Showing papers by "Roland E. Schmieder published in 1994"

Accelerated decline in renal perfusion with aging in essential hypertension

Abstract: The present cross-sectional study was designed to assess the effect of the severity of hypertensive cardiovascular disease and age on renal hemodynamics. In a homogeneous population of 157 white men (aged 15 to 87 years), we assessed renal and systemic hemodynamics by measuring mean arterial pressure invasively, renal blood flow by 131I-para-aminohippuric acid clearance, and cardiac output by the indocyanine dye dilution technique. Stepwise multiple regression analysis revealed the following independent determinants of renal blood flow: age (beta = -.42, P < .001), height (beta = +.14, P < .03), mean arterial pressure (beta = -.15, P < .02), and cardiac output (beta = +.19, P < .008). Renal blood flow corrected for height correlated inversely with age in all three groups. However, the renal fraction of cardiac output did not correlate with age in borderline hypertension (r = .17, P = NS) and in normotension (r = .12, P = NS), suggesting a parallel decline in renal blood flow and cardiac output with aging. In contrast, in established hypertension, the renal fraction of cardiac output was closely linked to age (r = .52, P < .001) and significantly steeper (P < .01) than in normotension or borderline hypertension. We conclude that unlike in normotensive subjects or patients with borderline hypertension, patients with established hypertension have an accelerated decline in renal perfusion with aging, reflecting selective functional or structural changes or both in the renal vascular bed.

Comparison of diastolic left ventricular filling and cardiac dysrhythmias in hypertensive patients with and without isolated septal hypertrophy

Abstract: Although many patients with hypertension develop isolated septal hypertrophy (ISH) rather than concentric or eccentric left ventricular (LV) hypertrophy, limited data are available on cardiac structure, function, and arrhythmias in hypertensive patients with ISH. Clinical features, hemodynamics, M-mode echocardiograms, and 24-hour electrocardiographic recordings were evaluated in 21 healthy normotensive subjects, 23 hypertensive patients without LV hypertrophy, 31 hypertensive patients with concentric LV hypertrophy, and 23 hypertensive patients with ISH to determine the prevalence and complexity of cardiac arrhythmias and diastolic LV filling abnormalities. Age, sex, race, obesity indexes, preload, ejection fraction, and LV contractility were similar in all 4 groups, and arterial pressure and afterload were statistically similar in the 3 hypertensive groups. Left atrial emptying index (p < 0.01) and peak LV filling rate (p < 0.01), 2 indexes of diastolic LV filling, were significantly reduced in the 3 hypertensive groups compared with the normotensive group. The duration of rapid LV filling, however, was significantly prolonged only in hypertensive patients with concentric LV hypertrophy and ISH (p < 0.05) but not in hypertensive patients without LV hypertrophy. The prevalence (p < 0.001) and complexity (p < 0.001) of ventricular ectopic activity was also significantly increased to a similar degree in hypertensive patients with concentric LV hypertrophy and in those with ISH compared with normotensive subjects or hypertensive patients without LV hypertrophy. The prevalence and complexity of atrial ectopic activity was only increased significantly (p < 0.001) in those with ISH.

Renal hemodynamic response to stress is influenced by ACE-inhibitors.

Abstract: Cardiovascular responses to new antihypertensive agents have been studied extensively under resting and stress conditions However, the effects of antihypertensive agents on renal hemodynamics have only been investigated at rest To test whether antihypertensive therapy leads to disparate renal hemodynamic effects during exposure to mental stress as opposed to resting conditions, we performed a double-blind, placebo-controlled crossover study In 17 normotensive healthy men, glomerular filtration rate (GFR; inulin clearance) and renal plasma flow (RPF; para-aminohippuric acid clearance) were measured at rest and after a standardized mental stress test, with or without one week's treatment with a new, long-acting ACE-inhibitor cilazapril 25 mg/day ACE-inhibition did not change resting blood pressure, RPF, GFR, or derived parameters, such as filtration fraction, renal vascular resistance and renal fraction of cardiac output Mental stress caused an acute increase in GFR (p < 0001) and filtration fraction with both treatments (0001) However, the increase in GFR and filtration with mental stress was greater (p < 005) with cilazapril treatment than with placebo Thus, renal hemodynamic responses to mental stress were influenced by ACE inhibitors We conclude that the impact of antihypertensive agents on renal hemodynamics during stress cannot a priori be delineated from measurements at rest

Nephroprotection by antihypertensive agents.

