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Biomedical subjects

F H Messerli

Publications and source records attributed to F H Messerli.

At least 19 recordsLinked to original sources
PubMed1992

Stress response pattern in obesity and systemic hypertension.

Under resting conditions obese hypertensive patients have been described as having a greater cardiac output and lower total peripheral resistance than lean hypertensive patients. To evaluate the hemodynamic patterns under stress conditions, we determined the hemodynamic response to mental stress (first study) and during isometric exercise (second study) in hypertensive patients with a body mass index > 27 kg/m2 (obese) and < 27 kg/m2 (lean). The cohort exposed to mental stress comprised 54 white male patients (30 were lean, 24 were obese) with untreated stage I or II essential hypertension according to the World Health Organization. Obese subjects responded with a higher increase in total peripheral resistance (p < 0.02) and lower increases in heart rate (p < 0.01), cardiac output (p < 0.01) and stroke volume (p < 0.02) when compared with their lean counterparts. This was independent of any differences in chemical or baseline hemodynamic characteristics at rest. The cohort exposed to isometric stress consisted of 57 patients (30 were lean, 27 were obese) with World Health Organization stage I or II essential hypertension. Obese subjects responded with exaggerated increases in systolic (p < 0.04) and diastolic (p < 0.01) pressures, and heart rate (p < 0.04) when compared with lean patients. Body mass index emerged as an independent determinant of the increase in systolic (r = 0.03) and diastolic (r = 0.01) pressure as well as of heart rate (r = 0.03). These results indicate that obese hypertensive patients respond to (1) mental stress with vasoconstriction instead of the expected vasodilation, and to (2) isometric stress with an exaggerated increase in arterial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Weight↗
PubMed1992

Hypertension, left ventricular hypertrophy, ventricular ectopy, and sudden death.

Left ventricular hypertrophy (LVH) is a common sequela of sustained arterial hypertension, although the correlation between spot blood pressure measurements and LV mass is not a close one. LVH has been shown to be a powerful blood pressure-independent risk factor for cardiovascular morbidity and mortality. LVH has been shown to trigger or to accelerate ventricular dysrhythmias, although the connection between ventricular dysrhythmias and sudden death is poorly documented. LVH can be reduced by specific antihypertensive therapy; however, not all drugs are equipotent in this regard. A reduction of LVH has been shown to be associated with a suppression of ventricular dysrythmias. Preliminary studies also indicate that the reduction of LVH may reduce its inherent excessive morbidity and mortality.

Antihypertensive Agents↗
PubMed1992

Left ventricular hypertrophy. Its relationship to obesity and hypertension.

Hypertension and obesity are closely related. Obese patients tend to have increased intravascular volume and cardiac output and decreased total peripheral vascular resistance and plasma renin activity. Lean patients with essential hypertension usually have increased total peripheral resistance. Left ventricular adaptation in obesity consists of eccentric left ventricular hypertrophy (LVH), regardless of the level of arterial pressure. Obesity and hypertension occurring together place a dual burden on the left ventricle and are associated with systolic and diastolic dysfunction, lipid abnormalities, insulin resistance, and a propensity for frequent, complex ventricular arrhythmias. Congestive heart failure and sudden death are common sequelae of obesity-hypertension and LVH. Treatment should include vigorous efforts at weight reduction and sodium restriction. Diuretics are ideal agents from a hemodynamic standpoint but often do not improve the total risk profile, with the possible exception of indapamide (Lozol). Calcium blockers may be ideal agents because of their favorable effects on both hemodynamics and total cardiovascular risk profile.

Arrhythmias, Cardiac↗
PubMed1992

Is the decrease in arterial pressure the sole factor for reduction of left ventricular hypertrophy?

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.

Blood Pressure↗
PubMed1992

Determinants of ventricular ectopy in hypertensive cardiac hypertrophy.

