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PubMed1996

[Epidemiologic features of congestive heart failure. Retrospective analysis of 2561 hospitalizations].

OBJECTIVES: The aim of this study was to characterise the epidemiology of congestive heart failure namely assessing demographic, etiologic and prognostic aspects, and the hospital admission trends in the last 6 years. METHODS: Retrospective analysis of computerised data concerning patients with congestive heart failure admitted to the department of Internal Medicine. LOCATION: A central hospital in the North of Portugal. SUBJECTS: Two thousand five hundred and sixty-one patients older than 10 years, admitted to the Internal Medicine Department of a central hospital in the North of Portugal between January 1, 1989 and December 31, 1994 and discharged with the principal or first listed diagnosis of congestive heart failure (ICD-9-CM code 4280). RESULTS: Eighty per cent of the patients had more than 60 years of age and the mean age was 69 years (female: 70.40 +/- 12.65; male: 66.24 +/- 12.25; p < 0.0001). Fifty-four per cent were females and 46 per cent males. The prevalence of congestive heart failure in the Internal Medicine Department was 4.8%. Between the ages of 15 and 44 years the hospital age-specific prevalence was between 16.1/10,000/year and 26.7/10,000/year for women and between 14.5/10,000/year and 16.1/10,000/year for men. For ages equal or greater than 75 years it was between 508.9/10,000/year and 561.3/10,000/year for women and between 300.2/10,000/year and 421.8/10,000/year for men. Possible causes of congestive heart failure were: valve disease in 26 per cent of patients, coronary artery disease in 24 per cent and hypertension in 20 per cent. The average case-fatality rate was 15.15% (female: 15.54%; male: 14.69%; chi 2 = 0.36; p > 0.55) evolving from 19.45% in 1989 to 12.59% in 1994 (chi 2 = 6.85; p < 0.01). Between the ages of 15 and 44 years the hospital cause-specific mortality rate was 16.2/100,000 and for ages equal or greater than 75 years it was 743.6/100,000. Stepwise logistic regression produced the following odds ratios for the variables significantly associated with dead during hospital admission: age (> or = 70 years)--1.48; infectious diseases--1.37; central nervous system diseases--2.28; chronic renal diseases--1.96; cardiac arrest--24.1; pulmonary embolism--2.26; acute renal failure--7.93; clinical signs of severe sodium and water retention--1.49; hyponatremia--3.39; other electrolyte abnormalities and acid-base balance disturbances--1.78. The simple linear regression of daily admissions on time produced a positive slope of 0.0002 (p < 0.002). CONCLUSIONS: The hospital prevalence of congestive heart failure is identical to other Western countries and is greater among the elderly patients. Valve disease, coronary artery disease and hypertension are the most frequent causes of congestive heart failure. An increasing trend in hospital admissions for congestive heart failure was observed. The hospital mortality was reduced in the last 6 years and was greater among the elderly patients. Age (> or = 70 years), the presence of comorbidity (infectious disease, central nervous system disease, acute renal failure, chronic renal disease and pulmonary embolism), hyponatremia, other electrolyte abnormalities and acid-base balance disturbances, resuscitated cardiac arrest and the presence of severe sodium and water retention have prognostic significance.

Aged↗

PubMed1993

Influence of congestive heart failure on endothelin levels and receptors in rabbits.

