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PubMed1993

[Pathophysiology and current therapy of congestive heart failure due to idiopathic cardiomyopathy].

Congestive heart failure (CHF) due to idiopathic cardiomyopathy is reviewed. CHF in dilated cardiomyopathy (DCM) is caused mainly by myocardial systolic dysfunction. Diuretics, angiotensin-converting enzyme (ACE) inhibitors and digitalis are the first choice drugs. ACE inhibitors have been shown to be effective in prolonging life and improving quality of life. Recently, long-term beta-blockade therapy has been shown to be useful. CHF in hypertrophic cardiomyopathy (HCM) is caused by decreased myocardial compliance. The beneficial effect of verapamil in HCM is related to improved relaxation and diastolic filing. Verapamil is also effective in relieving myocardial ischemia. Beta-blockade decreases pressure gradient and oxygen consumption. Idiopathic restrictive cardiomyopathy is a very rare disease and decreased myocardial compliance is responsible for CHF.

Adrenergic beta-Antagonists↗

PubMed2002

Efficacy of continuous hemodiafiltration for patients with congestive heart failure.

BACKGROUND/AIMS: The basic principle of treatment of congestive heart failure is achieving adequate control of preload and afterload through enhancement of cardiac contractility. In severe cases, however, we have usually applied continuous hemodiafiltration (CHDF) as a type of mechanical support. In this study, we investigated hemodynamic changes caused by CHDF in patients with congestive heart failure. METHODS: We treated seven patients with congestive heart failure complicated by multiple organ failure by CHDF over 72 h, during which we measured hemodynamic parameters to determine their changes. RESULTS: Implementation of CHDF resulted in a significant decrease in pulmonary artery occluded pressure and significant increases in cardiac index and left ventricular stroke work index. In addition, 72-hour cumulative water balance was found to be -1,791 +/- 2,119 ml, and systemic vascular resistance index decreased significantly. CONCLUSION: Hemodynamics of patients were improved with CHDF through strict control of preload and consequently tissue oxygen metabolism was improved.

Adult↗

PubMed1998

The influence of basal nitric oxide activity on pulmonary vascular resistance in patients with congestive heart failure.

Increased pulmonary resistance may reduce survival and treatment options in patients with congestive heart failure. Nitric oxide (NO) is a determinant of normal pulmonary resistance vessel tone. We tested the hypothesis that loss of NO function contributes to increased pulmonary vascular resistance index (PVRI) in congestive heart failure. Pulmonary arterial resistance vessel function was studied in 25 conscious adults. Three groups were studied: 8 controls, 9 patients with congestive heart failure and normal PVRI, and 8 patients with congestive heart failure and raised PVRI. Segmental arterial flow was determined with a Doppler wire and quantitative angiography. NG-monomethyl-L-arginine (L-NMMA) was used to inhibit NO, whereas phenylephrine was used as an endothelium-independent control. The response to inhibition of NO with L-NMMA was less in patients with congestive heart failure and elevated PVRI than in patients with congestive heart failure and normal PVRI (p <0.05). The difference in response between the congestive heart failure groups was specific to NO-dependent regulation because the response to the endothelium-independent constrictor phenylephrine was not different (p = 0.92). There was no difference in response to L-NMMA between controls and patients with congestive heart failure and normal PVRI. The response to L-NMMA correlated to PVRI. In adults with congestive heart failure, NO appears to play an important role in maintaining normal pulmonary resistance.

Adolescent↗

PubMed2002

Outcome of congestive heart failure in elderly persons: influence of left ventricular systolic function. The Cardiovascular Health Study.

BACKGROUND: Most persons with congestive heart failure are elderly, and many elderly persons with congestive heart failure have normal left ventricular systolic function. OBJECTIVE: To evaluate the relationship between left ventricular systolic function and outcome of congestive heart failure in elderly persons. DESIGN: Population-based longitudinal study of coronary heart disease and stroke. SETTING: Four U.S. sites: Forsyth County, North Carolina; Sacramento County, California; Allegheny County, Pennsylvania; and Washington County, Maryland. PARTICIPANTS: 5888 persons who were at least 65 years of age and were recruited from the community. MEASUREMENTS: Total mortality and cardiovascular morbidity and mortality. RESULTS: Of 5532 participants, 269 (4.9%) had congestive heart failure. Among these, left ventricular function was normal in 63%, borderline decreased in 15%, and overtly impaired in 22%. The mortality rate was 25 deaths per 1000 person-years in the reference group (no congestive heart failure and normal left ventricular function at baseline); 154 deaths per 1000 person-years in participants with congestive heart failure and impaired left ventricular systolic function; 87 and 115 deaths per 1000 person-years in participants with congestive heart failure and normal or borderline systolic function, respectively; and 89 deaths per 1000 person-years in persons with impaired left ventricular function but no congestive heart failure. Although the risk for death from congestive heart failure was lower in persons with normal systolic function than in those with impaired function, more deaths were associated with normal systolic function because more persons with heart failure fall into this category. CONCLUSIONS: Community-dwelling elderly persons, especially those with impaired left ventricular function, have a substantial risk for death from congestive heart failure. However, more deaths occur from heart failure in persons with normal systolic function because left ventricular function is more often normal than impaired in elderly persons with heart failure.

