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PubMedDate not supplied

Effects of cilazapril on ventricular arrhythmia in patients with congestive heart failure.

Angiotensin-converting enzyme (ACE) inhibitors reduce mortality and morbidity in patients with congestive heart failure. These effects may be mediated, at least in part, by suppression of lethal ventricular tachycardia (VT). The aims of this study were to examine whether the ACE inhibitor cilazapril reduces ventricular arrhythmia in patients with congestive heart failure and, if cilazapril does reduce ventricular arrhythmia, to determine whether this reduction is associated with suppression of sympathetic nerve activity in these patients. Thirty-two congestive heart failure patients (left ventricular ejection fraction, 35 +/- 6%; New York Heart Association class II or III) with VTs (Lown grade IVa or IVb) were randomly assigned to receive either conventional therapy, consisting of diuretics and digitalis (control group), or conventional therapy plus cilazapril (cilazapril group). Twenty-four-hour ambulatory electrocardiographic monitoring was performed at baseline and after 2 months of therapy. Plasma norepinephrine levels and heart rate variability (standard deviation about the mean RR interval) were compared at baseline and after 2 months of treatment. The control group demonstrated no significant change in arrhythmia frequency after 2 months of treatment. In the cilazapril group, however, the number of ventricular couplets and VT runs was significantly decreased. In association with this reduction, plasma norepinephrine levels were decreased, and heart rate variability was increased. These results suggest that cilazapril has antiarrhythmic effects, which may be produced by suppressing high sympathetic activity, in patients with congestive heart failure. It should be noted that the study group was small and that, although ventricular dysrhythmia was reduced with therapy, it remained substantial. Further study is needed to verify these results and to determine the exact causes of the reduction.

Aged↗
PubMed1986

A fixed-dose combination of furosemide and spironolactone in digitalized congestive heart failure patients.

Twenty-three optimally digitalized patients with congestive heart failure completed a 4-week treatment period with a fixed-drug association of 20 mg furosemide plus 50 mg spironolactone. Eleven patients responded with a 75% decrease in cardiac failure score on a daily dose of 1 capsule of the combination. The remaining 12 patients were initiated on the same dose, but needed, at the end of the first 14 days, an additional capsule (making a daily total of 40 mg furosemide and 100 mg spironolactone) over the next 2 weeks. On this dose, the patients achieved an average reduction of 52% in their cardiac failure score. There were no treatment failures. Electrolyte abnormalities and side-effects were not observed. The combination product, in a daily dose of 1 or 2 capsules, was found useful and well tolerated in the management of congestive heart failure.

Aged↗
PubMed1996

[Onset of dyspnea on exertion in elderly and young patients with congestive heart failure].

We previously reported that dyspnea on exertion in patients with congestive heart failure was not associated with pulmonary function ar rest, but was associated with the appearance of the anaerobic threshold and with the respiratory compensation point during exercise. Here we described a study of the influence of aging on the onset of dyspnea on exertion in elderly and in young patients with congestive heart failure. A total of 53 patients were studied: 35 were less than 65-year-old (average age, 47-year-old; 19 men and 16 women) and 18 were more than 65-year-old (average age, 70-year-old; 13 men and 5 women). All patients underwent maximal graded exercise testing on a bicycle ergometer. The workload increased according to a ramp protocol, and perceived exertion was evaluated with the Borg scale. The anaerobic threshold, the respiratory compensation point, and the peak VO2 were recorded. Values of 13 (somewhat hard) and 17 (very hard) on the Borg scale were considered to mark the start of dyspnea on exertion and an increase in dyspnea on exertion respectively. In the young patients, dyspnea on exertion began at about the time that the anaerobic threshold was reached, and it increased at about the time that the respiratory compensation point was reached. In contrast, elderly patients dyspnea on exertion began 70 seconds after the anaerobic threshold was reached, and it increased 30 seconds after the respiratory compensation point was reached. The VO2 at the start of dyspnea on exertion and the VO2 at the anaerobic threshold correlated more closely in the young patients than in the old patients. The same was true of the VO2 at the time that dyspnea on exertion increased and the VO2 at the respiratory compensation point. These findings suggest that elderly patients with congestive heart failure are less sensitive to the stimuli that cause dyspnea than are young patients.