Abstract: Arterial hypertension is one of the few factors confirmed to accelerate the development of renal failure. Conversely, several studies have documented that systematic reduction of the blood pressure slows the progression of renal failure. It is postulated that 24-h reduction of the blood pressure should be achieved, best controlled by ambulatory blood pressure monitoring, and that the elevated blood pressure should be reduced to at least below 140/90 mm Hg. In assessing the progression of renal failure, the renal plasma flow and the glomerular filtration rate are measured, because both renal hemodynamic parameters correlate with the degree of severity of histologic changes. Renal blood flow is increased by angiotensin-converting enzyme (ACE) inhibitors, and unchanged or slightly increased by calcium antagonists, whereas renal plasma flow is somewhat decreased by diuretics and beta-blockers. A further criterion for assessing the potential nephroprotective properties of antihypertensive agents is their influence on intraglomerular hemodynamics. According to animal studies, ACE inhibitors can prevent elevated intraglomerular pressure and the associated development of glomerulosclerosis. Retrospective and prospective studies could also demonstrate these findings in human subjects. Despite an equally effective reduction of systemic blood pressure by the antihypertensive medication, there was a lesser reduction in glomerular filtration rate with ACE inhibitors than when another conventional antihypertensive medication was used. It should be further clarified whether these favorable effects of ACE inhibitors were due also to antiproliferative properties (e.g., blockade of the growth-stimulating factor angiotensin II). The results for calcium antagonists are contradictory. Their protective properties in acute renal failure have been documented, but there are no clinical studies verifying the effect of long-term administration of calcium antagonists on the development of renal failure. To summarize, it has been confirmed to date that systemic antihypertensive therapy slows the progression of renal failure of any etiology, and there is initial proof that ACE inhibitors are superior to other antihypertensive agents in this respect.

Salt intake, blood pressure, and cardiovascular structure.

Abstract: Epidemiologic data revealed that a low sodium intake might have a favorable influence on blood pressure throughout an individual's lifetime. Sodium restriction was reported to lead to a modest fall in blood pressure in some studies, although a few groups of hypertensive patients experienced a rise in blood pressure. Left ventricular hypertrophy has been demonstrated to be related to cardiovascular morbidity and mortality independent of other risk factors. Dietary salt intake participates in the hypertrophic process independent of other determinants. Thus, 24-hour urinary sodium excretion has been reported to correlate with left ventricular mass independent of levels of arterial pressure. Three different mechanisms may link dietary salt intake to myocardial hypertrophy: the renin-angiotensin-aldosterone system, the sympathetic nervous system, and fluid volume homeostasis. Whether salt restriction reduces cardiovascular structural damage independent of arterial pressure has not been determined.

Efficacy and tolerance of low-dose loop diuretics in hypertension.

Abstract: Prospective studies have emphasized the key role for diuretics in the treatment of high blood pressure. Short-acting loop diuretics have not achieved the same acceptance as the thiazides in treatment of hypertension. Newer long-acting compounds, however, such as torasemide, have now been found to be as efficacious as the thiazides, particularly as they can be given once daily and have a low side-effect profile. Adverse laboratory side-effects are rare in hypertensive patients treated with torasemide; carbohydrate intolerance, dyslipidaemia, or hypokalaemia have seldom been observed during its long-term administration. For these reasons, torasemide is thera-peutically attractive due to its antihypertensive efficacy with once-daily administration, low incidence of adverse side-effects, and sustained improvement of the cardiovascular risk profile.

Obesity and hypertension.

Abstract: An increasing number of clinical trials have demonstrated that obese patients are more likely than lean individuals to be hypertensive. Moreover, both obesity and arterial hypertension have been identified as independent risk factors for cardiovascular disease. Pathophysiologically, obesity appears to have a major influence on the hemodynamic changes associated with hypertension. The available evidence suggests that at any given level of arterial pressure, obese hypertensive patients have a higher cardiac output and lower total peripheral resistance than do lean patients. Recent reports have indicated that obesity exerts a disparate effect on target organs in hypertension. Whereas at rest obesity seems to mitigate cardiovascular changes in the systemic vascular bed caused by hypertension, no such mitigation was observed in the renovasculature; left ventricular hypertrophy as a major cardiovascular risk factor was even exacerbated by the presence of obesity. The different hemodynamic patterns in obese hypertensive patients have recently been shown clinically relevant for treating hypertensive patients.