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Biomedical subjects

F H Messerli

Publications and source records attributed to F H Messerli.

At least 163 records · Page 9Linked to original sources
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↗
PubMed1991

Hemodynamic effects of celiprolol in essential hypertension.

The immediate and short-term (2 week) hemodynamic and humoral effects of the beta-1 antagonist, beta-2 agonist, celiprolol, were compared with those of more prolonged atenolol therapy in 12 patients with essential hypertension. Celiprolol produced an immediate dose-dependent decrease in mean arterial pressure (113 +/- 3 to 102 +/- 2 mm Hg; p less than 0.001) and total peripheral resistance (49 +/- 3 to 38 +/- 1 U/m2; p less than 0.005) that was associated with an increased heart rate (67 +/- 1 to 73 +/- 2 beats/min; p less than 0.01) and cardiac index (2,347 +/- 129 to 2,708 +/- 111 ml/min/m2; p less than 0.01). Both celiprolol and atenolol reduced mean arterial pressure with short-term treatment (p less than 0.01); this was associated with a reduced total peripheral resistance with celiprolol (from 24 +/- 1 to 21 +/- 1 U/m2; p less than 0.02) and was not observed with atenolol. Moreover, in contrast with atenolol, celiprolol did not change heart rate or stroke and cardiac indexes. Splanchnic and forearm vascular resistances decreased with celiprolol (p less than 0.05) but not with atenolol; neither beta-blocking drug altered renal blood flow. These results demonstrate that the hemodynamic effects of celiprolol were strikingly different from atenolol; celiprolol reduced arterial pressure and total peripheral and certain vascular resistances without altering heart rate, cardiac index or regional blood flows. These effects may be explained by celiprolol's cardiac beta-1 receptor inhibitory and peripheral beta-2 receptor agonistic effects.

Adrenergic beta-Antagonists↗
PubMed1991

Left ventricular filling in the systemic hypertension of obesity.

Cardiac structure and systolic as well as diastolic functions were evaluated by 2-dimensional M-mode echocardiography in lean and obese patients who were either hypertensive or normotensive. Diastolic function, as assessed by diminished normalized early peak filling rate and prolonged duration of rapid filling, was decreased in hypertensive patients compared with normotensive patients (p = 0.02). When compared with lean patients with similar blood pressure levels, obese patients exhibited a lower normalized peak filling rate (p = 0.0014) but no difference in duration of rapid filling. A significant correlation was observed between the normalized peak filling rate and either body mass index or left ventricular (LV) mass (r = 0.355 and r = -0.32, respectively; p less than 0.001). Obese patients had greater LV end-diastolic and systolic dimensions (p less than 0.005 and p less than 0.02, respectively), LV wall thickness (p less than 0.05) and LV mass (p less than 0.007) than lean patients. Impairment of LV filling was most pronounced in obese hypertensive patients. It is concluded that the burden on the left ventricle imposed by obesity causes cardiac enlargement and impairment of LV filling regardless of levels of arterial pressure.

Adult↗
PubMed1991

Cardiovascular effects of isradipine in essential hypertension.

The immediate and short-term cardiovascular effects of oral isradipine therapy were evaluated in 11 patients with mild to moderate systemic hypertension. Isradipine, 5 mg administered orally, induced a significant reduction in arterial pressure from 165 +/- 6/88 +/- 3 mm Hg to 140 +/- 5/76 +/- 2 mm Hg (p less than 0.001) within 2.5 hours by a decrease in total peripheral resistance associated with an increase in heart rate and cardiac output. Contrary to the acute effect, oral therapy with isradipine for 3 months reduced arterial pressure through a decrease in total peripheral resistance but without causing an increase in heart rate or cardiac output or activation of the sympathetic nervous system. Isradipine slightly reduced left ventricular mass and improved cardiac systolic function and left ventricular filling. Renal blood flow increased, and renal vascular resistance (p less than 0.01) and total blood volume (p less than 0.002) decreased without a change in either sodium excretion or body weight. Thus, isradipine, when given for 3 months, decreased arterial pressure by reducing total peripheral resistance without activation of reflexive mechanisms. Its favorable effects on systemic hemodynamics, total blood volume, renal blood flow, and cardiac structure and function suggest isradipine to be an excellent choice for antihypertensive therapy.

Adult↗
PubMed1991

Left ventricular hypertrophy: impact of calcium channel blocker therapy.

