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PubMed1994

Increased walking variability in elderly persons with congestive heart failure.

OBJECTIVES: To determine the effects of congestive heart failure on a person's ability to walk at a steady pace while ambulating at a self-determined rate. SETTING: Beth Israel Hospital, Boston, a primary and tertiary teaching hospital, and a social activity center for elderly adults living in the community. PARTICIPANTS: Eleven elderly subjects (aged 70-93 years) with well compensated congestive heart failure (NY Heart Association class I or II), seven elderly subjects (aged 70-79 years) without congestive heart failure, and 10 healthy young adult subjects (aged 20-30 years). MEASUREMENTS: Subjects walked for 8 minutes on level ground at their own selected walking rate. Footswitches were used to measure the time between steps. Step rate (steps/minute) and step rate variability were calculated for the entire walking period, for 30 seconds during the first minute of the walk, for 30 seconds during the last minute of the walk, and for the 30-second period when each subject's step rate variability was minimal. Group means and 5% and 95% confidence intervals were computed. MAIN RESULTS: All measures of walking variability were significantly increased in the elderly subjects with congestive heart failure, intermediate in the elderly controls, and lowest in the young subjects. There was no overlap between the three groups using the minimal 30-second variability (elderly CHF vs elderly controls: P < 0.001, elderly controls vs young: P < 0.001), and no overlap between elderly subjects with and without congestive heart failure when using the overall variability. For all four measures, there was no overlap in any of the confidence intervals, and all group means were significantly different (P < 0.05).

Adult↗
PubMedDate not supplied

Plasma cytokine levels in cardiac chambers of patients with mitral stenosis with congestive heart failure.

To ascertain whether elevated levels of circulating proinflammatory cytokines in patients with advanced heart failure are due to congestive heart failure or due to cachexia or infection complicating heart failure, we measured prospectively plasma concentrations of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), interleukin 2 (IL-2), and interleukin-6 (IL-6) in 12 patients with mitral stenosis with moderate congestive heart failure, but not with cachexia or infection. Blood samples were obtained from the peripheral vein and right and left atria of the patients during percutaneous mitral valvuloplasty. Levels of TNF-alpha, IL-1 beta, IL-2, and IL-6 in the plasma form the peripheral vein and right and left atria of these patients were not elevated compared with those from the peripheral vein of a control group of 10 normal subjects. On the other hand, plasma levels of TNF-alpha but not IL-1 beta, IL-2 or IL-6, were elevated in 4 of 9 patients with congestive heart failure complicated with cachexia and/or infection. Our results suggest that proinflammatory cytokine levels are not elevated in congestive heart failure uncomplicated with cachexia or infection.

Adult↗
PubMed2002

[Medical treatment of chronic congestive heart failure].

Medical treatment in congestive heart failure has been largely improved during the last 15 years. Treatment of left ventricular systolic dysfunction using angiotensin-converting-enzyme inhibitor is now confirmed in all NYHA classes, due to the important reduction in morbi-mortality. Betablockers have to be systematically associated in symptomatic classes. Among other drugs, only spironolactone has been shown efficient in severe NYHA classes. Diuretics in case of congestive symptoms, digoxin in order to reduce the frequency of hospitalization, and nitrates as adding therapy in severe classes may be also prescribed. However, treatment of left ventricular diastolic dysfunction remains under debate since up to date, no medication has shown a confirmed efficacy.

Drug Therapy, Combination↗
PubMed1987

Alterations in cardiac beta-adrenoceptor responsiveness and adenylate cyclase system by congestive heart failure in dogs.