Adolescent↗
PubMed2005

[Magnesium in congestive heart failure].

Magnesium deficit and other electrolyte abnormalities is a frequent disorder in patients with congestive heart failure. Overstimulation of the renin-angiotensin-aldosterone system, long-term administration of diuretics, digoxin, poor oral intake and impaired absorption contribute to these electrolytes abnormalities. Hypomagnesaemia and depletion of intracellular magnesium stores have been held responsible for a variety of cardiovascular and other functional abnormalities, including various arrhythmias, impairment of cardiac contractility, and vasoconstriction. Because sudden death is prevalent in congestive heart failure, a causal relationship between arrhythmias and magnesium deficiency has been proposed. Reportedly, administration of magnesium can suppress ventricular arrhythmias;however, it remains to be elucidated whether administration of magnesium prevents sudden death and improves prognosis of the patients with congestive heart failure. Nevertheless, since magnesium depletion may be prevalent in congestive heart failure and magnesium has anti-arrhythmic and beneficial cardiovascular effects, magnesium should be supplemented to the patients suspected to have its deficiency.

Arrhythmias, Cardiac↗
PubMedDate not supplied

Nesiritide (Natrecor): a new treatment for acutely decompensated congestive heart failure.

The care of the patient experiencing acutely decompensated congestive heart failure requires therapies that promote vasodilation and increase cardiac output while decreasing symptomatic hypotension and dysrhythmias. Nesiritide (Natrecor) is a new type of drug, recombinant human B-type natriuretic peptide (hBNP), approved for use in acutely decompensated congestive heart failure. The neurohormonal effects of endogenous BNP are reproduced by nesiritide. Indications, dosing, administration, and review of clinical trials are presented in this article.

Cardiotonic Agents↗
PubMed2006

Cardiac encephalopathy and congestive heart failure: a hypothesis about the relationship.

Many patients with congestive heart failure develop neurologic dysfunction. This may take the form of a cardiac encephalopathy that shares clinical features with other metabolic encephalopathies. The causes are multiple. There is a particular, previously unreported, syndrome that occasionally develops in some patients with congestive heart failure that resembles the findings in patients with normal pressure hydrocephalus. This syndrome is characterized by apathy and abulia with preserved alertness; it is caused by fluid retention within the cranial cavity. The syndrome may also develop in patients with other conditions that cause anasarca, e.g., severe liver or kidney disease or hypoalbuminemia. Because patients with these conditions are often quite ill, it has been difficult to verify the pathophysiologic aspects of the syndrome so that its mechanism must remain a hypothesis that awaits more definitive study in a series of patients. I have not seen this syndrome discussed in any cardiology or neurology texts or reports, and it seems to be completely unknown to cardiologists and neurologists. I have recognized about one patient per year with this syndrome.

Aged↗
PubMed1983

Respiratory gas analysis during exercise as a noninvasive measure of lactate concentration in chronic congestive heart failure.

Measurement of blood lactate during exercise in patients with chronic congestive heart failure provides a useful index of oxygen (O2) availability in working muscle. Bicarbonate buffering of lactate produces carbon dioxide (CO2) in excess of that resulting from oxidative metabolism. Therefore, calculation of excess CO2 production from measured CO2 production and O2 uptake may offer a noninvasive quantitative index of changes in blood lactate during exercise in these patients. To investigate this possibility, 22 patients with congestive heart failure and depressed left ventricular function were studied during progressive maximal upright bicycle exercise. Oxygen uptake, expired carbon dioxide, arterial lactate, O2 extraction, and cardiac output were measured at each 20 W incremental work load and peak exercise. Exercise increased VO2 from 3.5 +/- 0.9 ml/min/kg at rest to 13.1 +/- 2.9 ml/min/kg, O2 extraction from 49 +/- 9% at rest to 78 +/- 6%, lactate from 12 +/- 5 mg/dl at rest to 41 +/- 15 mg/dl, and cardiac index from 1.7 +/- 0.4 at rest to 3.8 +/- 1.2 liters/min/m2. The increase in lactate at each work load was linearly related to excess CO2 production (r = 0.92, p less than 0.01). Exercise was repeated the following day in 10 patients; measurements of excess CO2 production was highly reproducible (r = 0.98, p less than 0.01). Excess CO2 production also correlated with the decrease in bicarbonate produced by exercise (r = 0.81), supporting the hypothesis that excess CO2 is produced by bicarbonate buffering of lactate. Thus, calculation of excess carbon dioxide production from noninvasive measurement of respiratory gas exchange provides a reliable and reproducible method of continuously assessing alterations in lactate throughout bicycle exercise in patients with chronic congestive heart failure.

