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Biomedical subjects

F H Messerli

Publications and source records attributed to F H Messerli.

At least 109 records · Page 6Linked to original sources
PubMed1996

What, if anything, is controversial about calcium antagonists?

Recent publications purporting to show that calcium antagonists, when used for the treatment of hypertension or in the post myocardial infarction patient, would paradoxically increase the rate of heart attack and mortality have cast doubts on the safety and efficacy of this drug class. All three studies are retrospective, and have various drawbacks. Specifically, the metaanalysis of Furberg et al is fraught with mistakes, of borderline significance, and based on old data pertaining to short-acting nifedipine only (which should not be given in patients who have suffered an acute heart attack). The case control study of Psaty et al suggested that hypertensive patients who were treated with short-acting verapamil, diltiazem, and nifedipine had an excessive rate of myocardial infarction when compared with patients who were treated with diuretics. Two out of the three calcium antagonists that were used in this study were not approved for the treatment of hypertension by the US Food and Drug Administration. Some patients were taking these drugs only once a day whereas, because of their short duration of action, at least a three or four times daily regimen would be required to achieve an acceptable blood pressure control throughout a 24-h period. The cohort study of Pahor et al suggested distinct differences among various calcium antagonists with regard to survival. Blood pressure was controlled in < 40% of all patients, and in some patients blood pressure was never even measured. Recent studies, such as the Prospective Randomized Amlodipine Survival Evaluation (PRAISE), the third Vasodilator-Heart Failure Trial (VHeFT-III), the second Doppler Flow and Echocardiography in Functional Cardiac Insufficiency Assessment of Nisoldipine Therapy (DEFIANT II), the Angina Prognosis Study in Stockholm (APSIS), and the Shanghai Trial of Nifedipine in the Elderly (STONE), attest to the safety and efficacy of the newer long-acting calcium antagonists in patients with a wide spectrum of heart disease. Several ongoing trials including the Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) with amlodipine, the International Nifedipine-GITS Study: Intervention as a Goal in Hypertension Treatment (INSIGHT) with nifedipine, the Hypertension Optimal Treatment study (HOT) with felodipine, the Systolic Hypertension in the Elderly in Europe Trial (SYST-EUR) with nicardipine, the Second Swedish Trial in Old Patients with Hypertension (STOP II) with felodipine, and Nordic Diltiazem Study (NORDIL) with diltiazem, will give us morbidity and mortality data in patients with high blood pressure within the next few years. Until these results are available, we can be confident that the lowering of blood pressure and providing relief of patients with symptomatic angina can be achieved safely and efficiently with the presently available long-acting calcium antagonists.

Calcium Channel Blockers↗
PubMed1996

Fitness in the fit: does physical conditioning affect cardiovascular risk factors in middle-aged marathon runners?

OBJECTIVE: The study was designed to assess cardiovascular risk factors in marathon runners with different degrees of fitness. DESIGN: A total of 30 male middle-aged marathon runners were divided according to their marathon running time into fit (265 +/- 8 min), fitter (222 +/- 5 min) and fittest (178 +/-12 min). The three groups of 10 runners each were comparable in age, weight, and body surface area. Cardiovascular risk factors were assessed by measuring arterial pressure before and during exercise (150 watts) and determination of plasma lipoproteins, uric acid, glucose and white blood cell count before and after a marathon run. RESULTS: All measured laboratory values such as high-density lipoprotein cholesterol (P < 0.05), low-density lipoprotein cholesterol (P < 0.05), total cholesterol (non-significant), triglycerides (non-significant), blood sugar (non-significant), uric acid (P < 0.01) and white blood cell count (P < 0.05) indicated a lower cardiovascular risk in the fastest when compared with the slowest runners. Resting blood pressure was similar in the three groups but consistently lower at all levels of exercise in the fittest when compared with the less fit runners. The fittest runners also showed greater increases in high-density lipoprotein cholesterol after the marathon run (14% vs 8% in the slowest runners, P < 0.005). CONCLUSIONS: We conclude that even at the extreme end of a continuum such as represented by well-conditioned, middle-aged marathon runners, cardiovascular risk factors are related to the degree of fitness, as measured by the marathon running time.