Left ventricular hypertrophy (LVH) of the concentric type is the classic cardiac adaptation to sustained arterial hypertension. Data from the Framingham cohort have shown that patients with LVH have a severalfold higher risk of sudden death, acute myocardial infarction, and other cardiovascular morbidity than those with normal hearts. Common sequelae of LVH are ventricular ectopy, impaired ventricular contractility, myocardial ischemia, and decreased left ventricular filling. The benefits of antihypertensive therapy should not be limited to lowering arterial pressure, but should extend to preventing or reducing target organ damage. A variety of antihypertensive agents, such as calcium channel blockers, angiotensin-converting enzyme inhibitors, antiadrenergic drugs, and, to a lesser extent, beta blockers, have been shown to reduce LVH and to improve left ventricular filling. We have shown that calcium channel blockers diminish ventricular ectopy in parallel with the reduction of LVH, whereas antihypertensive therapy with diuretics neither reduced LVH nor suppressed ventricular ectopy, although it lowered arterial pressure to a similar extent. Whether or not these cardiac changes with antihypertensive therapies will improve cardiovascular morbidity and mortality in patients with LVH remains to be documented.

Arrhythmias, Cardiac↗
PubMed1991

Antihypertensive therapy. To stop or not to stop?

The benefits of continuous antihypertensive therapy have been extensively documented. However, lack of compliance with the prescribed regimen, excessive cost, and troublesome adverse effects of some antihypertensive agents led to the consideration of intermittent therapy or even complete discontinuation of therapy as an effective alternative to lifelong medication. Prospective studies dealing with this subject reported inconsistent results. Nevertheless, they allowed us to identify selection criteria of candidates for step-down or discontinuation of antihypertensive therapy. Such candidates include patients with mild essential hypertension who have one or more of the following characteristics: young age, normal body weight, low salt intake, no alcohol consumption, low pretreatment blood pressure, successful therapy with one drug only, and no or only minimal signs of target organ damage. Stopping antihypertensive therapy without subsequent rise in arterial pressure was shown to be possible in a subset of patients with mild essential hypertension for a period of months to years. This approach appears to be safe, provided that blood pressure is monitored frequently, and may improve compliance, save treatment costs, and reduce adverse effects of certain drugs, although its long-term consequences for morbidity and mortality remain to be determined.

Antihypertensive Agents↗
PubMed1991

Left ventricular filling and stress response pattern in essential hypertension.

PURPOSE: To evaluate whether impaired left ventricular filling determines the hemodynamic responses to isometric and orthostatic stress in a population with mild essential hypertension. PATIENTS AND METHODS: The study population consisted of 32 patients with essential hypertension who were subdivided into those with preserved left ventricular filling (15 patients) and those with impaired left ventricular filling (17 patients). Echocardiograms were obtained before hemodynamic assessment was performed. Isometric stress and head-up tilt tests were done with a recovery period of at least 10 minutes between each to allow for blood pressure and heart rate to return to baseline. Hemodynamic reassessment was performed during the last minute of each test and at the end of the recovery period. Plasma epinephrine, norepinephrine, and dopamine levels were determined by radioenzymatic method. RESULTS: Isometric stress increased mean arterial pressure by 30% (p less than 0.0001) by an increase in cardiac output (p less than 0.0001) and total peripheral resistance (p less than 0.0001) associated with an increase in plasma catecholamine levels (p less than 0.0001). Patients with preserved left ventricular filling had an increase in arterial pressure predominantly through an elevation in cardiac output (17%, p less than 0.0001) associated with a small increase in plasma norepinephrine levels (p less than 0.05) and in peripheral resistance (11%, p less than 0.05). In contrast, patients with impaired left ventricular filling had an increase in arterial pressure mainly through an increase in peripheral resistance (25%, p less than 0.0001) that was associated with a 45% elevation in plasma norepinephrine levels (p less than 0.0001). Orthostatic stress (passive head-up tilt) caused an exaggerated decrease in stroke volume (p less than 0.01) and cardiac output (p less than 0.01) in patients with impaired left ventricular filling when compared with those with preserved diastolic function. CONCLUSION: Impaired left ventricular filling blunts the response of the heart to isometric and orthostatic stress. As a consequence, hypertensive patients with impaired ventricular filling respond to these stressors with enhanced sympathetic stimulation and exaggerated vasoconstriction.

Adult↗
PubMed1991

Immediate and short-term cardiovascular effects of fosinopril, a new angiotensin-converting enzyme inhibitor, in patients with essential hypertension.

