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PubMed2006

Clinical advances in diastolic heart failure.

Congestive heart failure is a common cardiovascular disorder among adults and is a major cause of morbidity and mortality worldwide. Diastolic heart failure (DHF) is implicated in 1/3 to 1/2 of all heart failure cases and results from an abnormality of ventricular relaxation, compliance or filling. DHF differs from heart failure with reduced ejection fraction in epidemiology, pathophysiology, and natural history. Recent advances have improved our understanding of DHF. This review summarizes these advances and discusses their clinical implications as they pertain to the diagnosis and management of patients with DHF.

Aged↗
PubMed1991

Epidemiology and prognosis of heart failure.

Congestive heart failure (CHF) is a major cause of mortality and morbidity, and has a prognosis similar to that of several malignancies. There are increasing trends in both prevalence and incidence rates of CHF which points towards CHF becoming a major community health problem. Early detection of CHF is dependent upon criteria to define the initial stages of a condition which progresses slowly over many years. In western countries the dominant causes of CHF are hypertension and coronary heart disease, which account for more than 75% of the cases. Other precursors are diabetes and rheumatic heart disease. Independent risk factors for CHF are hypertension, smoking, obesity, and psychological stress. Early detection of CHF through identification of early symptoms such as dyspnea on exertion, treatment of known heart diseases, and treatment of risk factors may prevent its progress. Epidemiological data indicate that primary preventive efforts should be directed against hypertension, smoking and obesity. A multiple risk factor interventional approach seems to yield the best result since these risk factors act synergistically.

Cause of Death↗
PubMedDate not supplied

Myoplasty--a surgical option for end-stage heart failure.

Congestive heart failure is a growing problem in the Western world, which modern therapeutic options are doing little to ameliorate. Dynamic cardiomyoplasty may be one option which has great potential. This article reviews the use of skeletal muscle for circulatory assist and suggests that, with further work, it should take a significant place in the treatment armamentarium.

Assisted Circulation↗
PubMed1993

[The practical aspects of treatment in heart failure].

Congestive heart failure (CHF) has been treated for several years on empiric basis, until the results of the major clinical trials have made possible a pathophysiological approach to the treatment of patients with CHF. Studies from our laboratories have demonstrated that hemodynamic and neurohormonal responses to acute volume expansion are markedly impaired in patients with dilated cardiomyopathy and mild heart failure (NYHA Class I) and that pretreatment with ACE-inhibitors is able to prevent these abnormal responses. New insights into a more pathophysiological approach to CHF treatment are now possible by the development of new noninvasive techniques for the study of cardiac function. In particular, through radionuclide techniques we were able to demonstrate that patients with CHF show an exercise induced hemodynamic response different from that of normal subjects. Both ACE-inhibitors and digitalis were able to restore a normal response to exercise in patients with CHF.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2003

Endothelial nitric oxide synthase overexpression attenuates congestive heart failure in mice.

Congestive heart failure results in cardiovascular dysfunction and diminished vascular nitric oxide (NO) production. We hypothesized that overexpression of endothelial NO synthase (eNOS) within the endothelium would reduce the extent of contractile dysfunction in a murine model of infarct-induced congestive heart failure. We generated transgenic (TG) mice overexpressing the human eNOS gene. The TG mice displayed significantly enhanced eNOS protein levels and eNOS activity levels (10- to 12-fold greater) in the aorta and the coronary vasculature. Non-TG (NTg) and eNOS TG mice were subjected to permanent left anterior descending coronary artery occlusion and then observed for 1 mo. We assessed cardiac function in vivo by using echocardiography and ultraminiature ventricular pressure catheters. Myocardial infarct size was similar between study groups (approximately 70% of the risk zone). Survival was increased by 43% in the eNOS TG mice compared with NTg (P < 0.05). Fractional shortening and cardiac output were also significantly (P < 0.05) greater in the eNOS TG than in NTg. Interestingly, pulmonary edema was evident only in NTg mice, and no evidence of pulmonary edema was observed in the eNOS TG mice. Thus, targeted overexpression of the eNOS gene within the vascular endothelium in mice attenuates both cardiac and pulmonary dysfunction and dramatically improves survival during severe congestive heart failure.