Bicarbonates↗
PubMed2006

[Diuretics in therapy of "diuretic resistance" by patients with congestive heart failure].

Loop diuretics are integral part of overall therapy of severe congestive heart failure. Approximately 10-20 % of patients with congestive heart failure (NYHA class III-IV) do not respond satisfactorily to diuretic treatment. Despite its frequency, the term "diuretic resistance" remains inadequately defined. In general, failure to decrease the extracellular fluid volume despite liberal use of diuretics is often termed "diuretic resistance". The combination of diuretics, particularly of loop diuretic with thiazide agents, is recommended for prevention as well as treatment of this complication. Effective management is also continuous infusion of loop diuretic. If it is impossible to achieve adequate response by combination of diuretics, increasing of its dosage or/and frequency or continuous infusion, then dialysis methods may be employed (however it is not intended to discuss this option in this article).

Diuretics↗
PubMed2003

Randomized, double-blind, placebo-controlled, pilot trial of infliximab, a chimeric monoclonal antibody to tumor necrosis factor-alpha, in patients with moderate-to-severe heart failure: results of the anti-TNF Therapy Against Congestive Heart Failure (ATTACH) trial.

BACKGROUND: Preclinical and preliminary clinical data have suggested that tumor necrosis factor-alpha (TNFalpha) may play a role in the evolution and progression of heart failure and that inhibition of TNFalpha may favorably modify the course of the disease. We evaluated the efficacy and safety of infliximab, a chimeric monoclonal antibody to TNFalpha, in patients with moderate-to-severe heart failure. METHODS AND RESULTS: One hundred fifty patients with stable New York Heart Association class III or IV heart failure and left ventricular ejection fraction <or=35% were randomly assigned to receive placebo (n=49), infliximab 5 mg/kg (n=50), or infliximab 10 mg/kg (n=51) at 0, 2, and 6 weeks after randomization and were followed-up prospectively for 28 weeks. Neither dose of infliximab improved clinical status at 14 weeks, the primary endpoint of the study, despite suppression of inflammatory markers (C-reactive protein and interleukin-6) and a modest increase in ejection fraction in the patients receiving 5 mg/kg (P=0.013). Furthermore, after 28 weeks, 13, 10, and 20 patients were hospitalized for any reason in the placebo, 5 mg/kg infliximab, and 10 mg/kg infliximab groups, respectively. The combined risk of death from any cause or hospitalization for heart failure through 28 weeks was increased in the patients randomized to 10 mg/kg infliximab (hazard ratio 2.84, 95% confidence interval 1.01 to 7.97; nominal P=0.043). CONCLUSIONS: Short-term TNFalpha antagonism with infliximab did not improve and high doses (10 mg/kg) adversely affected the clinical condition of patients with moderate-to-severe chronic heart failure.

Antibodies, Monoclonal↗
PubMed1996

Early reduction of neurohumoral factors plays a key role in mediating the efficacy of beta-blocker therapy for congestive heart failure.

This study examined the role played by neurohumoral factors in mediating the effects of beta-blocker therapy for congestive heart failure. Fifteen patients with congestive heart failure underwent beta-blocker therapy. Plasma norepinephrine and alpha-atrial natriuretic peptide concentrations decreased 2 weeks after initiation of beta-blocker therapy. Decrease in plasma norepinephrine level persisted for 6 months. Lymphocyte beta-adrenoceptor density increased 2 weeks after therapy but was not increased 6 months later. Left ventricular ejection fraction was unchanged 2 weeks after therapy, but it increased 6 months after introduction of beta-blockers. Plasma norepinephrine level decreased 2 weeks after the therapy in the responders (increase in ejection fraction > 0.10) but not in the nonresponders. Thus early reduction of neurohumoral factor levels preceded the late improvement of left ventricular contractile function and may therefore be partly responsible for the efficacy of beta-blocker therapy for congestive heart failure.

