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Biomedical subjects

F H Messerli

Publications and source records attributed to F H Messerli.

At least 217 records · Page 12Linked to original sources
PubMed1987

Diltiazem maintains renal vasodilation without hyperfiltration in hypertension: studies in essential hypertension man and the spontaneously hypertensive rat.

The systemic and renal hemodynamic effects of diltiazem were determined in patients with mild to moderately severe essential hypertension and in rats with spontaneous hypertension (SHR). Seven patients were treated for one full year (300 mg/day, average dose) and 10 SHR and 10 normotensive Wistar-Kyoto (WKY) rats received 1 and 2 mg/kg, intravenously. In both man and rat with genetic hypertension, arterial pressure was reduced through a fall in total peripheral resistance without associated reflexive increases in heart rate and cardiac index; and the patients demonstrated no change in plasma volume. In both man and the SHR: renal blood flow increased (in SHR not statistically significant) as arterial pressure and renal vascular resistance fell; glomerular filtration rate (GFR) remained unchanged and the filtration fraction (FF) significantly fell; and calculated intrarenal hemodynamic indices (using the Gomez formulae) demonstrated falls in afferent and efferent glomerular arteriolar pressures and resistances and in intraglomerular pressures, thereby explaining the unchanged GFRs and the decline in FF. These findings in both hypertensive man and rat are in contrast with those of the normotensive WKY that only demonstrated a fall in afferent glomerular arteriolar resistance. Thus, these data demonstrate that diltiazem controlled arterial pressure in both forms of genetic hypertension associated with falls in systemic and renal arteriolar resistances and with improved intrarenal hemodynamics without glomerular hyperfiltration.

Adult↗
PubMed1987

Biventricular cardiac hypertrophy in essential hypertension.

Left ventricular hypertrophy (LVH) is the major adaptation of the heart to a prolonged increase in the left ventricular afterload in hypertension. However, the structure and function of the right ventricle have received little attention. The present study was designed to assess right ventricular structural changes in patients with established essential hypertension. To accomplish this, M-mode echocardiograms were obtained from 15 healthy normotensive subjects and 35 patients with essential hypertension-15 with normal left ventricles and 20 with clear-cut echocardiographic evidence of LVH. In comparison with the normotensive subjects, right ventricular wall thickness was increased almost twofold in the hypertensive patients with LVH (7.0 +/- 2.1 mm vs 3.7 +/- 0.8 mm; p less than 0.001); there was a significant, direct correlation between right and left ventricular wall thickness in the entire patient population (r = 0.65; p less than 0.001). Furthermore, the left atrial emptying index was significantly reduced in all patients with hypertension regardless of whether LVH was present (p less than 0.001) and suggests early diastolic functional involvement of the left ventricle in hypertension. We therefore conclude that right ventricular hypertrophy is associated with LVH in patients with hypertension, although the changes of LVH are frequently more obvious to the clinician.

Cardiomegaly↗
PubMed1987

Disparate hemodynamic responses to mental challenge after antihypertensive therapy with beta blockers and calcium entry blockers.

The hemodynamic response to mental challenge was studied in 40 male outpatients with mild essential hypertension. The patients were treated randomly either with a beta adrenoreceptor blocker (oxprenolol) or with a calcium entry blocker (nitrendipine). Cardiovascular reactivity was evaluated with two different mental arithmetic tasks before and six months after treatment by continuously measuring systolic and diastolic pressure (ultrasonic Doppler device), heart rate (electrocardiography), and stoke volume (impedance cardiography). Patients in both treatment groups had equal decreases in arterial pressure and the same pressures at rest. In patients receiving calcium entry blockers, mental challenge provoked an increase in stroke volume and a decrease in total peripheral resistance similar to results in the pretreatment phase. In contrast, beta adrenoreceptor blockade reversed the hemodynamic response pattern to a distinct decrease in stroke volume (p less than or equal to 0.05) and an increase in total peripheral resistance (p less than or equal to 0.05). In addition, an attenuated heart rate response (p less than or equal to 0.01) and a larger increase in diastolic pressure (p less than or equal to 0.01) were found in the beta blocker group compared with the calcium entry blocker group. Although beta blockers and calcium blockers produce equal decreases in arterial pressure, beta blockers evoke an abnormal hemodynamic response to mental challenge, whereas calcium entry blockers preserve the physiologic reactivity pattern of the untreated state.

Adrenergic beta-Antagonists↗
PubMed1987

Obesity hypertension.

Obesity and hypertension are two major risk factors for the cardiovascular system. Whereas arterial hypertension increases afterload to the left ventricle, obesity produces an increase in stroke volume and increases preload. As a result of this double burden, the heart adapts with eccentric left ventricular hypertrophy. Contractility becomes impaired early in the course of obesity hypertension, and ventricular ectopy is observed. As a consequence, the obese hypertensive patient is at a high risk for congestive heart failure and sudden death. Despite the synergistic effects of obesity and hypertension on the heart, patients appear to be relatively protected from nephrosclerosis and coronary artery disease. These epidemiologic observations are supported by the pathophysiologic changes that take place in obesity hypertension. At any given level of arterial pressure, cardiac output and renal blood flow are elevated in obese hypertensive patients, whereas systemic and renal vascular resistance are decreased when compared to lean hypertensive patients. Because total peripheral resistance is considered the hemodynamic hallmark of arterial hypertension, systemic vascular complications may be less pronounced in obesity hypertension. Weight loss decreases preload, afterload to the left ventricle, and the sympathetic drive to the heart. Protecting the heart from these hypertrophic stimuli should be a major goal of preventive cardiology.