Animals↗
PubMed1995

Amiodarone in patients with congestive heart failure and asymptomatic ventricular arrhythmia. Survival Trial of Antiarrhythmic Therapy in Congestive Heart Failure.

BACKGROUND: Asymptomatic ventricular arrhythmias in patients with congestive heart failure are associated with increased rates of overall mortality and sudden death. Amiodarone is now used widely to prevent ventricular tachycardia and fibrillation. We conducted a trial to determine whether amiodarone can reduce overall mortality in patients with congestive heart failure and asymptomatic ventricular arrhythmias. METHODS: We used a double-blind, placebo-controlled protocol in which 674 patients with symptoms of congestive heart failure, cardiac enlargement, 10 or more premature ventricular contractions per hour, and a left ventricular ejection fraction of 40 percent or less were randomly assigned to receive amiodarone (336 patients) or placebo (338 patients). The primary end point was overall mortality, and the median follow-up was 45 months (range, 0 to 54). RESULTS: There was no significant difference in overall mortality between the two treatment groups (P = 0.6). The two-year actuarial survival rate was 69.4 percent (95 percent confidence interval, 64.2 to 74.6) for the patients in the amiodarone group and 70.8 percent (95 percent confidence interval, 65.7 to 75.9) for those in the placebo group. At two years, the rate of sudden death was 15 percent in the amiodarone group and 19 percent in the placebo group (P = 0.43). There was a trend toward a reduction in overall mortality among the patients with nonischemic cardiomyopathy who received amiodarone (P = 0.07). Amiodarone was significantly more effective in suppressing ventricular arrhythmias and increased the left ventricular ejection fraction by 42 percent at two years. CONCLUSIONS: Although amiodarone was effective in suppressing ventricular arrhythmias and improving ventricular function, it did not reduce the incidence of sudden death or prolong survival among patients with heart failure, except for a trend toward reduced mortality among those with nonischemic cardiomyopathy.

Actuarial Analysis↗
PubMed2002

Clinical features and prognosis associated with a preserved left ventricular systolic function in a large cohort of congestive heart failure outpatients managed by cardiologists. Data from the Italian Network on Congestive Heart Failure.

BACKGROUND: The aim of this study was to evaluate the clinical characteristics, 1-year prognosis and therapeutic approach of heart failure with a preserved left ventricular systolic function in a large multicenter registry of patients referred to specialized heart failure clinics. METHODS: The study population consisted of 5164 outpatients (mean age 62 +/- 12 years, 78.8% male, 28.1% in NYHA functional class III-IV) with an available left ventricular ejection fraction (LVEF) measurement at the initial evaluation for enrollment in the Italian Network on Congestive Heart Failure. A 1-year follow-up was available for 2390 patients. RESULTS: 2859 out of 5164 patients (55.4%) had an LVEF < 35%, 1618 (31.3%) had an LVEF between 35 and 45%, and 687 patients (13.3%) had an LVEF > 45%. Patients with an LVEF > 45% were significantly older, more often female and presented a significantly higher prevalence of a hypertensive etiology, obesity and atrial fibrillation. The severity of the clinical picture, as indicated by a lower prevalence of NYHA class III-IV (17.2 vs 35.6%, p = 0.001) and a third heart sound (14.8 vs 33.5%, p = 0.001), was less in patients with an LVEF > 45%. The therapeutic approach differed significantly, with a larger use of calcium antagonists and beta-blockers in patients with an LVEF > 45%, while ACE-inhibitors, diuretics and digoxin were more often prescribed to those with an impaired LVEF. The 1-year mortality and morbidity (all cause and congestive heart failure worsening hospitalizations) were significantly lower in patients with a preserved left ventricular systolic function compared to those with left ventricular systolic dysfunction (8.9 vs 18.8% for mortality, p = 0.001, and 8.3 vs 16.5% for hospital readmissions due to worsening congestive heart failure, p = 0.001, respectively). CONCLUSIONS: Patients with congestive heart failure and a preserved left ventricular systolic function seem to constitute a distinct population not infrequently presenting even in the clinical setting of specialized heart failure clinics. Further studies are needed to establish a definitive and standardized diagnosis and the most appropriate therapy for congestive heart failure with a normal LVEF.