The effects of congestive heart failure on the physiological and biochemical functions of the cardiac beta-adrenoceptor-coupled adenylate cyclase system were studied in dogs with right heart failure produced by progressive pulmonary artery constriction and tricuspid avulsion. The cardiac inotropic response to dobutamine was attenuated in congestive heart failure, as determined by the right and left ventricular dP/dt responses. Adrenergic beta-receptor density, measured by [3H]dihydroalprenolol binding, was reduced in membrane fractions of the failing right ventricle, but not in the left ventricle. The functional activity of the adenylate cyclase system was studied in vitro by measuring the net cyclic AMP production following additions of isoproterenol, 5'-guanylylimidodiphosphate (Gpp(NH)p), forskolin, or manganese chloride, which act either directly on the beta-adrenergic receptors or on one of the post-receptor components of the adenylate cyclase system. Congestive heart failure reduced the net production of cyclic AMP by isoproterenol, Gpp(NH)p, and forskolin in both the right and left ventricles, but did not alter the effect of manganese chloride. Thus, beta-receptor down-regulation is chamber-specific, occurring only in the hemodynamically stressed right ventricle. In contrast, the post-receptor defect of the adenylate cyclase system occurred in both ventricles of the heart failure dogs. This decreased activation of adenylate cyclase by beta-agonists may be responsible, at least in part, for the diminished cardiac inotropic response to catecholamines in congestive heart failure.

5'-Nucleotidase↗
PubMedDate not supplied

Relationship of depression to increased risk of mortality and rehospitalization in patients with congestive heart failure.

BACKGROUND: Patients with congestive heart failure (CHF) may have a high prevalence of depression, which may increase the risk of adverse outcomes. OBJECTIVE: To determine the prevalence and relationship of depression to outcomes of patients hospitalized with CHF. METHODS: We screened patients aged 18 years or older having New York Heart Association class II or greater CHF, an ejection fraction of 35% or less, or both, admitted between March 1, 1997, and June 30, 1998, to the cardiology service of one hospital. Patients with a Beck Depression Inventory score of 10 or higher underwent a modified National Institute of Mental Health Diagnostic Interview Schedule to identify major depressive disorder. Primary care providers coordinated standard treatment for CHF and other medical and psychiatric disorders. We assessed all-cause mortality and readmission (rehospitalization) rates 3 months and 1 year after depression assessment. Logistic regression analyses were used to evaluate the independent prognostic value of depression after adjustment for clinical risk factors. RESULTS: Of 374 patients screened, 35.3% had a Beck Depression Inventory score of 10 or higher and 13.9% had major depressive disorder. Overall mortality was 7.9% at 3 months and 16.2% at 1 year. Major depression was associated with increased mortality at 3 months (odds ratio, 2.5 vs no depression; P =.08) and at 1 year (odds ratio, 2.23; P =.04) and readmission at 3 months (odds ratio, 1.90; P =.04) and at 1 year (odds ratio, 3.07; P =.005). These increased risks were independent of age, New York Heart Association class, baseline ejection fraction, and ischemic etiology of CHF. CONCLUSIONS: Major depression is common in patients hospitalized with CHF and is independently associated with a poor prognosis.

Adult↗
PubMed1994

Is there a role for positive inotropic agents in congestive heart failure: focus on mortality.

Congestive heart failure (CHF) is a common clinical syndrome that may result from a variety of etiologies. Impaired contractility can lead to pump failure and a number of hemodynamic and neurohormonal alterations. Vasodilator therapy improves symptoms and survival in patients with CHF due to systolic dysfunction. Inotropic therapy, on the other hand, has not been shown to improve survival and may even worsen survival. This article reviews the mechanism of action and clinical trials of inotropic therapy in patients with CHF.

Cardiotonic Agents↗
PubMedDate not supplied

The hemodynamic effects of ibopamine, a dopamine congener, in patients with congestive heart failure.

Ten patients with congestive heart failure underwent noninvasive and invasive hemodynamic testing before and sequentially after the administration of ibopamine to determine the cardiovascular effects of this oral dopamine congener. Single doses of 200, 400 and 600 mg were administered to all patients and 5 repeated doses of 200 or 400 mg were studied in 8. Hemodynamic effects occurred as early as 30 minutes and lasted up to 4 hours after dosing. In general, ibopamine elicited statistically significant dose-related increases in cardiac output and reductions in the derived resistance of the systemic and pulmonary circulations. A biphasic response in central and peripheral pressures was observed; up to 1 hour after administration, ibopamine elevated mean right and left atrial pressures and pulmonary and systemic arterial pressures with a significant reduction of these measurements beyond 1 hour. It did not alter heart rate. Repeated doses qualitatively affected hemodynamics similar to the initial dose and did not appear to be accompanied by short-term tolerance. While oral ibopamine elicits some favorable hemodynamic effects in humans with cardiac failure, the biphasic hemodynamic response is generally undesirable in the majority of these patients.