Heart Failure↗
PubMed1987

Immediate hemodynamic response to furosemide in patients undergoing chronic hemodialysis.

To evaluate the effect of furosemide on cardiovascular hemodynamics in patients with end-stage renal failure, we studied ten patients undergoing hemodialysis three times a week. Arterial pressure, heart rate, and cardiac output (indocyanine green dye) were measured in triplicate; total peripheral resistance and central blood volume were calculated by standard formulas. Hemodynamics were determined at baseline and 5, 10, 15, and 30 minutes after intravenous (IV) bolus injection of furosemide 60 mg. Furosemide produced a decrease in central blood volume of -13% +/- 2.2% from pretreatment values (P less than .01) that was most pronounced five minutes after injection, together with a fall in cardiac output (from 6.76 +/- 0.59 to 6.17 +/- 0.52 L/min, P less than .10). Stroke volume decreased with a maximum fall occurring after 15 minutes (from 84 +/- 7 to 79 +/- 7 mL/min, P less than .05), and total peripheral resistance increased (from 15.8 +/- 2.1 to 17.8 +/- 2.3 units, P less than .05) after furosemide. Arterial pressure and heart rate did not change. The decrease in central blood volume reflects a shift of the total blood volume from the cardiopulmonary circulation to the periphery, suggesting dilation of the peripheral venous bed. Thus, even in patients undergoing hemodialysis, furosemide acutely decreases left ventricular preload by venous dilation and should therefore prove to be beneficial in acute volume overload.

Adult↗
PubMed1987

Cardiovascular effects of verapamil in patients with essential hypertension.

The cardiovascular effects of intravenous verapamil and 3 months of oral administration of a slow-release form of verapamil (verapamil-SR) were studied in 10 patients with mild-to-moderate essential hypertension. Intravenous verapamil reduced arterial pressure by 15% (p less than .01) through a fall in total peripheral resistance of 29% (p less than .01); provoked a reflexive rise in heart rate (by 19%, p less than .02), cardiac output (by 74%, p less than .01), and plasma catecholamines; and shifted intravascular volume toward the cardiopulmonary circulation indicating peripheral venoconstriction. Quite in contrast to the immediate effects of the intravenous drug, oral therapy with verapamil-SR for 2 to 3 months lowered arterial pressure effectively (by 15%, p less than .01) by inducing vasodilation of 15% (p less than .02), but without causing reflex tachycardia, activation of the sympathetic-adrenergic or renin-angiotensin systems, or volume expansion. Oral therapy with verapamil-SR preserved systemic and renal blood flow and slightly reduced cardiac mass (by 6%, p less than .05) and renal vascular resistance (by 25%, p less than .05). Whereas intravenous verapamil tended to depress myocardial contractility, oral verapamil-SR did not at all affect myocardial contractility or left ventricular function. These cardiovascular effects make verapamil-SR an excellent agent for long-term antihypertensive therapy.

Administration, Oral↗
PubMed1987

Time course of regression of left ventricular hypertrophy in hypertensive patients treated with atenolol.

Regression of left ventricular hypertrophy occurs with a number of antihypertensive drugs, but the time course of this regression has not been defined clearly. We obtained echocardiograms at baseline and serially (on seven occasions) during a 1 year treatment period with the beta-adrenergic receptor inhibitor atenolol in 12 patients with previously untreated essential hypertension. To ensure control of blood pressure in all patients throughout the study, it was necessary to add a thiazide diuretic to the therapy of five patients. Baseline blood pressure was 155/100 mm Hg and fell to 136/84 mm Hg; there was a 20% reduction in heart rate. Posterior and septal wall thicknesses were reduced from 1.16 +/- 0.03 to 1.06 +/- 0.02 cm (p less than .05) and from 1.28 +/- 0.07 to 1.18 +/- 0.06 cm (p less than .05), respectively; this reduction became significant initially at 4 weeks. Left ventricular mass decreased from 144 +/- 9 to 127 +/- 7 g/m2 (p less than .05) and this fall first became statistically significant at 6 months. Significant reduction in electrocardiographic voltages was also seen at 6 months. Therefore, regression of left ventricular hypertrophy with atenolol-induced blood pressure control occurred as early as 4 weeks after starting therapy and was maintained thereafter without apparent compromise of left ventricular systolic function.

Adult↗
PubMed1987

Left atrial abnormalities indicating diastolic ventricular dysfunction in cardiopathy of obesity.