Congestive heart failure, both in man and in animals is associated with an increased plasma level of endothelin. To investigate further the potential role of the endothelin system, we designed a study to determine the effect of experimental congestive heart failure (CHF) on plasma and tissue immunoreactive-endothelin (irET) and on the density and affinity of endothelin-1 receptors in the heart and kidney. For this purpose, CHF was induced in rabbits by combined aortic valvular insufficiency and stenosis. When CHF was established, plasma and tissue irET levels were measured by radioimmunoassay and density and affinity of endothelin-1 receptors were measured by binding assay on tissue homogenates. Compared to control rabbits, plasma irET was significantly elevated in rabbits with CHF [1.04 +/- 0.15 vs. 0.04 +/- 0.01 fmol/ml, P < 0.001]. Tissue irET concentrations in ventricles and kidney were roughly 4 orders of magnitude higher than plasma concentrations. CHF decreased the tissue irET levels in left ventricle and kidney by 32 and 46%, respectively (P < 0.01), whereas CHF increased it by 58% in the right ventricle (P < 0.005). The density of ET-1 receptors was decreased in the right and left ventricles and in kidneys by 26, 36, and 61%, respectively (P < 0.05). Receptor affinity remained unchanged in response to CHF in both ventricles, whereas it increased in kidney [Kd (pM); 154 +/- 17 vs. 99 +/- 9, P < 0.01]. Thus, this study demonstrates that experimental CHF is not only characterized by elevated plasma irET levels but also by a decrease in tissue irET concentrations in the left ventricle and kidney, and by a down-regulation of ET-1 receptors both in the heart and kidney. Functional consequences of these changes need to be determined.

Animals↗

PubMed2006

[Diabetes mellitus and congestive heart failure: physiopathology and treatment].

Diabetes mellitus increases by 2.5 to 5 the relative risk of congestive heart failure. Besides the classical risk factors of congestive heart failure such as obesity, arterial hypertension and coronary artery disease that are frequently associated to type 2 diabetes, a diabetic cardiomyopathy plays also a role. This specific complication is related to metabolic factors and oxidative stress, leading to muscular cell apoptosis and fibrosis. The management of a diabetic patient with congestive heart failure has several specificities not only concerning the treatment of cardiac insufficiency but most importantly concerning antidiabetic therapy. The relationship between glitazones, peripheral oedema and risk of congestive heart failure is currently raising much interest and controversies.

Diabetes Mellitus, Type 2↗

PubMed2005

Mechanisms of neurohormonal activation in chronic congestive heart failure: pathophysiology and therapeutic implications.

Patients with chronic congestive heart failure have a sequential and incessant activation of those neurohormonal systems, which control body fluids, cardiac output and systemic blood pressure. Neurohormonal activation is initially selective and regional. Generalized activation is a late event in the natural history of congestive heart failure. Although the ultimate stimulus responsible for the activation of these neurohormonal systems is unknown, a decreased cardiac output and diminished effective blood volume have been proposed as the responsible mechanisms. However, extensive clinical and experimental research suggest that cardiac remodeling and loading of low-pressure cardiac receptors with sympathetic afferents could be the triggering events followed by unloading of high-pressure carotid receptors by decreased cardiac output and diminished effective blood volume.

Adrenergic beta-Antagonists↗

PubMed1988

Haemodynamic effects of urapidil in arterial hypertension and congestive heart failure.

An elevated total peripheral resistance is the haemodynamic hallmark of both arterial hypertension and congestive heart failure. In essential hypertension it is the main pathogenetic abnormality, whereas in congestive heart failure it is the result of vasoconstriction serving to compensate for the fall in cardiac output and arterial pressure. Any drug that lowers total peripheral resistance can, therefore, potentially favourably influence established hypertension as well as unload the left ventricle in congestive failure. In essential hypertension, urapidil lowers arterial pressure acutely by a fall in total peripheral resistance with a small compensatory increase in cardiac output. Concomitantly, renal and splanchnic blood flow increase and the resistance in these vascular beds falls. In congestive heart failure, the acute administration of urapidil increases cardiac index and lowers mean pulmonary artery wedge pressure and systemic vascular resistance by about 30%. At the same time, a mild fall in mean arterial pressure is observed. Long term non-invasive studies document that these acute haemodynamic effects remain preserved in both arterial hypertension and congestive heart failure. Urapidil seems, therefore, to be a promising agent for the treatment of haemodynamic disorders that are characterised by an elevation of total peripheral resistance, such as established essential hypertension and congestive heart failure.

Antihypertensive Agents↗

PubMed2002

Effects of metoprolol in chagasic patients with severe congestive heart failure.

