Showing papers by "Roland E. Schmieder published in 1993"
••
TL;DR: The findings in part negate the concept that obesity is able to exert a protective effect on early target organ damage in hypertensive patients and, in particular, on the heart.
Abstract: BACKGROUND Various prospective studies have found that lean hypertensive patients have greater cardiovascular morbidity and mortality than obese hypertensive subjects. It was therefore hypothesized that hypertension is more benign when associated with obesity. In the present study, we evaluated effects of obesity on early target organ damage in patients with essential hypertension. METHODS AND RESULTS In a total of 207 subjects, systemic and renal hemodynamics as well as left ventricular structure and function were assessed by measuring cardiac output (indocyanine green dye dilution), renal blood flow (clearance of 131I paraimmunohippuric acid), and mean arterial pressure (invasively) and by two-dimensionally guided M-mode echocardiographic findings. Systemic and renal vascular resistance, compliance of the large arteries evaluated by the stroke volume/pulse pressure index, and left ventricular mass served as parameters for early target organ damage. All individuals were categorized into four groups: lean and obese normotensive as well as lean and obese hypertensive subjects. In obese hypertensive patients, total peripheral resistance was significantly lower and stroke volume/pulse pressure index was higher than in the lean hypertensive group, almost reaching values of normotensive control subjects. No effect of obesity on the renal circulation was noted, whereas in hypertension, renal vascular resistance was elevated. The degree of left ventricular hypertrophy was more pronounced in the hypertensive groups than in their normotensive counterparts and progressively increased with obesity. Nevertheless, in obese hypertensive patients, left ventricular function, as measured by fractional fiber shortening and velocity of circumferential fiber shortening, was maintained despite the fact that the heart had been exposed to the double burden of an increased preload (obesity) and afterload (hypertension). CONCLUSIONS Obesity had a disparate effect on target organs in hypertension. At rest, obesity seemed to mitigate cardiovascular changes in the systemic vascular bed caused by hypertension. However, no such mitigation was observed in the renal vasculature, and left ventricular hypertrophy was even exacerbated by the presence of obesity. Our findings in part negate the concept that obesity is able to exert a protective effect on early target organ damage in hypertensive patients and, in particular, on the heart.
79 citations
••
TL;DR: Obesity affects the efficacy of metoprolol and isradipine in reducing blood pressure and after taking age and blood pressure before treatment into account there was a significant interaction between obesity and drug therapy.
Abstract: OBJECTIVE--To test the hypothesis that beta blockers lower blood pressure more effectively than calcium entry blockers in obese hypertensive patients and that calcium entry blockers are more effective in lean patients. DESIGN--Double blind, randomised controlled trial of treatment over six weeks. SETTING--Tertiary referral centre. SUBJECTS--42 white men with uncomplicated mild to moderate essential hypertension (World Health Organisation stage I or II); 36 completed the study. INTERVENTION--Patients were randomised to metoprolol 50-100 mg twice daily or isradipine 2.5-5.0 mg twice daily for six weeks after a two week run in phase. MAIN OUTCOME MEASURE--Blood pressure after six weeks of treatment. RESULTS--When stratified according to treatment and presence of obesity (body mass index
49 citations
••
TL;DR: It is suggested that despite a comparable reduction in total peripheral resistance at rest, fosinopril preserves a more physiologic hemodynamic response to isometric and orthostatic stress than isradipine.
Abstract: Optimal antihypertensive therapy should control blood pressure at rest and during stress while preserving the physiologic hemodynamic response. In patients with mild to moderate hypertension, the hemodynamic profile and catecholamine response at rest, during isometric, mental, and orthostatic stresses were compared before and 12 weeks after angiotensin-converting enzyme inhibition or calcium channel blockade. Antihypertensive therapy was titrated either with the angiotensin-converting enzyme inhibitor fosinopril (10 to 40 mg; n = 9) or with the calcium antagonist isradipine (5 to 20 mg; n = 10) until diastolic blood pressure < 90 mm Hg was achieved. Groups were comparable in race, sex, body mass index, pretreatment mean arterial pressure and response to isometric stress (25% increase in mean arterial pressure) before treatment. At rest, total peripheral resistance was reduced to the same extent (18%) in both groups. After fosinopril, the percent increase in stroke volume was higher and heart rate lower than with isradipine. During isometric stress, the percent increase in mean arterial pressure and cardiac output was higher, with isradipine (p < 0.05) reaching pretreatment levels. Plasma catecholamines were also higher with isradipine (p < 0.05), increasing by 100% with plasma norepinephrine compared with 16% before treatment. During orthostatic stress significant reductions in mean arterial pressure and stroke volume were observed after isradipine but not after fosinopril. Neither medication significantly modified the response to mental stress. Our data suggest that despite a comparable reduction in total peripheral resistance at rest, fosinopril preserves a more physiologic hemodynamic response to isometric and orthostatic stress than isradipine.(ABSTRACT TRUNCATED AT 250 WORDS)
16 citations
••
11 citations
••
9 citations