Aged↗

PubMed1998

Spontaneous conversion and maintenance of sinus rhythm by amiodarone in patients with heart failure and atrial fibrillation: observations from the veterans affairs congestive heart failure survival trial of antiarrhythmic therapy (CHF-STAT). The Department of Veterans Affairs CHF-STAT Investigators.

BACKGROUND: In a multicenter, double-blind, placebo-controlled study, the long-term effects of amiodarone on morbidity and mortality in patients with congestive heart failure (CHF) and atrial fibrillation (AF) were evaluated during a 4-year period. METHODS AND RESULTS: Of 667 patients with CHF, 103 (15%) had AF at baseline. Of these, 51 were randomized to amiodarone and 52 to placebo. The group with sinus rhythm and the group in AF were comparable except for a higher proportion of AF in patients with nonischemic versus ischemic cardiomyopathy (41% versus 27%, P<0.005). The mean ventricular response (VR) during AF over 24 hours was reduced by amiodarone at 2 weeks (20%, P=0.001), at 6 months (18%, P=0.001), and at 12 months (16%, P=0.006). Maximal VR was reduced 22% (P=0.001) at 2 weeks, 19% (P=0.001) at 6 months, and 14% (P=0.001) at 12 months. Sixteen of 51 patients on amiodarone and 4 of 52 on placebo converted to sinus rhythm during the study (chi2=9.23, P=0.002). During follow-up, 11 of 268 patients in sinus rhythm on amiodarone at baseline and 22 of the 263 in sinus rhythm on placebo developed AF; the difference was significant (chi2=12.88, P=0.005). Analysis of total mortality during follow-up showed a significantly lower mortality rate (P=0. 04) in patients in AF at baseline who subsequently converted to sinus rhythm on amiodarone than in those who did not convert to sinus rhythm on the drug. CONCLUSIONS: In patients with CHF, amiodarone has a significant potential to spontaneously convert patients in AF to sinus rhythm, with patients who convert having a lower mortality rate than those who do not. The drug prevented the development of new-onset AF and significantly reduced the VR in those with persistent AF.

Aged↗

PubMed2002

Pilot studies on the use of 3,5-diiodothyropropionic acid, a thyroid hormone analog, in the treatment of congestive heart failure.

After an initial safety study in 7 normal volunteers, a randomized double-blind comparison was made between 3,5-diiodothyropropionic acid (DITPA) and placebo in 19 patients with moderately severe congestive failure. In heart failure patients receiving the drug for 4 weeks, cardiac index was increased (p = 0.04) and systemic vascular resistance index was decreased (p = 0.02). Systolic cardiac function was unchanged but isovolumetric relaxation time was decreased significantly, suggesting improvement in diastolic function. Total serum cholesterol (p = 0.005) and triglycerides (p = 0.01) also were decreased significantly. DITPA could represent a useful new agent for treatment of congestive heart failure.

Adult↗

PubMed1990

Bronchial hyperresponsiveness in patients with chronic congestive heart failure.

To investigate the relationship between pulmonary congestion and bronchial responsiveness, we measured bronchial responsiveness to acetylcholine in 51 patients with left heart disorders. The measurement of bronchial responsiveness was performed by inhaling doses of acetylcholine chloride (0.08 to 20 mg/ml) and calculating the PC20-FEV1. The median value for PC20-FEV1 was above 20 mg/ml in the subjects without history of congestive heart failure (n = 18), was 5.29 mg/ml in the subjects with clinical evidence of congestive heart failure in the past days (n = 18; p less than 0.01), and was 5.74 mg/ml in the subjects with clinical evidence of congestive heart failure at the time of study (n = 15; p less than 0.01). The hemodynamic variables by cardiac catheterization and the clinical symptoms were not correlated with the grade of bronchial responsiveness. These results suggest that the bronchial responsiveness was increased in most of the patients with chronic congestive heart failure. We concluded that continuous pulmonary congestion may contribute to the pathogenesis of bronchial hyperresponsiveness.