Left ventricular hypertrophy in arterial hypertension has repeatedly been documented to trigger or aggravate ventricular ectopy. To determine cardiovascular mechanisms underlying ventricular ectopy, we examined 53 hypertensive patients with mild to moderate nondilated left ventricular hypertrophy by 24-hour echocardiographic monitoring and two-dimensional (2-D)-guided M-mode echocardiography. Patients with more severe ectopy (Lown's class II to IV) were older and had greater increases in left ventricular mass, ejection fraction, velocity of circumferential fiber shortening, end-diastolic volume index, and left ventricular stroke work than patients with less severe ectopy (Lown's class 0 to I). Left ventricular mass, end-diastolic diameter, stroke volume, stroke work, ejection rate, velocity of circumferential fiber shortening, and fractional fiber shortening were enhanced in a subgroup with complex ventricular ectopy (multiform or paired premature ventricular beats or runs of ventricular tachycardia) when compared with a subgroup matched with respect to age, sex, body surface area, and mean arterial pressure, which had uniform monofocal ventricular beats occurring with a frequency of less than 10/hr only. Our 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. Whether or not the pattern of ventricular ectopy will identify hypertensive patients with left ventricular hypertrophy who are at increased risk of sudden death remains to be determined.

Adult↗
PubMed1992

Preserved ventricular pump function after a marked reduction of left ventricular mass.

OBJECTIVES: This study was designed to evaluate the long-term effects of combination therapy with an angiotensin-converting enzyme inhibitor and a beta-adrenergic blocking agent on the relation between the decrease in arterial pressure at rest and during exercise and the decrease in left ventricular mass. BACKGROUND: A variety of antihypertensive drugs including angiotensin-converting enzyme inhibitors and beta-blockers have been shown to reduce ventricular hypertrophy, although little is known about combination therapy and the time course of such a reduction. METHODS: Twenty-one patients with previously untreated essential hypertension were treated with a low dose combination of 50 mg of atenolol and 10 mg of enalapril once daily for 39 months. Cardiovascular findings were assessed by two-dimensionally guided M-mode echocardiography in the pretreatment phase and after 6 and 39 months of combination therapy. RESULTS: Combination therapy reduced arterial pressure at rest from 161/108 to 130/86 mm Hg (p less than 0.001) and exercise arterial pressure at 100 W from 192/112 to 167/95 mm Hg (p less than 0.001). After 6 months of treatment, significant decreases in interventricular septal thickness (9%, p less than 0.001), posterior wall thickness (9%, p less than 0.001) and left ventricular mass index (16%, p less than 0.001) were demonstrated on the echocardiogram. After 39 months of therapy, reductions in these values were 28% (p less than 0.001), 29% (p less than 0.001) and 40% (p less than 0.001), respectively. CONCLUSIONS: Long-term treatment with combination therapy of atenolol and enalapril produced significant reductions in arterial pressure at rest and during exercise accompanied by a marked reduction of left ventricular mass. However, whereas arterial pressure decreased immediately and remained unchanged, left ventricular mass decreased more gradually and continued to decrease throughout the treatment period of greater than 3 years. Despite this marked reduction in left ventricular mass, left ventricular pump function was well preserved during rest and exercise.

Adrenergic beta-Antagonists↗
PubMed1992

Depressed systolic and diastolic cardiac function after prolonged aerobic exercise in healthy subjects.

We studied 11 healthy untrained volunteers (aged 28.9 +/- 4.6 years) during 60 minutes of aerobic ergometric exercise with constant heart rates of 130 to 140 beats/minute. We found a continuous and significant decrease in systolic and diastolic pressure from 175 +/- 18/77 +/- 7 mmHg in the 5th minute to 144 +/- 14/68 +/- 6 mmHg in the 60th minute of exercise. Cardiac function and structure were assessed by M-mode echocardiography before exercise, after 5 minutes and after 60 minutes of exercise at comparable heart rates. The results demonstrated significant decreases in cardiac output, ejection fraction, and diastolic posterior wall velocity and an increase in total peripheral resistance after 60 minutes of exercise. We conclude that the decrease in blood pressure during long-term aerobic exercise in healthy untrained subjects might be at least influenced by a decrease in left ventricular filling and contractility, possibly indicating cardiac fatigue.