Adult↗
PubMed2000

Natriuretic peptides in the pathophysiology of congestive heart failure.

A hallmark of congestive heart failure (CHF) is the activation of the cardiac endocrine system, in particular atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). The natriuretic peptides are a group of structurally similar but genetically distinct peptides that have diverse actions in cardiovascular, renal, and endocrine homeostasis. ANP and BNP are of myocardial cell origin and C-type natriuretic peptide (CNP) is of endothelial origin. ANP and BNP bind to the natriuretic peptide-A receptor (NPR-A), which, via 3',5'-cyclic guanosine monophosphate (cGMP), mediates natriuresis, vasodilatation, renin inhibition, antimitogenesis, and lusitropic properties. CNP lacks natriuretic actions but possesses vasodilating and growth inhibiting actions via the guanylyl cyclase-linked natriuretic peptide-B receptor. All three peptides are cleared by the natriuretic peptide-C receptor and degraded by the ectoenzyme neutral endopeptidase 24.11, both of which are widely expressed in kidney, lung, and vascular wall. Recently, a fourth member of the natriuretic peptide, Dendroaspis natriuretic peptide (DNP) has been reported to be present in human plasma and atrial myocardium and is elevated in plasma of human CHF.

Amino Acid Sequence↗
PubMed1995

Prognostic importance of the length of ventricular tachycardia in patients with nonischemic congestive heart failure.

In patients with congestive heart failure the frequency of ventricular arrhythmias poorly predicts mortality. It is unknown whether the length of ventricular tachycardia is a better predictor of mortality in these patients. We therefore investigated the prognostic importance of the length of the longest run of ventricular tachycardia, the frequency of ventricular tachycardia, and the frequency of ventricular premature depolarizations with 24-hour ambulatory electrocardiographic recordings in 122 patients with heart failure. We also determined whether the cause of heart failure affects the prognostic importance of these parameters. Each ambulatory electrocardiographic recording was evaluated for the frequency of ventricular premature depolarizations and ventricular tachycardia and for the length of the longest run of ventricular tachycardia. For each electrocardiographic parameter patients were divided into groups based on the median value of that parameter. Mortality among groups was compared in all patients and then separately for nonischemic and ischemic patients. Neither the frequency of ventricular premature depolarizations nor the frequency of ventricular tachycardia predicted mortality whether or not cause was considered. When all patients were examined, the length of ventricular tachycardia did predict an increased risk of death. However, when cause was considered, length of ventricular tachycardia predicted mortality only in the nonischemic patients and not in the ischemic patients. We conclude that the length of ventricular tachycardia may be the best electrocardiographic predictor of mortality in patients with nonischemic heart failure.

Aged↗
PubMed1983

Platelet alpha 2 adrenoreceptors in chronic congestive heart failure.