Immediate and short-term cardiovascular effects of a new angiotensin-converting enzyme inhibitor, fosinopril, were assessed in 10 patients with mild to moderate essential hypertension. Administration of a 10 mg oral dose of fosinopril reduced mean arterial pressure (p less than 0.001) as a result of a 24% fall in total peripheral resistance (p less than 0.001). Short-term therapy (12 weeks) maintained the decrease in mean arterial pressure (p less than 0.05) by decreasing total peripheral resistance (p less than 0.01), without reflexive cardiac stimulation or expanding intravascular volume. Renal vascular resistance decreased (p less than 0.05) while renal blood flow, glomerular filtration rate and filtration fraction remained unchanged. The response pattern to mental, isometric and orthostatic stress was similarly unchanged. Left ventricular mass diminished by 11% (p less than 0.01); myocardial contractility was unaffected. Afterload was reduced (p less than 0.05), and velocity of circumferential fiber shortening and stroke volume increased (p less than 0.05). Thus, arterial pressure reduction produced by fosinopril was associated with improved systemic and renal hemodynamics and reduced left ventricular mass.

Adult↗
PubMed1991

Regression of increased left ventricular mass by antihypertensives.

Left ventricular hypertrophy (LVH) is both a target organ response to chronic arterial hypertension and a disorder that may be responsible for cardiovascular events. Although an increase in ventricular wall thickness may initially be compensatory and decrease wall stress, numerous studies have indicated that LVH is associated with a reduction in coronary flow reserve, diastolic and systolic ventricular dysfunction, and ventricular arrhythmias, all of which predispose to morbid cardiovascular events, including acute coronary syndromes, congestive myocardial failure, and sudden death. Reduction in LVH has been accomplished with beneficial effects on diastolic function and ventricular arrhythmias, without pressure-induced deterioration in systolic or diastolic function. Although therapy with diuretics and vasodilators effectively lowers arterial pressure, these therapies are not usually associated with significant regression of LVH. Calcium channel blockers, angiotensin converting enzyme (ACE) inhibitors, beta-adrenergic blockers, central adrenergic blocking agents, and possibly alpha-adrenergic blockers and diuretics with vasodilatory properties are associated with reductions in LV mass. However, studies are still needed to determine the relative effects of various antihypertensive therapies on LVH regression, coronary flow reserve, ventricular function, ventricular ectopy, and most importantly, on protection against major cardiac morbidity and mortality inherent to LVH.

Antihypertensive Agents↗
PubMed1991

Left ventricular hypertrophy: an independent risk factor.

Left ventricular hypertrophy (LVH), an increase in the muscle mass of the left ventricle, has been identified as a powerful risk factor for future cardiovascular morbidity and mortality. The risk of acute myocardial infarction, congestive heart failure, sudden death, and other cardiovascular events increases six- to eightfold with the presence of LVH. 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. Hypertension, obesity, advanced age, valvular heart disease, and other disorders that cause an increase in the hemodynamic burden can lead to LVH. Left ventricular hypertrophy and its sequelae can be reduced by specific antihypertensive therapy but, despite these promising findings, future epidemiological studies are necessary to document the clinical benefits of a reduction of LVH.

Cardiomegaly↗
PubMed1991

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

Left ventricular hypertrophy (LVH) has been identified as a significant risk factor for future cardiovascular morbidity and mortality. LVH and its sequelae such as myocardial ischemia, impaired filling and contractility, ventricular arrhythmias, and congestive heart failure can be reduced by specific antihypertensive agents. Future clinical trials will determine whether a reduction of LVH will ultimately improve its inherent ominous prognosis.

Antihypertensive Agents↗
PubMed1990

Glomerular hyperfiltration indicates early target organ damage in essential hypertension.

In 111 patients with essential hypertension (World Health Organization stage I or II), we examined the relationship between renal hemodynamics and left ventricular hypertrophy. Left ventricular structure was determined by two-dimensional guided M-mode echocardiography, renal blood flow by iodine I 131 aminohippuric acid clearance, and glomerular filtration rate by creatinine clearance. The glomerular filtration rate correlated with left ventricular mass (r = .52) and left ventricular cross-sectional area (r = .21). Conversely, at a similar age, body mass index, body surface area, and arterial pressure, hypertensive patients with left ventricular hypertrophy disclosed a higher glomerular filtration rate and filtration fraction than those without left ventricular hypertrophy, whereas renal blood flow and renal vascular resistance measurements were not significantly different. Thus, at similar levels of arterial pressure and renal blood flow, glomerular hyperfiltration was linked to early cardiac structural changes in essential hypertension. We conclude that, in a hypertensive patient with normal renal function, a high glomerular filtration rate may be an indicator for early target organ damage in essential hypertension.

Adult↗