BACKGROUND: Beta-blockers are the most effective and promising treatment for congestive heart failure secondary to left ventricular dysfunction and sympathetic activation. METHODS: Since chagasic patients with severe congestive heart failure have left ventricular systolic dysfunction and neurohormonal activation, we administered metoprolol to nine chagasic patients who were in severe congestive heart failure. Metoprolol (5 mg p.o. daily) was uptitrated on a weekly basis. RESULTS: Patients were receiving digitalis, diuretics and angiotensin converting enzyme inhibitors and had left ventricular dilatation (6.77+/-0.89 cm), depressed ejection fraction (0.20+/-0.06), low systolic blood pressure (93+/-11 mm Hg), sinus tachycardia (115+/-17 beats/min) and sympathetic activation 400+/-246 pg/ml). One patient was in New York Heart Association Functional class III and eight patients were in functional class IV. At the end of the fifth week of treatment (metoprolol 25 mg), seven patients were in functional class III and two were in functional class II. Heart rate decreased to 85+/-15 beats/min (P<0.05) and the systolic blood pressure increased to 108+/-18 mm Hg (P<0.01). There were no significant changes in left ventricular ejection fraction. By the end of the tenth week of treatment (metoprolol 50 mg), four patients were now in functional class I and five were in functional class II. Left ventricular ejection fraction increased to 0.27+/-0.05 (P<0.01) and the left ventricular systolic diameter decreased from 6.38+/-0.90 at baseline to 5.89+/-0.59 and 5.76+/-0.96 after 25 and 50 mg of metoprolol treatment, respectively (P<0.04). Plasma norepinephrine decreased non-significantly to 288+/-91 pg/ml. CONCLUSION: Beta-blockers improve the clinical status and the left ventricular function of chagasic patients with severe congestive heart failure.

Adrenergic beta-Antagonists↗

PubMed1992

Impaired endothelium-mediated vasodilation in the peripheral vasculature of patients with congestive heart failure.

Impaired endothelial-dependent vasodilation has been demonstrated in two animal models of congestive heart failure and in the coronary circulation of patients with idiopathic dilated cardiomyopathy. To determine whether this impairment contributes to the abnormal peripheral vasomotor tone in patients with congestive heart failure, the local vascular response to intraarterial infusions of graded concentrations (10(-8) M to 10(-5) M) of acetylcholine (an endothelial-dependent vasodilator) and nitroglycerin (a direct-acting vasodilator) was studied in the superficial femoral artery of 19 patients with congestive heart failure (New York Heart Association classes I to IV) and 6 age-matched normal control subjects. The local vascular response was determined from the arterial blood flow velocity pattern obtained by transcutaneous Doppler ultrasonography. Acetylcholine, 10(-5) M, induced a pattern characteristic of vasodilation in all six normal subjects; mean blood flow velocity for the group significantly increased from 11.9 +/- 2.7 to 44.8 +/- 20.9 cm/s (p less than 0.05). In contrast, the same dose of acetylcholine induced a blood flow velocity pattern characteristic of vasodilation in only 4 of the 19 patients with congestive heart failure. Group mean blood flow velocity did not change significantly. Nitroglycerin, 10(-7) M, induced vasodilation in all 6 normal subjects but in only 1 of 19 patients. Nitroglycerin, 10(-5) M, was administered to 10 patients; all 10 demonstrated a pattern characteristic of vasodilation. Thus, acetylcholine-mediated endothelial-dependent vasodilation appears to be impaired in the peripheral vasculature of patients with congestive heart failure. Both endothelial dysfunction and abnormal vascular smooth muscle responsiveness may contribute to abnormal peripheral vasomotor tone.

Acetylcholine↗

PubMed1984

Haemodynamic evaluation of ibopamine in severe congestive heart failure.

Ten patients suffering from refractory congestive heart failure were treated orally with Ibopamine 100 mg. The haemodynamic effects were evaluated with a Swan-Ganz catheter and thermodilution technique, 1 and 2 h after treatment. Ibopamine significantly increased the cardiac index and stroke work index, and decreased pulmonary pressure and the pulmonary and peripheral vascular resistances without affecting heart rate or blood pressure.

