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Biomedical subjects

F H Messerli

Publications and source records attributed to F H Messerli.

At least 127 records · Page 7Linked to original sources
PubMed1994

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

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.

Adult↗
PubMed1994

Disparate structural effects on left and right ventricles by angiotensin-converting enzyme inhibitors and calcium antagonists in essential hypertension.

Reduced left ventricular (LV) mass and wall thicknesses with angiotensin-converting enzyme (ACE) inhibitors and calcium antagonists occur in essential hypertension. Experimental studies have shown that reduction in LV mass is related to hemodynamic as well as nonhemodynamic factors that may influence LV and also right ventricular (RV) structure. Sixty-eight patients with essential hypertension were studied echocardiographically 4 to 8 weeks after antihypertensive therapy was initiated. LV dimensions and wall thicknesses, as well as RV free wall thickness, were measured using 2-dimensionally guided techniques. Patients were divided in 2 groups: those receiving either ACE inhibitors or calcium antagonists. This short-term therapeutic period produced similar hemodynamic changes and reductions in LV mass in both groups. In these 2 groups of patients, we found opposite effects in RV free wall thickness. Thus, RV wall thickness increased from 0.44 +/- 0.02 to 0.56 +/- 0.02 cm (p < 0.01) after therapy in the calcium antagonist group, whereas no change was found in the ACE inhibitor group (0.36 +/- 0.04 vs 0.34 +/- 0.04). These structural changes suggest that ACE inhibitors and calcium antagonists produce dissimilar effects on cardiac cell growth and growth reversal, which may be mediated through different nonhemodynamic effects after short-term therapy.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1994

Ventricular dysrhythmias, left ventricular hypertrophy, and sudden death.

Left ventricular hypertrophy has been documented to be a powerful risk factor for sudden death, acute myocardial infarction, and other cardiovascular morbidity and mortality. The major determinant of left ventricular mass is the hemodynamic burden. However, the hypertrophic process is modified by demographic parameters (age, sex, race), nutritional parameters (salt intake, alcohol, obesity), and neuroendocrine factors (angiotensin, catecholamines, growth hormones, etc.). Ventricular ectopy and more serious arrhythmias are commonly seen in patients with left ventricular hypertrophy. Specific antihypertensive therapy will reduce left ventricular hypertrophy, although not all antihypertensive drugs are equipotent in this regard. A reduction in left ventricular hypertrophy has been shown to diminish left-ventricular-hypertrophy-associated arrhythmias. However, it remains to be shown that patients with left ventricular hypertrophy and ventricular ectopy are at a higher risk of sudden death than those without ventricular ectopy and that the reduction of left-ventricular-hypertrophy-associated ventricular ectopy indeed confers a clinical benefit that exceeds the one from the reduction in arterial pressure alone.

Antihypertensive Agents↗
PubMed1994

Salt intake, blood pressure, and cardiovascular structure.

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.

Animals↗
PubMed1994

Is a decrease in arterial pressure during long-term aerobic exercise caused by a fall in cardiac pump function?

Ten healthy normotensive volunteers demonstrated a progressive decrease (p < 0.01) in systolic and diastolic pressures during 1 hour of aerobic exercise. Cardiac function and structure were assessed by M-mode echocardiography before exercise and, at the same heart rate, after 5 minutes of exercise and after 60 minutes of exercise. After 5 minutes of exercise, heart rate, cardiac output, ejection fraction, fractional fiber shortening, and contractility index significantly increased (p < 0.01, p < 0.05, respectively) and total peripheral resistance decreased (p < 0.01) compared with resting values. When compared with the values at minute 5, there was a decrease (p < 0.01) in cardiac output, ejection fraction, fractional fiber shortening, and contractility index (p < 0.05) and an increase (p < 0.05) in total peripheral resistance after 60 minutes of exercise. We conclude that the gradual decrease in arterial pressure seen with prolonged aerobic exercise is the result of a fall in cardiac pump function (as measured by cardiac output, ejection fraction, fractional fiber shortening, and contractility index), possibly indicating cardiac fatigue.)

Adult↗
PubMed1994

Accelerated decline in renal perfusion with aging in essential hypertension.

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.

Adolescent↗
PubMed1994

Cardiovascular adaptation to cyclosporine-induced hypertension.

Arterial hypertension is a complication of cyclosporine therapy in heart transplant recipients. We studied cardiovascular adaptation to cyclosporine-induced hypertension by determining haemodynamic and echocardiographic indexes in 25 cardiac transplant recipients matched by mean arterial pressure, age, sex, height and weight to 25 patients with established essential hypertension. Twenty-five normotensive subjects matched by age, sex and body habitus were used as controls. Systemic vascular resistance was 15% higher (P = 0.07) and cardiac and stroke volume indices were 20% and 25% lower (P < 0.01), respectively, in the hypertensive cardiac transplant recipients compared with patients with essential hypertension. Patients with essential hypertension and hypertensive cardiac transplant recipients had greater posterior wall thickness and left ventricular mass index than normotensive subjects (P < 0.01); however, hypertensive cardiac transplant recipients had a greater left ventricular mass (245 +/- 7 vs. 223 +/- 8 g, P < 0.05) than patients with markedly established essential hypertension. Left ventricular ejection fraction was significantly lower in hypertensive cardiac transplant recipients when compared with either normotensives or patients with established essential hypertension. These results indicate that established essential and cardiac transplant hypertension are associated with markedly increased systemic vascular resistance. However, after heart transplantation, hypertension is associated with higher systemic vascular resistance, lower cardiac output, stroke volume and stroke work compared with patients with established essential hypertension at the same level of mean arterial pressure. The cardiac adaptation to cyclosporine-induced hypertension has more severe concentric left ventricular hypertrophy and impaired left ventricular systolic performance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1994

Left ventricular mass and cardiac function in patients with essential hypertension.

