Showing papers by "Roland E. Schmieder published in 1988"
TL;DR: Dietary salt intake is identified as a strong determinant of cardiac structural adaptation to a persistent increase in arterial pressure and a high salt intake might aggravate and, conversely, dietary salt restriction might prevent (or at least mitigate) the development of left ventricular hypertrophy in patients with essential hypertension.
Abstract: Because a given increase in afterload does not consistently produce the same degree of left ventricular hypertrophy, we evaluated several clinical, hemodynamic, and endocrine factors that are prone to modify the adaptation of left ventricular structure in patients with mild essential hypertension (World Health Organization stages I or II). Dietary salt intake assessed by sodium excretion over 24 hours was a powerful determinant of posterior wall thickness (r = 0.64, p less than 0.001), relative wall thickness (r = 0.67, p less than 0.001), and left ventricular mass (r = 0.37, p less than 0.05). In contrast, diastolic pressure, body mass index, hematocrit, and epinephrine were found to be weaker determinants of left ventricular structure (r = 0.31-0.40, p less than 0.05). A stepwise multiple regression analysis revealed that sodium excretion was the strongest predictor for posterior wall thickness (p less than 0.02) and relative wall thickness (p less than 0.05) independent of the other examined variables. These results identify dietary salt intake as a strong determinant of cardiac structural adaptation to a persistent increase in arterial pressure. Consequently, a high salt intake might aggravate and, conversely, dietary salt restriction might prevent (or at least mitigate) the development of left ventricular hypertrophy in patients with essential hypertension.
277 citations
TL;DR: Although the risk of developing congestive heart failure increases in parallel with the degree of obesity, load-dependent indexes of left ventricular function are found to be reduced in patients with morbid obesity only, and some obese patients have depressed myocardial contractility despite well-preserved pump function.
Abstract: Although the risk of developing congestive heart failure increases in parallel with the degree of obesity, load-dependent indexes of left ventricular function are found to be reduced in patients with morbid obesity only. We used the ratio of end-systolic wall stress to end-systolic volume index, which is load-independent, to assess myocardial contractility in 23 nonobese, 28 mildly obese and 26 moderately obese patients with mild to moderate essential hypertension. Although load-dependent indexes (i.e., ejection fraction, fractional fiber shortening and velocity of circumferential fiber shortening) were similar in the 3 groups, end-systolic wall stress to end-systolic volume index was lower in the moderately obese group (2.63 ± 0.4, p
103 citations
TL;DR: The decrease in arterial pressure produced by lisinopril was associated with improved renal hemodynamics and reduced left ventricular mass, and was mediated through arteriolar dilation.
Abstract: The immediate and short-term effects of lisinopril, a new converting enzyme inhibitor, on systemic and regional hemodynamics, cardiac structure and function and humoral indexes were evaluated in 10 patients with mild to moderate essential hypertension. A single oral dose of 5 mg lisinopril reduced mean arterial pressure from 118 to 104 mm Hg (p < 0.01) and significantly increased (p < 0.05) all load-dependent indexes of ventricular function (i.e., ejection fraction, velocity of circumferential fiber shortening and fractional fiber shortening rate). After 10 to 12 weeks of once-daily administration of lisinopril, mean arterial pressure remained reduced over a full 24-hour period (p < 0.01), and was mediated through arteriolar dilation as expressed by the dose correlation (r = 0.93, p < 0.01) between changes in mean arterial pressure and changes in total peripheral resistance. Cardiac index decreased from 3.06 to 2.68 liters/min/m2 (p < 0.01) without correlation to the decrease in arterial pressure (r = 0.06). Despite this reduction in cardiac index, renal blood flow increased from 861 to 1,053 ml/min (p < 0.05) and renal vascular resistance decreased from 14 to 9 units (p < 0.01). Left ventricular mass index decreased from 124 to 109 g/m2 (p < 0.05), and left ventricular function remained unchanged. Thus, the decrease in arterial pressure produced by lisinopril was associated with improved renal hemodynamics and reduced left ventricular mass.
60 citations
TL;DR: Angiotensin II emerged as a determinant of left ventricular structural adaptation in essential hypertension.
46 citations
TL;DR: Enalapril induced a twofold greater reduction than captopril (14%) or lisinopril(12%) and renal hemodynamic effects may be drug specific and not uniform for all ACE inhibitors.
17 citations
TL;DR: In this paper, the authors analyzed the hemodynamic, endocrine and volume characteristics of isolated septal hypertrophy (ISH) in established systemic hypertension, and compared 22 patients with ISH to 23 patients with symmetric hyper-trophy and to 28 without left ventricular (LV) hyper-phy.
Abstract: To analyze the hemodynamic, endocrine and volume characteristics of isolated septal hypertrophy (ISH) in established systemic hypertension, 22 patients with ISH were compared to 23 patients with symmetric hypertrophy and to 28 without left ventricular (LV) hypertrophy. Mean arterial pressure and 24-hour ambulatory pressure readings did not differ between the 2 groups. At the same level of arterial pressure, patients with ISH had a high cardiac index (p
11 citations