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Biomedical subjects

F H Messerli

Publications and source records attributed to F H Messerli.

At least 271 records · Page 15Linked to original sources
PubMed1983

Disparate cardiovascular effects of obesity and arterial hypertension.

Since obesity and essential hypertension frequently coexist, a study was designed to analyze some of their cardiovascular effects. Twenty-eight obese patients, half of whom were normotensive and half with established hypertension, were matched for mean arterial pressure with 28 corresponding lean subjects. Systemic and renal hemodynamics, intravascular volume, plasma renin activity, and circulating catecholamine levels were measured. Obese patients had increased cardiac output (p less than 0.001), stroke volume (p less than 0.001), central blood volume (p less than 0.02), plasma and total blood volume (p less than 0.01), and decreased total peripheral resistance (p less than 0.001). In contrast, cardiac output, central blood volume, and stroke volume of hypertensive patients were normal, but they had increased total peripheral (p less than 0.001) and renal vascular resistance (p less than 0.001) and a contracted intravascular volume. Left ventricular stroke work was elevated to a similar level in obesity (p less than 0.001) and hypertension (p less than 0.02), but the increase was caused by an expanded stroke volume in the former and by an increase in systolic pressure in the latter. It is concluded that the disparate effects of obesity and hypertension on total peripheral resistance and intravascular volume counteract and may even offset each other. Thus, obesity may mitigate the effects of chronically elevated total peripheral resistance (and therefore end-organ damage) in essential hypertension. Since both entities affect the heart through different mechanisms, their presence in the same patient results in a double burden to the left ventricle, thereby gently enhancing the long-term risk of congestive failure.

Adult↗
PubMed1983

Racial differences in cardiac adaptation to essential hypertension determined by echocardiographic indexes.

Epidemiologic data point to racial differences in cardiac adaptation to hypertension. In this study, echocardiography and measurement of systemic hemodynamics were performed in 30 black and 30 white patients with untreated essential hypertension. Each black patient was matched with a white patient for age, sex and mean arterial pressure. Wall thickness measurements were similar, but left ventricular mass index was significantly increased in blacks (probability [p] less than 0.05). There was a nonsignificant increase in the number of black patients with posterior wall thickness greater than 1.1 cm. Only in black patients was posterior wall thickness related to systolic (r = 0.45; p = 0.008) and diastolic (r = 0.44; p = 0.0042) pressure and to total peripheral resistance (r = 0.32; p less than 0.046). Thus, although ventricular wall thickness changes are similar in black and white patients, qualitative differences exist in the cardiac adaptive process to systemic hypertension.

Adaptation, Physiological↗
PubMed1983

Hemodynamic effects of intravenous labetalol in essential hypertension.

Labetalol inhibits alpha- and beta-adrenergic receptors. Systemic and regional hemodynamic alterations after intravenous labetalol and its cardiovascular reflexive and metabolic effects were evaluated in 12 subjects with mild to moderately severe essential hypertension. Supine systolic, diastolic, and mean pressures were reduced (from 180/101 and 125 to 149/86 and 109 mm Hg; P less than 0.001). The fall was accentuated during head-up tilt and was accompanied by decreased cardiac output and central blood volume in subjects in both the supine and tilted positions. Neither heart rate nor total peripheral resistance was changed by labetalol, suggesting that venodilation resulting from alpha-adrenergic-receptor inhibition played an important role in arterial pressure reduction.

Adult↗
PubMed1983

Cardiac status in juvenile borderline hypertension.

A prospective M-mode echocardiographic study was done to look for early cardiovascular changes in children prone to hypertension with blood pressures between the 75th and 95th percentiles for age. Average systolic/diastolic pressures in 27 children with borderline hypertension were 137/89 mm Hg compared to 110/68 mm Hg for the 26 controls. Echocardiographic measurements were normalized for comparison using two methods. The borderline hypertensive group mean values were significantly greater than controls for left ventricular wall thickness (p less than 0.05 for method 1; p less than 0.001 for method 2), left ventricular mass (p less than 0.001; p less than 0.005) and left ventricular wall thickness to radius ratio (p less than 0.001, both methods). Echocardiographic estimates of left ventricular function were lower in the hypertensive group. This study suggests that cardiac hypertrophy can be shown by noninvasive means in some children before arterial pressure becomes elevated. To assess the incidence and possible consequences of early target organ changes, more extensive clinical evaluation of borderline hypertension in children is recommended.

Adolescent↗
PubMed1983

Cardiovascular changes after weight reduction in obesity hypertension.

Intravascular volumes and systemic and regional hemodynamic variables were measured before and after weight reduction in 12 patients with obesity and essential hypertension. These findings were compared with those in nine patients who did not have any weight loss. Reduction of mean arterial pressure significantly correlated with the fall in total body weight (r = 0.46, p less than 0.05). Total circulating and cardiopulmonary blood volumes were significantly reduced (p less than 0.05 and p less than 0.01, respectively), and these changes permitted a decreased venous return and cardiac output (p less than 0.01). This fall in cardiac output was directly related to a contracted total blood volume (r = 0.49, p less than 0.05) and decreased cardiopulmonary blood volume (r = 0.52, p less than 0.05). Patients who did not lose weight showed no changes in any of these hemodynamic measurements. In addition, weight loss was associated with reduced resting circulating levels of plasma norepinephrine (p less than 0.01), suggesting that diminished adrenergic function may also be related to weight reduction and its associated fall in arterial pressure.

Blood Pressure↗
PubMed1983

Dimorphic cardiac adaptation to obesity and arterial hypertension.