Two-dimensional guided M-mode echocardiography was used to estimate left ventricular mass and left ventricular performance in 140 untreated hypertensive patients, 38 (27%) of whom had left ventricular hypertrophy. Left ventricular contractility as reflected by ratio of end-systolic wall stress to end-systolic volume index and normalised early left ventricular peak filling rate were decreased in the patients with left ventricular hypertrophy compared with those without hypertrophy and correlated inversely with the left ventricular mass (r = -0.44; P < 0.0001 and r = -0.31; P = 0.0004, respectively). Positive correlations were found between the peak filling rate and either the ejection fraction or the contractility index (r = 0.44; P < 0.0001 and r = 0.24; P = 0.004, respectively). Left ventricular mass also correlated with mean arterial pressure in the whole study population (r = 0.43; P < 0.0001). The data suggest that with the development of left ventricular hypertrophy both contractility and filling of the left ventricle become progressively impaired in hypertensive patients. The decline in cardiac function with progressive left ventricular hypertrophy may represent a pathophysiological correlate of the epidemiological observation identifying left ventricular hypertrophy as one of the most powerful risk factors for future cardiovascular morbidity and mortality. The present study shows that with development of left ventricular hypertrophy in essential hypertension both contractility and filling of the left ventricle become progressively impaired.

Adolescent↗
PubMed1993

Disparate cardiovascular response to stress tests during isradipine and fosinopril therapy.

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)

Cardiovascular System↗
PubMed1993

[Ventricular arrhythmia and sudden cardiac death: the significance of left ventricular hypertrophy as risk factor].

Left ventricular hypertrophy is a frequent and early manifestation of cardiac structural adaptation in patients with essential hypertension. Prospective studies have clearly demonstrated that left ventricular hypertrophy represents a risk factor for cardiovascular morbidity and mortality, including sudden cardiac death. The increased risk is independent of the impact of high blood pressure and other risk factors on the cardiovascular system. Various clinical studies noted increased prevalence and severity of premature ventricular beats in hypertensive patients with left ventricular hypertrophy. Hypertrophy of myocardial cells, dilation of the left ventricle, increased stress of subendocardial myocardium and impaired coronary reserve are discussed as a possible pathogenetic link between myocardial hypertrophy and ventricular arrhythmias. Therapeutically, the primary goal for ventricular arrhythmias in hypertensive patients with left ventricular hypertrophy is regression of left ventricular mass. For this purpose, centrally sympatholytic agents, angiotensin converting enzyme inhibitors, betablockers and calcium antagonists have been found to be effective. Recently we observed that a reduction of left ventricular hypertrophy was associated with a decreased prevalence and severity of ventricular arrhythmias. Nevertheless, prospective studies are required to demonstrate whether reduction of severe ventricular arrhythmias helps to prevent sudden cardiac death due to left ventricular hypertrophy in hypertension.

Antihypertensive Agents↗
PubMed1993

Left ventricular hypertrophy: should it be reduced?

Left ventricular hypertrophy (LVH) is a structural adaptation of the heart to sustained hypertension, serving to normalize increased wall stress. Recent clinical studies have indicated that LVH is a powerful pressure-independent risk factor for cardiovascular morbidity and mortality, particularly sudden death, acute myocardial infarction, and congestive failure. The pathophysiologic sequelae of LVH consist of reduced ventricular filling and contractility, ventricular dysrhythmias, and diminished coronary reserve or myocardial ischemia. LVH can be reduced by antihypertensive therapy, although not all drugs are equipotent in this regard. Angiotensin-converting enzyme (ACE) inhibition seems to be the most powerful monotherapeutic modality for reducing LVH. Recent studies have shown that such a reduction also improves the pathophysiologic sequelae of LVH and maintains left ventricular pump function. Although the reversal of these pathophysiologic events is encouraging, it remains unknown whether reducing LVH will ultimately decrease the excessive risk of sudden death, acute myocardial infarction, and congestive heart failure that has been associated with this disorder independently of arterial pressure.

Heart↗
PubMed1993

Reduction of left ventricular hypertrophy: how beneficial?

Left ventricular hypertrophy (LVH) can no longer be considered a compensatory adaptation of the heart serving to normalize the increased wall stress in hypertension. Recent studies have indicated that LVH is a powerful pressure-independent risk factor for cardiovascular morbidity and mortality. The pathophysiologic sequelae of LVH are reduced ventricular filling and contractility, ventricular dysrhythmias, and diminished coronary reserve or myocardial ischemia. Left ventricular hypertrophy can be reduced by antihypertensive therapy, although not all drugs are equipotent in this regard. Recent studies have shown that such a reduction also improves the pathophysiologic sequelae of LVH, that is, ventricular filling, coronary reserve, and ventricular dysrhythmias, and maintains left ventricular pump function. Although the reversal of these pathophysiologic findings is encouraging, it remains unknown whether a reduction of LVH will ultimately reduce the excessive risk of sudden death, acute myocardial infarction, and congestive heart failure that has been associated with this disorder independent of arterial pressure.

Calcium Channel Blockers↗
PubMed1993

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