Adrenergic beta-Antagonists↗
PubMed2001

Congestive heart failure after treatment for Wilms' tumor: a report from the National Wilms' Tumor Study group.

PURPOSE: We determined the frequency of and risk factors for congestive heart failure following treatment for Wilms' tumor that included doxorubicin. PATIENTS AND METHODS: Flow sheets and medical records were reviewed to identify cases of congestive heart failure in a cohort of patients treated on National Wilms' Tumor Studies (NWTS)-1, -2, -3, and -4. The frequency of congestive heart failure was estimated using the Kaplan-Meier method. A case-control study was conducted to determine the relationship among cumulative doxorubicin dose, site(s), total dose of abdominal and thoracic irradiation, sex, and the frequency of congestive heart failure. RESULTS: The cumulative frequency of congestive heart failure was 4.4% at 20 years after diagnosis among patients treated initially with doxorubicin and 17.4% at 20 years after diagnosis among those treated with doxorubicin for their first or subsequent relapse of Wilms' tumor. The relative risk (RR) of congestive heart failure was increased in females (RR = 4.5; P =.004) and by cumulative doxorubicin dose (RR = 3.3/100 mg/m(2); P <.001), lung irradiation (RR = 1.6/10 Gy; P =.037), and left abdominal irradiation (RR = 1.8/10 Gy; P =.013). CONCLUSION: We conclude that congestive heart failure is a risk of treatment with doxorubicin for Wilms' tumor. Additional follow-up of those children treated on NWTS-4 will be necessary to determine if the decrease in dose to 150 mg/m(2) significantly reduces this risk.

Actuarial Analysis↗
PubMed1991

Oxygen free radicals and congestive heart failure.

Plasma lipid peroxides (malondialdehyde) and thiols were measured in 45 patients with congestive heart failure and 45 controls. Malondialdehyde concentrations were significantly higher in the patients with congestive heart failure (median 9.0 nmol/ml interquartile range (IQR) 7.9-10.2) than in the controls (median 7.7 nmol/ml (IQR 6.9-9.2)). Plasma thiols were significantly lower in congestive heart failure (median 420 mumol/l (IQR 379-480)) than in the controls (median 463 mumol/l (IQR 445-525)). There was a significant but weak negative correlation between malondialdehyde and left ventricular ejection fraction (r = -0.35) and a positive correlation between plasma thiols and left ventricular ejection fraction (r = 0.39). This study provides clinical support for experimental data indicating that free radicals may be important in heart failure. It also suggests that the degree of free radical production may be linked to the severity of the disease.

Adult↗
PubMed1994

Diuretic treatment for the sodium retention of congestive heart failure.

The use of diuretics for the treatment of sodium retention in congestive heart failure was evaluated. Particular focus was given to the altered renal response to diuretics in patients with heart failure and adverse responses to diuretic therapy. Highlighted information included historical aspects of the development of diuretics, mechanisms of sodium retention, the physiologic and clinical response to diuretics, and the altered pharmacokinetics and pharmacodynamics of diuretics in congestive heart failure. Despite more than 60 years of empiric diuretic use in heart failure, the actual database regarding the long-term efficacy, adverse effects, and altered mortality outcome in heart failure is relatively small. Existent pharmacokinetic and pharmacodynamic data are typically not collected within the context of heart failure efficacy trials. In addition to altered electrolyte transport and total-body electrolyte depletion, diuretics may be associated with adverse neurohormonal activation. Thus, guidelines for acute and long-term therapy with diuretics in heart failure remain somewhat empiric. Diuretics will remain a mainstay for the treatment of edema in congestive heart failure but must be accompanied by moderate sodium restriction. However, large clinical trials of diuretics would be necessary to demonstrate that improved clinical efficacy with edema reduction is not offset by adverse effects, which include electrolyte depletion, ventricular arrhythmias, and subsequent increased mortality.

Administration, Oral↗
PubMed2006

[Quality of life and functional status in congestive heart failure].