Acetylcholine↗

PubMedDate not supplied

Effect of congestive heart failure on the intrinsic metabolic capacity of the liver in the dog.

The intrinsic metabolic capacity of the liver at end-stage heart failure in the pacing overdrive dog model of congestive heart failure was evaluated ex vivo. Congestive heart failure was induced in seven adult mongrel dogs (20-30 kg) by cardiac electrical pacing at a frequency of 240 stimuli/min until the development of overt heart failure; seven other dogs served as controls. The animals were then anesthetized and the right ventricular papillary muscles and samples from the left lateral hepatic lobes were collected. The degree of myocardial dysfunction as well as the total amount and the activities of cytochromes P-450 were evaluated. Tension, maximum rate of tension rise, and Vmax were significantly lower (40-60%) in the paced than in the control dogs, indicating a marked myocardial dysfunction. Moreover, significant decreases in total cytochrome P-450 (0.31 +/- 0.04 vs. 0.53 +/- 0.03 nmol/mg of microsomal protein, p less than 0.01) and in the intensity of four different electrophoretic protein bands (molecular masses of 46, 48, 50, and 59 kDa) occurred in the dogs with congestive heart failure. The decrease in total cytochrome P-450 was accompanied by a significant reduction in aminopyrine N-demethylase activity (1.74 +/- 0.25 vs. 2.91 +/- 0.40 nmol/min/mg of microsomal protein, p less than 0.05). Immunoblot analysis using antibodies to two different dog liver phenobarbital-inducible cytochromes P-450 demonstrated that PBD-1 (a P-450IIIA) was not affected by congestive heart failure, whereas PBD-2 (a P-450IIB) was markedly decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1984

Relation between hemodynamic and ventilatory responses in determining exercise capacity in severe congestive heart failure.

The cause of exercise intolerance in congestive heart failure is unclear. Hemodynamic and ventilatory responses were measured during symptomatic maximal upright bicycle exercise in 28 patients with chronic severe left ventricular failure who achieved a maximal oxygen uptake of only 12 +/- 4 ml/min/kg (+/- standard deviation). All patients reached anaerobic metabolism as the respiratory exchange ratio rose and arterial pH fell significantly. Pulmonary capillary wedge pressure increased from 20 +/- 10 mm Hg at rest to 38 +/- 9 mm Hg at peak exercise and cardiac index increased from 2.51 +/- 0.73 to 4.54 +/- 1.65 liters/min/m2 (both p less than 0.001). Systemic vascular resistance decreased, but pulmonary vascular resistance did not change during exercise. Despite the marked pulmonary venous hypertension at peak exercise, blood gases were unchanged (PaO2, 96 +/- 15 mm Hg; PaCO2, 35 +/- 7 mm Hg). Systemic arterial oxygen content increased from 16 +/- 2 to 17 +/- 2 vol% (p less than 0.01). Changes in pulmonary capillary wedge pressure did not correlate with changes in arterial oxygen content. Results were similar whether patients were limited by dyspnea or fatigue. Thus, exercise intolerance in patients with severe left ventricular failure is associated with marked elevation of pulmonary capillary wedge pressure and anaerobic metabolism without hypoxemia or altered carbon dioxide tension. These findings suggest that exercise ability in congestive heart failure is more dependent on cardiac output than on ventilatory consequences of pulmonary congestion.

Adult↗

PubMed1990

Rapid ventricular pacing in pigs: an experimental model of congestive heart failure.

To develop an improved animal model of congestive heart failure, 11 female farm pigs (wt, 42-46 kg) underwent rapid ventricular pacing at 230 beats/min for 7 days with a modified Medtronic unipolar pacemaker connected to an apical pacing lead. After 7 days the pacemaker was turned off, anesthesia induced, the chest opened, and cardiac hemodynamic and dimensional studies were performed. Results were subsequently compared with data from 12 control pigs that received no pacing. Two pigs died before measurements could be determined. Cardiac output in the paced animals (0.061 +/- 0.018 l.min-1.kg-1) was significantly less (P less than 0.05) than in control pigs (0.085 +/- 0.016 l.min-1.kg-1), when compared at the same resting heart rate. Left ventricular (LV) end-diastolic pressure (23.2 +/- 7.7 vs. 8.6 +/- 3.6 mmHg, P less than 0.01) and right ventricular (RV) end-diastolic pressure (9.0 +/- 3.1 vs. 4.4 +/- 1.7 mmHg, P less than 0.01) were significantly greater in the paced pigs. Significant increases in both septal-lateral LV end-diastolic dimension (60.3 +/- 3.9 vs. 52.1 +/- 7.2 mm, P less than 0.01) and RV end-diastolic dimension (47.2 +/- 5.7 vs. 40.8 +/- 4.7 mm, P less than 0.05) indicated biventricular dilation in the paced pigs. They also exhibited a significantly greater heart weight-to-total body weight ratio and clinical evidence of congestive heart failure, with hepatomegaly and ascites. These results demonstrate that 1 wk of rapid ventricular pacing at 230 beats/min produces a realistic model of congestive heart failure in the pig.