Patients with chronic congestive heart failure (CHF) are known to have elevated plasma concentrations of norepinephrine. Although this elevation of catecholamines in plasma may facilitate myocardial contractility, it may also be toxic to the myocardium in the long term. The alpha 2 adrenoreceptor located on noradrenergic nerve terminals regulates neuronal norepinephrine release by feedback inhibition. This receptor is also located on human blood platelets. This study determines the status of platelet alpha 2 adrenoreceptors in 16 patients with CHF (class I and II in 7 and class III and IV in 9) and in 26 normal volunteers. Specific high-affinity binding of the alpha 2 agonist 3H-clonidine and the alpha 2 antagonist 3H-yohimbine was used to determine the number (Bmax) of alpha 2 receptors and the dissociation constant (KD) for the 2 ligands. In the control population, the Bmax (in fmol/mg protein) for 3H-clonidine was 33 +/- 2 and for 3H-yohimbine was 165 +/- 12. There was a 25% difference in the maximum number of specific binding sites for 3H-clonidine in the class III/IV group (Bmax 24 +/- 2, p less than 0.05) and a 43% difference in the maximum number of specific binding sites for 3H-yohimbine (Bmax 94 +/- 9; p less than 0.005). There was a smaller but nonsignificant difference in the number of receptors on platelets from patients in the class I and II group. The KD's were similar in all 3 groups. These differences correlated well with the increases in plasma norepinephrine levels between the normal group (273.8 +/- 44.1 pg/ml) and the class III/IV group (1333.5 +/- 244.9, p less than 0.0005). This study supports the hypothesis that increased levels of circulating norepinephrine in CHF lead to a decrease in platelet alpha 2 adrenoreceptors. Further studies should be performed to determine whether pharmacologic stimulation of these receptors might lead to a decrease in the neuronal release of that norepinephrine which might be toxic to the myocardium. Monitoring of platelet alpha 2 adrenoreceptor number may provide a guide to therapy of CHF.

Adult↗
PubMed1985

Epidemiology of congestive heart failure.

The incidence of congestive heart failure (CHF) is influenced by a variety of factors, including availability of medical care, socioeconomic status, geography, nutrition and race. The etiology of CHF in China, England, Botswana and Sweden will be examined and compared with prospective findings from Boston and Detroit. Because the therapy used in the treatment of CHF varies with the underlying causes, which may be as diverse as rheumatic fever, systemic hypertension and viral infection, the importance of fully determining its pathogenesis is emphasized.

Cardiomyopathy, Dilated↗
PubMed1987

Usefulness of calcium antagonists for congestive heart failure.

In patients with congestive heart failure (CHF) due to dilated cardiomyopathy, nifedipine, diltiazem and several of the newer calcium antagonists including nicardipine, nitrendipine, felodipine and PN 200-110 (isradipine) improve left ventricular function. Because of its relatively more pronounced negative inotropic and chronotropic actions, verapamil is generally not tolerated by patients with left ventricular failure. In addition, even relatively vascular-selective agents such as nifedipine can occasionally cause significant left ventricular depression, particularly if combined with beta-adrenergic blocking agents. Comparative studies using nitroprusside to cause an equivalent decrease in arterial pressure indicate that nifedipine acts predominantly on the arterial vasculature, and that a small but significant decrease in contractility occurs, apparently due to a direct myocardial action. Although diltiazem causes a depression in myocardial contractility in dogs with volume overload heart failure, limited data show no significant negative inotropic action in patients with heart failure. The negative inotropic effects, if any, of newer and possibly more vascular-selective agents are not yet known. Calcium antagonists appear to act predominantly on the limb and coronary vasculature, with relatively less effect on renal and hepatic vessels. In patients with CHF, nifedipine causes an increase in coronary blood flow and a decrease in the aorto-coronary sinus oxygen difference indicating an improvement in myocardial energetics. Although nifedipine causes an increase in cardiac index and decreases in systemic vascular resistance and pulmonary capillary wedge pressure during exercise, the limited data available fail to show a short- or long-term increase in exercise capacity. Nifedipine causes an increase in plasma renin activity, possibly due to a direct action on the kidney.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium Channel Blockers↗
PubMed1987

31P nuclear magnetic resonance evidence of abnormal skeletal muscle metabolism in patients with congestive heart failure.