Adult↗
PubMed1996

Hypertension and coronary artery disease in the elderly.

Both hypertension and coronary artery disease are common in the geriatric population, and a variety of pathogenetic links exist between the two disorders. In the elderly patient, coronary artery disease is often asymptomatic and more difficult to recognize clinically. Antihypertensive therapy has been shown to reduce morbidity and mortality from coronary artery disease in the elderly to some extent. A more specific and individualized approach is more likely to increase these therapeutic benefits.

Aged↗
PubMed1996

Prevention and reduction of left ventricular hypertrophy in the elderly.

Left ventricular hypertrophy (LVH) is both a target organ response to arterial hypertension and a disorder that may be responsible for increasing risk of cardiovascular events, including coronary artery disease (CAD) events, in the elderly population. Hypertension and obesity are the strongest risk factors for LVH, and both disorders are more likely to occur with age. Not surprisingly, the prevalence of LVH markedly increases with age. Although LVH may initially be a compensatory mechanism to reduce ventricular wall stress, substantial data indicate that as LVH progresses, coronary flow reserve is reduced, and CAD events are increased. Furthermore, LVH leads to systolic and particularly, diastolic ventricular dysfunction, and an increase in the prevalence and complexity of ventricular dysrhythmias. All types of cardiovascular morbidity and mortality also are increased in patients with LVH. Pharmacologic and nonpharmacologic strategies that may decrease LVH and potentially reduce cardiovascular morbidity and mortality in the elderly are reviewed.

Aged↗
PubMed1995

[The compliance of the large elastic arteries after blood pressure-lowering therapy with a calcium antagonist].

A decrease in the vascular compliance of the large elastic vessels (reduction of their "Windkessel" function) is of decisive importance for the pathogenesis and prognosis of cardiovascular complications such as arteriosclerosis, left ventricular hypertrophy and heart failure. The effect of the antihypertensive calcium antagonist isradipine on the "Windkessel" function of the aorta was measured in terms of the central haemodynamics in ten patients (eight men, two women; mean age 58 +/- 3 years) with essential hypertension (WHO stage I-II) before and 3 months after treatment. The mean arterial blood pressure was obtained invasively from the aortic arch, cardiac output or stroke volume being obtained by the indicator dilution method. The ratio stroke volume/blood pressure amplitude was calculated as a measure of vascular compliance. After 3 months of treatment with isradipine the mean arterial blood pressure fell from 114 +/- 4 to 97 +/- 3 mm Hg (P < 0.01), and total peripheral resistance from 22 +/- 1 to 18 +/- 1 U, P < 0.05), while vascular compliance rose from 1.07 +/- 0.10 to 1.58 +/- 0.10 ml/mm Hg, P < 0.05. The increase in compliance resulted from both the fall in blood pressure per se and the pressure-independent increase in the distensibility of the vessel wall (87 +/- 8% as against 107 +/- 13%, P < 0.05). As the fall in afterload favoured regression in left ventricular hypertrophy and heart failure, this pressure-independent structural and (or) functional change in the great elastic arteries could be decisive for the cardiovascular prognosis of hypertensives.

Aorta↗
PubMed1995

High blood pressure. A side effect of drugs, poisons, and food.