Adult↗

PubMed1994

Volumes and Na+/H+ antiporter activity of lymphocytes in patients with congestive heart failure.

Previous studies in patients with congestive heart failure (CHF) treated with diuretics and/or digoxin have shown abnormalities of cellular volume and electrolytes in biopsies of skeletal muscle. These abnormalities seem to play an important role with regard to the dysregulation of peripheral vascular resistance and characteristic clinical features of CHF, for example, muscular weakness. This study assessed the effect of angiotension-converting enzyme (ACE) inhibitor therapy on cell volume and cell volume regulation in patients with CHF. Cell diameters of human mononuclear leukocytes (HML) were determined electronically by a Coulter Counter. Cell diameters for 19 patients with decreased left ventricular ejection fraction (determined via levocardiography) on therapy with ACE inhibitors (group 1) were compared to those of HML from patients on diuretics alone (group 2, n = 16). The activity of the Na+/H+ antiporter was determined by cell swelling in isotonic propionate. The control group consisted of 20 normal, age- and sex-matched volunteers. HML diameters were significantly increased from 7.16 +/- 0.07 in normals to 7.24 +/- 0.08 microns (group 1; P < 0.01) and 7.23 +/- 0.11 microns (group 2; P < 0.05), indicating an abnormal regulation of cell volume. There were no statistically significant correlations between the individual ejection fraction or digoxin therapy and average cell diameters. In both patient groups ethylisopropylamiloride-sensitive swelling rates were normal compared to the control group indicating a normal activity of the Na+/H+ antiporter. In conclusion, increased cell sizes reflect a structural change in HML rather than a rapidly reversible functional abnormality which was not affected different by ACE inhibition and diuretic therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2003

Beta-blockers for congestive heart failure.

The prognosis of patients with congestive heart failure (CHF) can be significantly improved with drug therapy targeted at the renin-angiotensin and adrenergic nervous system. beta-adrenergic blocking drugs, once contraindicated in CHF, have now been shown to improve survival in CHF.

Adrenergic beta-Antagonists↗

PubMed1982

Captopril pharmacokinetics and the acute hemodynamic and hormonal response in patients with severe chronic congestive heart failure.

Twelve patients with severe chronic congestive heart failure (CHF) underwent simultaneous evaluation of the pharmacokinetic, pharmacodynamic, and neurohumoral actions of a single 25 mg oral dose of the angiotensin-converting enzyme (ACE) inhibitor captopril (CPT). Following drug administration, which raised plasma renin activity (PRA) and thereby indicated significant ACE inhibition, both free (unchanged) and total CPT (including active metabolites) were detectable in the blood with 40 minutes and peak blood levels of the agent were recorded 1 hour after CPT. Total CPT concentration was higher and persisted longer than free CPT, which became virtually nondetectable 8 hours after ingestion. Concomitantly, left ventricular function was markedly augmented by the oral ACE inhibition in all patients, with the magnitude of this improvement being closely related to the baseline PRA. Thus, the overall hemodynamic response to CPT, which rapidly appears in the bloodstream following drug intake in patients with advanced CHF, is a function of the extent of baseline renin-angiotensin-aldosterone activity.

Adult↗

PubMed1985

Comparative hemodynamic effects of intravenous dobutamine and MDL-17,043, a new cardioactive drug, in severe congestive heart failure.