OBJECTIVE: To assess health related quality of life of patients with congestive heart failure (CHF), to correlate quality of life with other functional parameters; maximal oxygen uptake (peak VO2) with submaximal tests (two minute walking test and shuttle walk test) and New York Heart Association (NYHA) with other clinical variables. METHODS: We evaluated 35 stable congestive heart failure patients (NYHA II-III). Functional status was assessed by NYHA classification, maximal oxygen uptake (peak VO2) and submaximal tests (two minute walk test and shuttle walk test). Health related quality of life was measured with short form 36 health survey (SF 36). RESULTS: NYHA functional class was correlated with social functioning of SF 36, peak VO2 and shuttle walk test. Peak VO2 was correlated with most of the parameters of SF 36. On the other hand 2 minute walk test and shuttle walk test were correlated with social functioning of SF 36. There was a correlation between peak VO2 and submaximal test, but there was no correlation between left ventricular ejection fraction, peak VO2 and NYHA class. CONCLUSION: Social functioning is impaired in patients with congestive heart failure. There is a correlation between maximal and submaximal tests. The maximal and submaximal tests can explain some degree of quality of life. Functional status can be explained with peak VO2 and shuttle walk test apart from NYHA class.

Adult↗
PubMed1995

Improvement of cardiac performance by intravenous infusion of L-arginine in patients with moderate congestive heart failure.

OBJECTIVES: The aim of this study was to evaluate the hemodynamic effect of L-arginine infusion in patients with congestive heart failure. BACKGROUND: Endothelium-dependent vasodilation is impaired in patients with congestive heart failure. Nitric oxide, which was identified as endothelium-derived relaxing factor, is generated by nitric oxide synthase from L-arginine. Our hypothesis was that administration of L-arginine in patients with congestive heart failure may increase nitric oxide production and have a beneficial hemodynamic effect. METHODS: Twelve patients with congestive heart failure (New York Heart Association class II or III) due to coronary artery disease (left ventricular ejection fraction < 35%) were given 20 g of L-arginine by intravenous infusion over 1 h at a constant rate. Stroke volume, cardiac output and left ventricular ejection fraction were determined with Doppler echocardiography at baseline and at 30 and 60 min and 1 h after the end of infusion. Blood and urinary levels of nitrite/nitrate (NO2/NO3), stable metabolites of nitric oxide, were measured and clearance was calculated. RESULTS: One hour of infusion of L-arginine resulted in a significant increase in stroke volume (from 68 +/- 18 ml to 76 +/- 23 ml [mean +/- SD], p = 0.014) and cardiac output (from 4.07 +/- 1.22 liters/min to 4.7 +/- 1.42 liters/min, p = 0.006) without a change in heart rate. Mean arterial blood pressure decreased (from 102 +/- 11 mm Hg to 89 +/- 9.5 mm Hg, p < 0.002), and systemic vascular resistance decreased significantly. Within 1 h after cessation of L-arginine infusion, blood pressure, stroke volume, cardiac output and systemic vascular resistance were statistically not different from baseline values. Clearance of NO2/NO3 increased significantly during L-arginine administration (from 13.28 +/- 0.42 ml/min to 29.97 +/- 1.09 ml/min, p < 0.001). CONCLUSIONS: Infusion of L-arginine in patients with congestive heart failure results in increased production of nitric oxide, peripheral vasodilation and increased cardiac output, suggesting a beneficial hemodynamic and possibly therapeutic profile.

Aged↗
PubMed1989

Clinical relevance of long-term therapy with levodopa and orally active dopamine analogues in patients with chronic congestive heart failure.