Adult↗
PubMed1992

Hypertension, left ventricular hypertrophy, ventricular arrhythmias and sudden death.

LVH is a common sequela of arterial hypertension; it increases the risk of sudden death and other cardiovascular morbidity and mortality independent of arterial pressure and has been associated with ventricular arrhythmias. Electrophysiological studies suggest a connection between ventricular arrhythmias in patients with LVH and sudden death. LVH can be reduced by specific antihypertensive therapy, although not all drugs are equipotent in this regard. A reduction in LVH has been shown to diminish ventricular ectopy. Preliminary findings suggest that a reduction of LVH and associated arrhythmias may reduce its inherent cardiovascular risk.

Death, Sudden, Cardiac↗
PubMed1992

Selection of antihypertensive therapy: cardiac and extracardiac considerations.

There are four possible pathophysiological mechanisms which may relate left ventricular hypertrophy (LVH) with cardiovascular morbidity and mortality: LVH diminishes left ventricular filling; LVH decreases coronary reserve and hampers myocardial oxygenation; LVH is commonly associated with ventricular arrhythmias, and with long-standing LVH, left ventricular contractility decreases. LVH can be reduced by a range of antihypertensive drugs, although not all drugs are equipotent in this regard. Two recent meta-analyses have indicated that ACE inhibitors are among the most powerful monotherapeutic modalities to reduce LVH. Calcium channel blockers are almost as effective, whereas beta-blockers and diuretics seem to have a lesser effect, despite equipotent antihypertensive properties. Reducing LVH with ACE inhibitors and calcium channel blockers has been shown to improve contractility and left ventricular filling, and diminish ventricular ectopy. A preliminary study also indicates that coronary reserve increases after reduction in LVH. Despite these promising pathophysiological signs, it remains unknown whether or not a reduction in LVH will reduce morbidity and mortality over and above the reduction achieved by a reduction in arterial pressure alone.

Antihypertensive Agents↗
PubMed1992

Does a reduction in left ventricular hypertrophy reduce cardiovascular morbidity and mortality?

Left ventricular hypertrophy is an important risk factor for sudden death and other cardiovascular morbidity and mortality irrespective of the level of arterial blood pressure. Left ventricular hypertrophy, i.e. an increase in wall thickness at the expense of left ventricular volume, is an adaptive mechanism observed in patients with long standing arterial hypertension. Severe left ventricular hypertrophy is associated with a reduction in left ventricular compliance, impaired coronary reserve, ventricular ectopy, and impaired contractile function. Left ventricular hypertrophy can be reduced by antihypertensive therapy; however, not all antihypertensive agents have the same effect on left ventricular hypertrophy despite their similar effects on arterial blood pressure. Angiotensin converting enzyme (ACE) inhibitors appear to be the most powerful agents for reducing left ventricular hypertrophy, followed by the nondihydropyridine calcium antagonists. In addition to reducing left ventricular mass and arterial blood pressure, certain calcium antagonists also improve left ventricular filling, suppress ventricular ectopy, and maintain or enhance contractile function. However, despite these beneficial effects, it is not known whether the risk of cardiovascular morbidity and mortality can be prevented or reduced by specific antihypertensive agents.

Cardiovascular Diseases↗
PubMed1992

End-organ disease in hypertension: what have we learned?