Electrocardiograms and M-mode echocardiograms were evaluated in lean and obese patients, either normotensive or hypertensive, who were paired for mean arterial pressure, age, and sex. Electrocardiographic evidence of left atrial abnormalities (LAA) occurred more frequently (p less than 0.01) and left atrial size was greater in the obese than in the lean patients (p less than 0.01). The left atrial emptying index, an indicator of early diastolic ventricular function, was reduced in obese patients (p less than 0.01), most markedly in those with obesity-hypertension. The left atrial emptying index was reduced in obese patients with electrocardiographic LAA compared to obese patients without this electrocardiographic sign (p less than 0.02). A close correlation (r = 0.61, p less than 0.001) was obtained between the left atrial emptying index and atrial ECG abnormalities. These left atrial abnormalities in obesity and particularly in obesity-hypertension indicate diastolic ventricular dysfunction.

Adult↗
PubMed1987

Disparate cardiovascular findings in men and women with essential hypertension.

We measured systemic hemodynamic, volume, and endocrine findings in 100 hypertensive women matched to 100 men by mean arterial pressure, age, race, and body surface area. Women had a higher resting heart rate, cardiac index, and pulse pressure and lower total peripheral resistance (all p less than 0.01) than men with the same pressure level. Isometric stress caused an increase in arterial pressure that was almost 50% higher in men than in women. The sexual difference in cardiovascular findings was significant before but not after menopause. For any level of arterial pressure, total peripheral resistance (and therefore the risk of hypertensive cardiovascular disease) was lower in women than in men. We conclude that premenopausal women are hemodynamically younger than men of the same chronologic age. Our study identifies a pathophysiologic mechanism for the clinical and epidemiologic finding that essential hypertension is less lethal in women than in men.

Adult↗
PubMed1987

Diagnostic information provided by ambulatory blood pressure monitoring.

Ambulatory blood pressure monitoring allows one to evaluate the blood pressure profile over a 24-hr period. It has been demonstrated that an average of daily pressure readings is more predictive of cardiovascular complications of hypertension than casual monitoring of blood pressure. On the other hand, there is no conclusive evidence that the higher degree of blood pressure variability found in hypertensive patients is related to increased hypertensive morbidity. The absence of a physiological decrease in arterial pressure during sleep is associated with complications of hypertension such as atherosclerosis and left ventricular hypertrophy as well as with impairments of the autonomic nervous system.

Ambulatory Care↗
PubMed1986

Use of diuretic agents in obese or black patients with systemic hypertension.

Any increase in arterial pressure is the result of either an increase in cardiac output, an increase in total peripheral resistance or a combination of the two. Hypertension is not a homogeneous disease, however, and different mechanisms may be operative during the life span of the patient. Hypertension in the young, nonobese patient is usually hemodynamically characterized by high cardiac output, normal to slightly contracted intravascular volume and numerically normal total peripheral resistance. In contrast, hypertension in the middle-aged or elderly patient is usually hemodynamically characterized by normal to low cardiac output, contracted intravascular volume and high total peripheral resistance. Two further subgroups of hypertensive patients can be identified: obese patients, whose hypertension is characterized by high cardiac output, expanded intravascular volume and normal or low total peripheral resistance, and black patients, whose hemodynamic and fluid volume findings are similar to those of their white counterparts, but who tend to have lower heart rates and greater responsiveness to intravascular volume depletion than white hypertensive subjects. A rational therapeutic approach to essential hypertension should take into account these variable pathophysiologic features. Thiazide diuretics continue to be appropriate and generally well-tolerated choices for initial antihypertensive therapy in obese or in black patients. Many obese patients or black patients, however, are likely to develop early left ventricular (LV) hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Osler's maneuver, pseudohypertension, and true hypertension in the elderly.

Up to half of the geriatric population has been reported to have arterial hypertension and, therefore, an augmented risk of heart attack, stroke, congestive heart failure, and sudden death. Recent studies indicate that mechanisms serving to elevate arterial pressure in the elderly diametrically differ from those in younger patients with similar elevation of arterial pressure. Elderly hypertensive patients have a low cardiac output, elevated vascular resistance, impaired tissue flow, and increased arterial stiffness. Arterial stiffness, if marked, can give rise to pseudohypertension--an entity often responsible for inappropriate diagnosis and inappropriate therapy in the geriatric population. Pseudohypertension can be suspected from a simple bedside maneuver that was hinted at by Sir William Osler almost a century ago. Arterial hypertension seems to accelerate the physiologic process of aging in the cardiovascular system and threatens, therefore, to set the biologic clock at a faster pace. Hopefully, antihypertensive agents more closely tailored to underlying mechanisms of pressure elevation will reverse hypertensive damage to target organs and thereby reset the aging process of the cardiovascular system at a slower pace.

Adult↗
PubMed1986

Norepinephrine-induced hypertension in Guillain Barré syndrome.

Systemic haemodynamics, plasma catecholamine levels and diurnal variation of arterial pressure were studied in a 20-year-old patient with hypertension during Guillain Barré syndrome after complete resolution of the illness. Transient arterial hypertension during the course of Guillain Barré syndrome is characterized by an increased total peripheral resistance associated with elevated circulating norepinephrine levels, suggesting an over-activity of the sympathetic nervous system as the underlying mechanism of the elevated blood pressure.

Adult↗