Beneficial effects of long-term treatment with dopamine analogues in patients with congestive heart failure may result from their vasodilating properties, in particular from renal artery vasodilation. Oral application of levodopa results in increased dopamine plasma levels and can improve cardiac performance and renal function in patients with congestive heart failure. A daily levodopa dosage of at least 4 g appears to a prerequisite for long-term response to the drug. Because of frequent side effects including nausea, vomiting, and dyskinesia at this dosage, the clinical usefulness of levodopa seems to be limited to a minority of patients. Ventricular arrhythmias have been shown to increase significantly during long-term levodopa therapy, probably due to stimulation of myocardial beta receptors. Increased ventricular arrhythmias or significant central nervous side effects have not been observed after administration of ibopamine and fenoldopam, which are orally active analogues of dopamine. Both agents exhibit potent arterial vasodilating properties and have been shown to increase cardiac performance in patients with congestive heart failure after short-term administration. The long-term beneficial effects of ibopamine and fenoldopam in the treatment of congestive heart failure have not yet been clarified. However, available results are encouraging and warrant further clinical evaluation of these agents, as well as the development of new analogues of dopamine, in particular of potent vascular dopamine agonists.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed2004

Renal, but not systemic, hemodynamic effects of dopamine are influenced by the severity of congestive heart failure.

OBJECTIVE: To determine whether the short-term systemic and renal hemodynamic response to dopamine is influenced by clinical severity of congestive heart failure. DESIGN: Effects of increasing doses of dopamine were assessed in patients consecutively admitted for acutely decompensated congestive heart failure. SETTING: Intensive care unit. PATIENTS: We enrolled 16 congestive heart failure patients stratified by clinical severity (New York Heart Association [NYHA] class III, n = 8; NYHA class IV, n = 8) and two additional NYHA class III patients as controls. INTERVENTIONS: Measurements were carried out throughout five 20-min experimental periods: baseline, dopamine infusion at 2, 4, and 6 microg x kg(-1) x min(-1), and recovery. Controls received a similar amount of saline. MEASUREMENTS AND MAIN RESULTS: Systemic and renal hemodynamics were determined respectively by right cardiac catheterization and radioisotopes (iodine 131-labeled hippuran and iodine 125-labeled iothalamate clearance). The peak increase in heart rate and cardiac index occurred at a dopamine dose of 4-6 microg x kg(-1) x min(-1). The dose-response relation was similar in NYHA classes III and IV. Improvement in effective renal plasma flow and glomerular filtration rate, peaking at 4 microg x kg(-1) x min(-1), was more rapid and marked in NYHA class III than class IV patients, in whom the renal fraction of cardiac output failed to increase. The systemic and renal effects of dopamine were independent of age. No change occurred in controls. CONCLUSIONS: The dose of dopamine producing an optimal improvement of systemic and renal hemodynamics in congestive heart failure is higher than usually reported. A greater clinical severity of congestive heart failure impairs the renal effects of dopamine, probably through a selective loss in renal vasodilating capacity.

Acute Disease↗
PubMed1998

Prognostic value of congestive heart failure history in patients undergoing percutaneous coronary interventions.

OBJECTIVES: We sought to determine the prognostic significance of a history of congestive heart failure above that provided by baseline ejection fraction in patients undergoing percutaneous coronary interventions. BACKGROUND: Left ventricular function is a known predictor of survival in patients with coronary artery disease, as is a history of congestive heart failure. The contribution of heart failure history independent of left ventricular function is unknown. METHODS: Data were pooled from four interventional trials and the Duke University database. The combined dataset included 5,260 patients undergoing percutaneous interventions, 334 with and 4,926 without a history of heart failure. Patients were defined by the treating physician as having a clinical history of heart failure at the time of enrollment. RESULTS: The 30-day and 6-month mortality were higher in patients with a clinical history of congestive heart failure than in those without such a history (2% vs. <1%, p=0.002 at 30 days, 5% vs. 1%, p=0.001 at 6 months). Heart failure history did not influence the incidence of myocardial infarction, use of angioplasty or the use of bypass surgery during follow-up. Multivariable analysis revealed that heart failure history added significantly to ejection fraction in predicting intermediate-term (6-month) mortality (p=0.01). Stepwise logistic regression also revealed heart failure history to be an independent predictor of 6-month mortality (odds risk 1.9, 95% confidence interval 1.1 to 3.5). CONCLUSIONS: A clinical history of congestive heart failure is associated with increased early and intermediate-term mortality in patients undergoing percutaneous revascularization. Congestive heart failure history appears to provide prognostic information independent of that available from a patient's left ventricular function. These findings suggest that patients with a clinical history of congestive heart failure who undergo a percutaneous intervention should be closely monitored, especially those with the lowest ejection fractions.

Aged↗