The major target organs that suffer from sustained hypertension are the heart, kidneys, and brain. Cardiac adaptation to arterial hypertension consists of left ventricular hypertrophy (LVH) of the concentric type, that is, an increase in wall thickness at the expense of chamber volume. However, LVH can no longer be considered a simple adaptive myocardial process serving to compensate for the increase in afterload and bring left ventricular wall stress back to normal. Data from the Framingham cohort have shown that the occurrence of LVH drastically increases the risk of sudden death and other cardiovascular morbidity and mortality irrespective of the levels of arterial pressure. Renal adaptation to arterial hypertension consists of a decrease in renal blood flow with elevations in filtration fraction and renal vascular resistance. With progressive hypertensive cardiovascular disease, glomerular filtration rate will fall as well. Recent data in patients with mild-to-moderate hypertension demonstrate that despite "efficacious" antihypertensive therapy, one-third to one-half of hypertensive patients may experience a significant decline in renal function. Cerebrovascular adaptation to hypertension consists of micro- and macrovascular disease leading to vascular dementia, or ischemic or hemorrhagic stroke. Cerebrovascular autoregulation, the mechanism by which cerebral blood flow is maintained, despite changes in arterial pressure, may be altered in hypertension.

Humans↗
PubMed1992

Combination therapy in hypertension.

In patients in whom monotherapy does not control blood pressure a second agent is required. Common combinations in clinical practice are a beta-blocker plus a diuretic, an angiotensin converting enzyme (ACE) inhibitor plus a diuretic, a beta-blocker plus a dihydropyridine calcium antagonist, and an ACE inhibitor plus a calcium antagonist. Since both ACE inhibitors and calcium antagonists are metabolically inert and exert favorable effects on target organ disease, their combination is of particular interest. When combined, these two drug classes have additive effects on antihypertensive efficacy, reduction of left ventricular hypertrophy, and protection of the renal circulation. However, whether or not these favorable pathophysiologic changes induced with combination therapy of ACE inhibitors and calcium antagonists will translate into a reduction of morbidity and mortality remains to be documented.

Antihypertensive Agents↗
PubMed1992

Left ventricular hypertrophy as a coronary risk factor.

Left ventricular hypertrophy (LVH) is one of the most powerful risk factors known for cardiovascular disease. It is associated with impaired left ventricular filling, ventricular ectopy, impaired left ventricular contractility, and myocardial ischemia. Myocardial ischemia has a multifactorial pathogenesis and results from an increased oxygen demand (due to increased hemodynamic burden and increased muscle mass) and a decreased oxygen supply secondary to microvascular disease and coronary artery disease.

Coronary Disease↗
PubMed1992

Effect of antihypertensive therapy on left ventricular hypertrophy and on its pathophysiologic sequelae.

Recent evidence has shown that a decrease in left ventricular hypertrophy (LVH) by antihypertensive agents suppresses ventricular ectopy, improves ventricular filling, and maintains or even enhances LV function. However, not all antihypertensive drugs reverse LVH or reduce ectopy in spite of their ability to lower blood pressure. Preliminary data suggest that the reversal of LVH is linked to a decrease in cardiovascular morbidity and mortality.

Antihypertensive Agents↗
PubMed1991

Hemodynamic comparison of two nifedipine formulations in patients with essential hypertension.

The hemodynamic and humoral effects and trough-to-peak 24-hour blood pressure responses of 2 nifedipine formulations, capsules and continuous-release once-daily formulation tablets, were evaluated in 10 patients with mild to moderate essential hypertension. Both formulations reduced mean arterial pressure similarly from 120 +/- 3 (baseline) to 107 +/- 2 (p less than 0.005) and 105 +/- 2 mm Hg (p less than 0.005) and total peripheral resistance index from 65 +/- 9 (baseline) to 47 +/- 4 (p less than 0.05) and 45 +/- 3 U/m2 (p less than 0.05), respectively. Renal, splanchnic and total forearm (including skin and skeletal muscle) blood flows were maintained or even increased slightly associated with reductions in regional vascular resistances. Decreases in renal, total forearm and skeletal muscle resistances were significant (p less than 0.05) with the capsules, but the decrease was only significant in renal resistance with the long-acting tablets. Intravascular volume did not expand with reduction in arterial pressure. This antihypertensive effect was not related to baseline plasma renin activity levels or age. Nifedipine tablets provided a better control of mean arterial pressure (66%) than did capsules (44%).

Capsules↗