In 14 patients with severe congestive heart failure (CHF) due to ischemic heart disease or idiopathic dilated cardiomyopathy, the hemodynamic response to intravenous infusion of dobutamine (D) was compared to that of a new non-catechol, non-glycoside, inotropic and vasodilator agent, MDL-17,043 (MDL) administered in incremental intravenous doses. D and MDL produced comparable increases in cardiac index (L/min/m2) (1.8 +/- 0.4 to 2.9 +/- 0.8 and 1.7 +/- 0.3 to 3.3 +/- 0.6, respectively; both p = 0.001) and stroke volume index (ml/beat/m2) (24 +/- 8 to 35 +/- 9 and 22 +/- 7 to 39 +/- 11, respectively; both p = 0.001). Both D and MDL reduced left ventricular filling pressure (29 +/- 5 to 24 +/- 5 and 29 +/- 6 to 17 +2- 6 mm Hg, respectively; both p less than 0.05), and mean right atrial pressure (11 +/- 4 to 8 +/- 4 and 13 +/- 5 to 6 +/- 4 mm Hg, respectively; both p = 0.001). The overall changes in heart rate and mean arterial pressure were small with both D and MDL. However, MDL in comparison to D resulted in a significantly lower left ventricular filling pressure (p = 0.001), mean pulmonary arterial pressure (p = 0.001), and mean arterial pressure (p less than 0.05). The salutary hemodynamic effects of MDL on cardiac index and left ventricular filling pressure were sustained for an average of 9.6 hours, whereas the effects of D dissipated within 30 minutes of stopping the infusion. No serious adverse effects were noted during acute administration with either drug. Therefore, intravenous MDL may be a useful substitute for D in the acute therapy of severe CHF.

Aged↗

PubMed1985

Potential for altering the natural history of congestive heart failure: need for large clinical trials.

Congestive heart failure (CHF) is a major clinical and public health problem; moreover, its incidence is increasing. Once this syndrome is manifest, the mortality rate is very high. To date, none of the drugs available for its treatment has been shown to reduce mortality. It is theoretically possible that in patients with overt CHF, drug treatment may not alter prognosis. This hypothesis suggests that patients at high risk of heart failure should be treated before CHF becomes manifest. Alternatively, the trials of patients with manifest CHF may have been unpromising, simply because they were too small. These considerations indicate an urgent need for very large studies of both categories of patients--a "prevention" trial in those without overt CHF and a "treatment" trial in those with overt CHF.

Aged↗

PubMed1985

Measurement of cardiac output during exercise by the thermodilution and direct Fick techniques in patients with chronic congestive heart failure.

Nine men with chronic stable congestive heart failure (New York Heart Association class II or III) were studied. Oxygen consumption was measured continuously and cardiac output (CO) determined by thermodilution and from the Fick equation at the end of each stage of treadmill exercise. CO measured by the 2 techniques was similar (r = 0.98) over the range of 2.5 to 13 liters/min (43 separate estimations). Tricuspid regurgitation developed in 2 patients during exercise, which resulted in unphysiologic estimates of CO (more than 30 liters/min) by thermodilution. In these circumstances estimation of CO by the direct Fick technique is superior. With this exception, CO measured by thermodilution was accurate even during exercise and provided results similar to those using the direct Fick technique.

Adolescent↗

PubMed1987

A preliminary report of the effects of orally administered enoximone on regional hemodynamics in congestive heart failure.

Twelve patients with moderately severe congestive heart failure underwent the simultaneous determination of central and regional hemodynamics after administration of placebo and enoximone. The regions examined hemodynamically included renal, hepatic-splanchnic and upper limb. Enoximone was studied in 2 doses, 1 and 2 mg/kg, and administered in a double-blind, placebo-controlled, crossover design. At these doses enoximone elicited a significantly greater increase in cardiac output and a greater decrease in systemic vascular resistance than placebo. Systemic blood pressure was not significantly altered. Enoximone did not significantly change the flow or resistance of renal or hepatic-splanchnic vascular beds. Limb vascular resistance decreased modestly after enoximone with a significant augmentation (+12% to 17%) of limb blood flow compared with placebo. The initial oral administration of the 1 and 2 mg/kg doses of enoximone improved central hemodynamic parameters with apparent preferential reduction of limb vascular resistance and augmentation of blood flow to the limb region (peripheral musculoskeletal system).

Administration, Oral↗

PubMed1990

Hemodynamic effects of oral nicorandil in congestive heart failure.