A variety of therapeutic agents or chemical substances can induce either a transient or a sustained increase in blood pressure. These agents increase arterial pressure by either causing sodium retention and extracellular volume expansion or directly or indirectly activating the sympathetic nervous system. Some agents act directly on arteriolar smooth muscle. For certain agents, the mechanism of pressure elevation is mixed or unknown. Paradoxically, some agents that are used to lower arterial pressure may acutely increase arterial pressure. Also, a rebound increase in pressure may be encountered after discontinuation of certain antihypertensive agents. In general, these chemically induced increases in arterial pressure are small and transient; however, severe hypertension involving encephalopathy, stroke, and irreversible renal failure has been reported. Careful evaluation of a patient's drug regimen may identify chemically induced hypertension and prevent the need for evaluation and therapy. This study reviews the therapeutic agents or chemical substances that elevate blood pressure and their mechanisms of action.

Drug-Related Side Effects and Adverse Reactions↗
PubMed1995

Central blood volume: a determinant of early cardiac adaptation in arterial hypertension?

OBJECTIVES: This study was undertaken to assess the influence of the fluid volume state on cardiac adaptation to hypertension. BACKGROUND: Left ventricular hypertrophy is an important predictor of hypertensive complications. We analyzed volume status and its impact on cardiac structural changes in early hypertension. METHODS: In 33 normotensive subjects, 40 patients with borderline hypertension and 63 patients with established essential hypertension, mean arterial pressure was measured invasively; total blood volume was measured by iodine-125-labeled plasma albumin and hematocrit; central blood volume by indocyanine green dye dilution curve; and diastolic diameter and left ventricular mass by two-dimensional-guided M-mode echocardiography. RESULTS: Central blood volume was approximately 20% higher in patients with stage I borderline hypertension than in normotensive subjects ([mean +/- SD] 3,001 +/- 663 vs. 2,493 +/- 542 ml, p < 0.05), whereas total blood volume was similar in all three groups. This shift in intravascular volume toward the cardiopulmonary circulation was accompanied by a significant increase in diastolic diameter (5.29 +/- 0.80 vs. 4.86 +/- 0.77 cm, p < 0.05) and in left ventricular mass (239.4 +/- 90.6 vs. 183.5 +/- 68.8 g, p < 0.05) in patients with borderline hypertension compared with subjects with normotension. In patients with established essential hypertension, volume status of stroke volume and diastolic dimension returned to normal values, whereas left ventricular mass increased further. CONCLUSIONS: We conclude that the early phase of hypertension is characterized by centripetal distribution of intravascular volume, leading to an increased preload to the left ventricle. This change in volume status appears to be related to cardiac structural adaptation to an increase in arterial pressure.

Adaptation, Physiological↗
PubMed1995

Gender-specific cardiovascular adaptation due to circadian blood pressure variations in essential hypertension.

To determine the effects of circadian variation in arterial pressure on early hypertensive target organ disease, we examined systemic hemodynamics (cardiac output by indocyanine green dye dilution), renal hemodynamics (renal plasma flow by iodine-131 para-aminohippuric acid clearance), left ventricular structure and function (2D-guided M-mode echocardiogram), and 24-h ambulatory blood pressure in 20 women and 46 men with untreated essential hypertension. Both gender groups were subdivided into "dippers" and "nondippers" according to the physiologic nocturnal decrease in mean arterial pressure by 10% of daytime values. Systemic and renal hemodynamics, neurohumoral findings (norepinephrine, epinephrine, dopamine, plasma renin activity), causal blood pressure values, duration of hypertension, and body weight did not differ between the two groups. In contrast, left ventricular mass and mass index was higher in female nondippers than dippers (255 +/- 68 v 184 +/- 81 g, and 137 +/- 30 v 102 +/- 39 g/m2, P < .05, respectively), while in men no significant differences were found (234 +/- 48 v 240 +/- 54 g, and 119 +/- 27 v 121 +/- 13 g/m2, P = NS, respectively). Relative wall thickness (0.45 +/- 0.06 v 0.39 +/- 0.06, P < .05) and posterior wall thickness (1.1 +/- 0.1 v 0.89 +/- 0.2 mm, P < .05) were also found to be greater in female nondippers than in dippers, whereas no significant differences were obtained in men. Thus, the degree of left ventricular hypertrophy correlated with the circadian blood pressure variations in women only, which indicates that left ventricular structure may be more load-dependent in women than in men with essential hypertension.