Cardiovascular function and structure were evaluated by M-mode echocardiography and systemic hemodynamics in paired lean and obese patients, either hypertensive or normotensive. Compared to lean patients, obese patients had greater left atrial (p less than 0.0001), ventricular (p less than 0.001), and aortic root (p less than 0.002) diameters; posterior and septal wall thickness (p less than 0.001); and ventricular mass, cardiac output, stroke volume, and stroke work (all p less than 0.0001). Hypertensive patients had increased posterior wall thickness, end diastolic wall stress, stroke work (p less than 0.01), and a lower radius to posterior wall thickness ratio indicating concentric hypertrophy (p less than 0.001) when compared to normotensive patients. Cardiac adaptation to obesity consists of left ventricular dilatation and hypertrophy (eccentric hypertrophy) irrespective of arterial pressure levels. In contrast, essential hypertension solely produces concentric hypertrophy. Both obesity and hypertension increase left ventricular stroke work by disparate hemodynamic mechanisms; their presence in the same patient will tax the heart and increase the long-term risk of congestive failure.

Adult↗
PubMed1982

Cardiovascular effects of obesity and hypertension.

Although often coexisting in the same patient, obesity and essential hypertension exert disparate cardiovascular effects. An excess of adipose tissue augments cardiac output, stroke volume, and left ventricular filling pressure, expands intravascular volume, and lowers total peripheral resistance. In contrast, essential hypertension in a non-obese patient is associated with a contracted intravascular volume, high total peripheral resistance, and normal cardiac output, but increased left ventricular stroke work due to high afterload. Left ventricular adaptation will consist of eccentric hypertrophy in the obese (irrespective of arterial pressure) and concentric hypertrophy in the non-obese hypertension patient. The combination of obesity and hypertension burdens the heart with high preload and high afterload, thereby greatly enhancing the risk of congestive heart failure. Peripheral resistance and intravascular volume may be normal in mildly hypertension obese patients because of the mutually antagonising effects of the increase in arterial pressure and the increase in body weight. The fall in arterial pressure associated with weight loss seems to be caused by a decrease in adrenergic activity which leads to a fall in cardiac output without change in vascular resistance. Obesity hypertension may be the result of an inappropriately raised cardiac output in the presence of a relatively restricted arterial capacity due to the low vascularity of adipose tissue. In morbid obesity increased blood viscosity may contribute to the raised arterial pressure.

Blood Pressure↗
PubMed1982

Diurnal variations of cardiac rhythm, arterial pressure, and urinary catecholamines in borderline and established essential hypertension.

Ambulatory continuous ECG and arterial pressure (BP) were recorded simultaneously (Delmar Avionics Pressurometer II) for 24 hours in 13 age-matched normotensive subjects, 11 patients with borderline hypertension (HBP), and in 10 patients with uncomplicated established essential HBP. Urinary concentrations of epinephrine, norepinephrine, and dopamine were simultaneously collected over four successive 4-hour periods and one 8-hour period. Prevalence and total number of ventricular and supraventricular ectopic beats was low and not affected by arterial BP. Twenty-four-hour rate (HR) and 4-hourly excretion of epinephrine, norepinephrine, and dopamine were comparable between normotensive and HBP persons and no correlation between urinary catecholamines and arterial BP (systolic, diastolic, or mean), HR, or prevalence of ectopic beats was found in any of the three groups or in the total study population. We conclude that HBP patients without ECG evidence of left ventricular hypertrophy do not have a higher prevalence of supraventricular or ventricular ectopic beats. Urinary catecholamines are not related to circadian fluctuations or variability in arterial BP, HR, or prevalence of ectopic beats.

Blood Pressure↗
PubMed1982

Early hypertension and cardiac work.

Myocardial function and ventricular work in early essential hypertension were assessed by comparing systemic hemodynamics and echocardiographic data in 33 normotensive subjects and 38 hypertensive patients, all without left ventricular hypertrophy. External work (tension-time index and cardiac work) and internal work (fiber shortening velocity) were significantly increased in the patients with mild hypertension. Because factors other than blood pressure contribute to cardiac work, antihypertensive therapy must favorably affect both blood pressure and cardiac work.

Adult↗
PubMed1982

Baroreceptor stimulation and isometric exercise in normotensive and borderline hypertensive subjects.

1. The effects of carotid baroreceptor stimulation (neck chamber) on systemic haemodynamics were determined for normotensive and borderline hypertensive subjects during periods of resting and isometric exercise. 2. Both groups reacted to baroreceptor stimulation with a similar decrease in mean arterial pressure and cardiac index at rest and during isometric exercise, but baseline heart rate decreased more in borderline hypertensive patients. 3. Baroreceptor stimulation elicited the same haemodynamic response at rest and during exercise-induced arterial pressure increase. Since the magnitude of arterial pressure had no bearing on the subsequent response, these data suggest resetting of baroreceptors during this short-term blood pressure increase.

Adult↗
PubMed1982

Hemodynamics, biochemical and reflexive changes produced by atenolol in hypertension.

Hemodynamic (systemic and regional), metabolic and cardiovascular reflexive variables were measured before and after 4 weeks of beta blockade with atenolol in 10 patients with mild essential hypertension. Atenolol reduced mean arterial pressure, heart rate, cardiac index (all p less than 0.005) and renal vascular resistance (p less than 0.01) and increased total peripheral resistance (p less than 0.005). Glomerular filtration rate and renal blood flow were unchanged; plasma renin activity fell 43%. Reflexive cardioacceleration during the Valsalva maneuver and upright passive tilt was blunted. No changes were observed in circulating fluid volumes. In six patients followed for 1 year, blood pressure and heart rate were maintained at levels similar to those during the first 4 weeks. Atenolol was shown to be an effective oral antihypertensive that has no apparent deleterious hemodynamic effects on the renal and splanchnic circulations.

Adrenergic beta-Antagonists↗