Animals↗

PubMed1979

Risk factors for doxorubicin-induced congestive heart failure.

Potential risk factors responsible for development of doxorubicin-induced congestive heart failure were examined through retrospective analysis of 4018 patient records. The overall incidence of drug-induced congestive heart failure was 2.2% (88 cases). The probability of incurring doxorubicin-induced congestive heart failure was related to the total dose of doxorubicin administered. There was a continuum of increasing risk as the cumulative amount of administered drug increased. A weekly dose schedule of doxorubicin was associated with a significantly lower incidence of congestive heart failure than was the usually employed every 3-week schedule. An increase in drug-related congestive heart failure was also seen with advancing patient age. Performance status, sex, race, and tumor type were not risk factors. These data will enable clinicians to better estimate the risk/benefit ratio in individual patients receiving prolonged administration of doxorubicin. They also provide a basis for the investigation of less cardiotoxic anthracycline analogues or for designing measures to prevent doxorubicin-induced cardiomyopathy.

Adolescent↗

PubMed1999

A novel biochemical approach to congestive heart failure: cardiac troponin T.

BACKGROUND: The major structural characteristic of congestive heart failure is myocardial cell death. The aim of our study was to determine whether the level of cardiac troponin T, a protein specific for cardiac necrosis, was increased in patients with congestive heart failure. METHODS AND RESULTS: Plasma samples were obtained from 33 patients and 47 healthy control subjects. Quantitative determination of cardiac troponin T was achieved with a second-generation enzyme immunoassay without cross-reactivity with the skeletal muscle troponin T. The mean circulating level of cardiac troponin T was 0.140 +/- 0.439 ng/mL in patients with heart failure and 0.0002 +/- 0.001 ng/mL in the healthy controls (P =. 0001). To evaluate the relation between structural degradation and functional impairment, patients in heart failure were categorized according to their radionuclide left ventricular ejection fraction (LVEF). In the 23 patients with LVEF </=45%, cardiac troponin T was 0.163 +/- 0.50 ng/mL, a level significantly higher than that in patients with LVEF >45% (P =.04). There was also a negative correlation between cardiac troponin T and LVEF (R = -0.41, P =.01). CONCLUSIONS: These data show that cardiac troponin T is increased in patients with congestive heart failure and that the level parallels the severity of the disease. We conclude that cardiac troponin T is a suitable candidate-marker molecule to monitor congestive heart failure from a structural perspective.

Adult↗

PubMed1990

Neuroendocrine activity in congestive heart failure.

The increased neuroendocrine activity in patients with congestive heart failure appears to be a generalized attempt to maintain blood pressure at the expense of reduced cardiac performance and salt and water retention. It is likely that baroreceptor dysfunction contributes to increased sympathetic nervous system activity in patients with congestive heart failure. The usual tonic inhibitory messages emanating from baro- and mechanoreceptors in the great vessels and heart fail to adjust sympathetic traffic from the brain to the periphery, leading to uninhibited sympathetic tone. Arginine vasopressin and plasma renin activity may be increased secondarily; however, plasma renin activity activation could also be induced by a low-salt diet and diuretic use. Preliminary baseline data indicate that patients with left ventricular dysfunction (ejection fraction less than or equal to 35%) but no or very mild symptoms of heart failure have increased plasma levels of norepinephrine, atrial natriuretic factor and arginine vasopressin, while plasma renin activity is normal, suggesting that neuroendocrine activity contributes to the pathogenesis of congestive heart failure. Neurohormones such as angiotensin II may alter gene expression, leading to changes in the shape and size of the cell. Remodeling of the heart and blood vessels is associated with both heart failure and hypertension. Angiotensin-converting enzyme inhibitors have been demonstrated to retard or reverse the remodeling process under certain experimental conditions. Studies are currently under way to test this possibility in patients.

Heart Failure↗

PubMed1992

The Rational for the Use of Ã -Blockers in the Treatment of Congestive Heart Failure.

