease in arterial pressure per se is the only or the main determinant for reduction of LVH. An analysis of the underlying pathogenic mechanisms suggests the presence of multiple interacting pathogenic factors in the development of LVH. Conversely, disparate rates of reduction of LVH with various antihypertensive drugs as well as conflicting results in different hypertensive patients point to the existence of blood pressure-independent factors influencing reduction of LVH.

3 citations


Journal Article
TL;DR: Sympatholytic substances, angiotensin-converting enzyme (ACE) inhibitors, and calcium antagonists are antihypertensive agents that effected adequate reductions in blood pressure as well as regression of left ventricular hypertrophy.
Abstract: One of the earliest structural changes in the heart adapting to hypertension is left ventricular hypertrophy. which can now be exactly measured by echocardiography.Left ventricular hypertrophy increases the incidence of coronary artery disease, heart failure, and sudden death severalfold, independent of the blood pressure levels. Left ventricular hypertrophy requires specific antihypertensive therapy that controls both high blood pressure and increased left ventricular mass

2 citations


Journal ArticleDOI
TL;DR: Results indicate that β-blockade is effective in reducing cardiac responsiveness but, because of vascular counterregulatory mechanisms, BP responsiveness is not decreased, and calcium antagonism preserves the physiological hemodynamic profile while reducing BP responsiveness to stress.
Abstract: The effects of the calcium antagonist isradipine and the β-blocker metoprolol, which are based on different antihypertensive therapeutic principles, were evaluated in 52 men with mild-to-moderate hypertension in a 6-week, double-blind, randomized study. Mental stress-testing was performed before and after active treatment. With isradipine (n=26), the stress-induced responses of cardiac output and total peripheral resistance were not significantly changed, but the blood pressure (BP) response, specifically the diastolic response, was decreased

1 citations