Adaptation, Physiological↗
PubMed1995

Obesity-related hypertension: mechanisms, cardiovascular risks, and heredity.

Recent investigations cast some doubts on the status of insulin resistance as a trigger in hyperinsulinemia-associated hypertension or obesity-related hypertension, or both. Major epidemiological studies have shown that central adiposity is a powerful risk factor for stroke or coronary artery disease when accompanied by hypertension or hypertriglyceridemia. New heredity studies have failed to identify a common gene that may explain obesity-related hypertension.

Animals↗
PubMed1995

How should renal hemodynamic data be indexed in obesity?

Clearance data are customarily indexed to body surface area of 1.73 m2. This study examined whether this standard procedure gives correct values for renal perfusion in obese subjects. In 215 subjects who varied in age, gender, height, weight, obesity, and mean arterial blood pressure, RPF was determined by measuring the clearance of (131I)para-aminohippuric acid. Multiple regression analysis of the whole study group revealed that age (beta = -0.44, P < 0.001), height (beta = +0.25, P < 0.01), and arterial blood pressure (beta = -0.19, P < 0.01) were independent predictors of RPF, but that weight or body mass index was not. When related to body surface area, RPF appeared to decline with increasing obesity as follows: normal weight, 609 +/- 153 mL/min per 1.73 m2; overweight, 572 +/- 149 mL/min per 1.73 m2; severely overweight, 530 +/- 145 mL/min per 1.73 m2 (P < 0.012). In contrast, RPF related to height reflected a pattern concordant with the multiple regression analysis: normal weight, 3.76 +/- 0.9 mL/min per meter; overweight, 3.86 +/- 1.0 mL/min per meter; and severely overweight, 3.86 +/- 1.0 mL/min per meter (not significant). A separate repetition of the whole analysis for both normotensive (N = 55) and hypertensive subjects (N = 160) revealed a result similar to that found for the whole group. Thus, our results show that obesity was not a determinant of RPF, and when related to body surface area, inappropriately low values of RPF were calculated for obese patients. It was concluded that RPF values correlate with height and not with surface area in obese subjects.

Adolescent↗
PubMed1995

Cardiac rehabilitation, exercise training, and preventive cardiology research at Ochsner Heart and Vascular Institute.

We review data from our institution demonstrating the benefits of cardiac rehabilitation and exercise training on coronary risk factors, exercise capacity, behavioral characteristics, and quality of life in various subgroups of patients. In addition, we discuss our research in several other areas of preventive cardiology, including lipid disorders, hypertension, left ventricular hypertrophy, fish oils, and antioxidants. We believe that we are now in a very exciting era in which a multifactorial approach to the primary and secondary prevention of coronary artery disease is needed in order to further reduce morbidity and mortality rates.

Antioxidants↗
PubMed1995

Hypertension and left-ventricular hypertrophy.

Left-ventricular hypertrophy (LVH), the primary cardiac manifestation of hypertension, has been identified as the most powerful risk factor for future cardiovascular events causing morbidity and mortality, such as myocardial infarction, congestive heart failure, sudden death, and so forth. The increase in myocardial mass lowers coronary reserve and enhances cardiac oxygen requirements, gives rise to ventricular ectopy, and impairs left-ventricular filling and contractility. Besides hypertension, other risk factors such as obesity, advanced age, valvular heart disease, and other pathologic disorders can cause an increase in the hemodynamic burden and lead to LVH. Nonhemodynamic determinants of left-ventricular mass include dietary salt intake, alcohol, and neurohormones. LVH and its sequelae can be reduced by specific antihypertensive therapy, but despite these promising findings, future epidemiologic studies are necessary to document the clinical benefits of a reduction in LVH.

Cardiovascular Diseases↗