Limited clinical data suggest that in particular types of congestive heart failure, the cautious use of low-dose Ã -blockers may be beneficial, despite the well-known cardiodepressant effect of these drugs. Downregulation of cardiac Ã -adrenoceptors has been demonstrated repeatedly in various forms of congestive heart failure. This phenomenon is caused by the long-term exposure of these receptors to endogenous noradrenaline (a Ã -adrenoceptor agonist), which is known to reach markedly elevated plasma concentrations in severe congestive heart failure. As but one example, the downregulation of Ã -adrenoceptors explains the well-known tachyphylaxis in the inotropic response to Ã -adrenoceptor agonists such as dobutamine. A beneficial effect of low-dose Ã -blockers has been shown for metoprolol and bucindolol given for several months. Most studies with such agents have been done in patients with severe congestive heart failure resulting from dilated cardiomyopathy. The beneficial effect of such therapy may be explained by Ã -adrenoceptor upregulation, thus allowing a better response to endogenous noradrenaline. Alternatively, the therapy may exert its effect by inhibiting tachycardia, which is known to accompany congestive heart failure.

Journal Article↗

PubMed1999

Congestive heart failure in the community: trends in incidence and survival in a 10-year period.

OBJECTIVE: To compare the incidence of congestive heart failure and the survival in patients with congestive heart failure in Rochester, Minn, in 1981 with that observed in 1991. METHODS: Population-based, descriptive epidemiological study with ecological and individual level comparisons over time. Olmsted County, Minnesota, where the Rochester Epidemiology Project provides passive surveillance of the population for health outcomes. All 248 patients fulfilled the Framingham criteria, 107 patients presenting with the new onset of congestive heart failure in 1981 and 141 patients in 1991. The community inpatient and outpatient medical records of all incident cases were reviewed to evaluate the presenting characteristics of patients at diagnosis. RESULTS: The incidence of congestive heart failure after adjustment for age and sex to the US population was not significantly different in the 1991 cohort compared with that in 1981 (3.0 per 1000 person-years; 95% confidence interval, 2.5-3.5 vs 2.8 per 1000 person-years; 95% confidence interval, 2.2-3.3; P = .55). The survival of patients with new diagnosis of congestive heart failure was similar in the 2 cohorts (P = .53). Survival adjusted for age, sex, and New York Heart Association functional class was not significantly different in patients with congestive heart failure in 1981 and 1991 (relative risk, 0.907; P = .55). CONCLUSIONS: These data suggest that recent advances in management of cardiovascular disease, as used in the community, had not yet impacted incidence or survival of patients with congestive heart failure in the community during the 10-year study period. This highlights the need to continue efforts to ensure that advances in diagnosis and therapy are incorporated into the care of patients with congestive heart failure in the community.

Age Distribution↗

PubMed2006

Surgical aspects of congestive heart failure.

Despite tremendous advances in the medical management of congestive heart failure the gold standard for the treatment of end stage congestive heart failure remains cardiac transplantation. The acknowledged critical limitation of sufficient suitable organ donors has resulted in the refinement and development of novel surgical alternatives for the treatment of congestive heart failure. These approaches include the extension of current conventional cardiac operations such as mitral valve repair to the failing ventricle, surgically reconstructing the size and shape of the failing left ventricle in order to optimize geometry and render it a more efficient pump, and partial or complete replacement of the ventricle with a mechanical device. The continued evolution of such therapies is likely to one day have a significant epidemiologic impact on patients suffering from end stage heart failure.

Aortic Valve↗

PubMed1989

Are inotropic agents contraindicated in congestive heart failure?

The myocardium in the patient with congestive heart failure is abnormal and probably unable to generate sufficient chemical energy to meet the heart's mechanical needs. Such a condition of "energy starvation" would have several important implications; among these is that inotropic stimulation, by increasing energy utilization, could accelerate the progressive death of myocardial cells that characterizes end-stage heart failure. An important goal of therapy in these patients, therefore, is to reduce cardiac energy expenditure. This can be accomplished by unloading the failing heart, which has already been shown to prolong survival in patients with severe congestive heart failure. Slowing the progressive death of myocardial cells may also be accomplished by the administration of negative, rather than positive, inotropic drugs.

Cardiotonic Agents↗

PubMed1978

Loculated interlobar air-fluid collection in congestive heart failure.

Two patients are described who had congestive heart failure with loculated interlobar air-fluid collections. Although pseudotumor (interlobar effusion) is a well-known finding in congestive heart failure, the additional presence of air is unique. Both are somewhat related to the underlying failure.

Aged↗