In patients with congestive heart failure (CHF), exercise limitation correlates poorly with central hemodynamic abnormalities, suggesting that additional abnormalities in skeletal muscle blood flow or metabolism play an important pathophysiologic role. Therefore, muscle metabolism was examined by 31P nuclear magnetic resonance (NMR) at rest and during repetitive bulb squeeze exercise in 11 patients with New York Heart Association class II to IV CHF and 7 age-matched control subjects. Serial spectra were obtained at rest, at 2 levels of exercise and during recovery. At rest, the only abnormal finding was an elevated inorganic phosphate (Pi) concentration (5.0 +/- 1.5 vs 3.6 +/- 0.4 mM, p less than 0.01). At the lower exercise level, phosphocreatine (PCr) utilization, which was followed as the ratio of [PCr]/[( PCr] + [Pi]), was greater (0.36 +/- 0.16 vs 0.53 +/- 0.10, p less than 0.02), and pH fell more rapidly and to a lower value (6.38 +/- 0.25 vs 6.85 +/- 0.17, p less than 0.001). At the higher level of exercise, the patients could not work effectively and the group differences narrowed. Compared with control subjects, acidification was disproportionately greater in relation to PCr depletion in patients, further suggesting excessive dependence on glycolytic metabolism. The Pi peak was prominently double in 5 patients, indicating presence of a population of muscle fibers undergoing unusually active glycolysis. PCr resynthesis, a reflection of oxidative phosphorylation, was delayed in 4 patients. These findings indicate that in many patients with CHF, exercising muscle has marked metabolic changes consistent with impaired substrate availability and altered biochemistry.

Adenosine Triphosphate↗
PubMed1991

Peripheral adaptations in congestive heart failure: a review.

In congestive heart failure, peripheral adaptive mechanisms play a significant and largely underestimated role. In acute heart failure, sympathetic-mediated peripheral vasoconstriction together with chronotropic and inotropic actions serves to maintain perfusion pressure and blood supply to the vital organs. In chronic heart failure, activation of the renin-angiotensin system increases peripheral vascular resistance and arterial tone and decreases arterial compliance and vasodilator capacity. Endothelium-mediated, flow-dependent vasodilation is reduced as a consequence of reduced blood flow. Deconditioning renders the blood vessels incapable of dilating in response to increased flow. Simultaneously, reduced blood flow and inactivity are induced by deconditioning, with functional and structural consequences within the skeletal muscle. Exercise performance is limited by reduced overall blood flow, reduced conductance of the feeding arteries, elevated tone of the resistance vessels, reduced vasodilator capacity, impaired dissipation of heat from the working muscle, and functional and structural changes of the skeletal muscle due to underperfusion and inactivity. The adaptive mechanisms operate at different time scales. Under therapeutic intervention, their reversibility also follows different time constants. Restoration of the vasodilator capacity of the large arteries and of the abnormalities of skeletal muscle in heart failure requires time. Vasodilation with reduced pre- and/or afterload will retard progression of the superimposed ventricular dilation and hypertrophy, and therefore retard the progress of the disease. However, restoration of the peripheral blood flow and of organ function will require time. Restoration of the vascular compliance and of the full amplitude of adaptive flow-dependent vasodilation in the large arteries requires weeks or months. Similarly, restoration of functionally and morphologically altered skeletal muscle can be expected to be reversible over a longer time period.

Blood Circulation↗
PubMed1995

Acute electrophysiologic effects of amiodarone in patients with congestive heart failure.

Patients with severe congestive heart failure (CHF) are at increased risk for atrial and ventricular arrhythmias and sudden cardiac death. Amiodarone is generally well tolerated by this population and has a low proarrhythmic potential. Because of its peculiar kinetics, amiodarone requires a prolonged loading period, necessitating lengthy hospitalizations in a monitored setting. This study was planned prospectively to assess the electrophysiologic effects of an abbreviated high-dose oral load of amiodarone in patients with severe CHF and known or suspected life-threatening ventricular arrhythmias. Fifteen patients with stable CHF and known or suspected life-threatening ventricular arrhythmias underwent baseline electrophysiologic study. The study was repeated after administration of oral amiodarone, 50 mg/kg/day for 2 days in 8 divided doses (mean dose 6.9 +/- 0.4 g). After amiodarone administration, there was prolongation in virtually all conduction times and refractory periods. The prolongation of refractoriness was most pronounced in the atrium. Ventricular effective refractory periods demonstrated reverse frequency dependence. We conclude that a brief high-dose oral load of amiodarone is well tolerated by patients with CHF. It has marked and diffuse electrophysiologic actions suggestive of class I and III effects in addition to antiadrenergic and calcium blocking action. These effects are especially pronounced in the atrium.

Administration, Oral↗