Twenty-five patients with congestive heart failure (CHF) underwent a double-blind randomized study of the acute hemodynamic effects of orally administered nicorandil, a newly developed vasodilator drug. A dose range of 10 to 60 mg was studied. Nicorandil, at a dose of 60 mg, caused statistically significant decreases in systemic systolic and diastolic blood pressure, right atrial pressure, pulmonary capillary wedge pressure, systemic and pulmonary vascular resistance and systolic and diastolic pulmonary arterial pressure. A brief increase in cardiac index attributable to an increase in stroke volume without a change in heart rate was also observed. A dose of 40 mg produced similar results in cardiac index and systemic and pulmonary vascular resistance, but changes in other hemodynamic parameters were much smaller in magnitude and usually not of statistical significance. No significant hemodynamic response was seen to doses of 10 and 20 mg of nicorandil. Duration of action was short with nearly all hemodynamic parameters returning close to baseline within 3 hours. This rapid decrease in activity occurred in concert with a rapid plasma clearance of nicorandil as determined by serial measurements of plasma drug concentration. This study suggests that first-dose orally administered nicorandil elicits favorable, but brief, hemodynamic effects in CHF at doses greater than or equal to 40 mg.

Administration, Oral↗

PubMed2004

Time trends in the use of beta-blockers and other pharmacotherapies in older adults with congestive heart failure.

BACKGROUND: Evidence supporting pharmacotherapy of congestive heart failure (CHF) has grown substantially over the past decade and includes large, placebo-controlled trials with mortality end points. We describe beta-blocker and other medication temporal treatment trends of CHF in the Cardiovascular Health Study, a community-based cohort study of 5888 adults > or =65 years of age. METHODS: Prescription medication data were collected from hospital discharge summaries for incident CHF events and at in-study annual clinic visits for prevalent CHF cases from 1989 to 2000. Change in use of agents over time was estimated by using generalized estimating equations while adjusting for potential confounding factors of age, sex, race, and cardiovascular and pulmonary comorbidities. RESULTS: Among 1033 incident CHF events, beta-blocker use after diagnosis increased an average of 2.4 percentage points annually (95% CI, 1.5 to 3.4 points) from 1989 to 2000. The increasing trend was consistent throughout follow-up. Among participants with coronary disease and/or hypertension and among those with low ejection fractions (<45%), beta-blocker use remained flat from 1989 to 1994 and increased 4.7 points annually (2.5 to 6.9) and 10.0 points annually (6.1 to 13.8), respectively, from 1995 to 2000. Among participants without coronary disease or hypertension, there was no overall increase in use. Use of renin-angiotensin system inhibitors increased 2.3 points annually (1.0 to 3.5), digoxin use decreased 2.4 points annually (-3.6 to -1.1), and loop diuretic use remained flat between 1989 and 2000. In general, treatment trends were similar for prevalent CHF. CONCLUSIONS: Treatment of CHF has changed gradually in the 1990s and may in part reflect the influence of CHF clinical trial evidence.

Adrenergic beta-Antagonists↗

PubMed2005

On the mechanism of augmentation of electrocardiogram QRS complexes in patients with congestive heart failure responding to diuresis.

Patients with congestive heart failure (CHF) responding to diuresis reveal marked augmentation of the QRS complexes (AUG-QRS) in their electrocardiograms (ECGs). Recently, such change in the ECG has been observed in patients with anasarca (AN) of varying etiology commensurate with partial alleviation of the volume overload; similar ECG change has been noted in patients with end-stage renal failure after hemodialysis. The mechanism for the AUG-QRS in patients with CHF has been debated, and many have ascribed this ECG change to the "Brody effect," linking the AUG-QRS to reduction of intracardiac blood volumes resulting from diuresis. However, the Brody effect (a theoretical formulation not fully validated by experimentation and associated with controversy in its clinical implementation) has not provided a satisfactory explanation for the AUG-QRS in patients with CHF. In contrast, the described association between amelioration of AN in a diverse patient population and AUG-QRS suggests that this ECG change in patients with CHF is due to an increased electrical resistance of the passive body volume conductor, resulting from water loss effected by diuresis. This thesis is supported by theoretical work, animal experimentation, and clinical evidence.

Body Water↗