Aged↗
PubMed1986

Effect of propranolol after acute myocardial infarction in patients with congestive heart failure.

The incidence of congestive heart failure was studied in the Beta Blocker Heart Attack Trial in which postmyocardial infarction patients between the ages of 30 and 69 years, with no contraindication to propranolol, were randomly assigned to receive placebo (n = 1921) or propranolol 180 or 240 mg daily (n = 1916) 5 to 21 days after admission to the hospital for the event. Survivors of acute myocardial infarction with compensated or mild congestive heart failure, including those on digitalis and diuretics, were included in the study. A history of congestive heart failure before randomization characterized 710 (18.5%) patients: 345 (18.0%) in the propranolol group and 365 (19.0%) in the placebo group. The incidence of definite congestive heart failure after randomization and during the study was 6.7% in both groups. In patients with a history of congestive heart failure before randomization, 51 of 345 (14.8%) in the propranolol group and 46 of 365 (12.6%) in the placebo group developed congestive heart failure during an average 25 month follow-up. In the patients with no history of congestive heart failure, 5% in the propranolol group developed congestive heart failure and 5.3% in the placebo group developed congestive heart failure. Baseline characteristics predictive of the occurrence of congestive heart failure by multivariate analyses included an increased cardiothoracic ratio, diabetes, increased heart rate, low baseline weight, prior myocardial infarction, age, and more than 10 ventricular premature beats per hour.(ABSTRACT TRUNCATED AT 250 WORDS)

Heart Failure↗
PubMedDate not supplied

Pharmacotherapy in congestive heart failure: COX-2 inhibition: a cautionary note in congestive heart failure.

NSAIDs have been a mainstay of therapy for rheumatologic diseases for a number of years. Unfortunately, their use was accompanied by sometimes unacceptable gastrointestinal and/or renal side effects. Therefore, safer treatment options were sought. In the process of such a search, selective cyclo-oxygenase-2 inhibitors were identified. Drugs in this class have anti-inflammatory properties similar to NSAIDs and did not produce anywhere near the same pattern of NSAID-related gastrotoxicity. The enthusiasm for this class of drugs would appear, at least on the surface, to be well grounded. However, establishing the renal side effect profile of the selective cyclo-oxygenase-2 inhibitors would appear to be a work in progress. Formal studies with selective cyclo-oxygenase-2 inhibitors have not been conducted in the congestive heart failure population. Information does though exist for other patient cohorts--similarly "prostaglandin-dependent" for their integrity of renal function, such as the elderly and sodium-deplete individual. These data would strongly suggest that the selective cyclo-oxygenase-2 inhibitors could decrease glomerular filtration rate and stimulate salt and water retention, comparable to what occurs with nonselective NSAIDs. To date, no compelling information exists, which supports the notion that differences exist among the currently available selective cyclo-oxygenase-2 inhibitors--celecoxib and--in the potential to negatively impact renal function in this and similarly compromised patient populations. (c)2000 by CHF, Inc.

Journal Article↗
PubMed1986

Congestive heart failure in children.

Congestive heart failure in children is unusual as a presenting problem, and the nonspecific nature of the signs and symptoms in the pediatric population makes recognition difficult. Congenital heart disease is most common in the infant whereas older children most commonly develop congestive heart failure due to cardiomyopathy, myocarditis, electrolyte abnormalities, dysrhythmias, and, more rarely, endocarditis, and rheumatic carditis. Management focuses upon stabilization of the airway and ventilation while improving circulatory function. This is achieved by the use of inotropic agents, combined with attention to the volume and pressure overload, pulmonary problems, dysrhythmias, and ongoing follow-up.

Cardiotonic Agents↗
PubMed1988

Congestive heart failure in thyrotoxicosis.

Congestive heart failure due to thyrotoxicosis without preexisting heart disease is rare. Indeed, the very existence of a thyrotoxic heart disease has been much discussed. We describe a 44-year-old woman in whom thyrotoxicosis was found to be the sole cause of congestive heart failure.

Adult↗
PubMed2006

Secondary hyperparathyroidism in patients with untreated and treated congestive heart failure.

BACKGROUND: The congestive heart failure syndrome includes a systemic illness with wasting of soft tissues and bone. We hypothesized secondary hyperparathyroidism (HPT) would be found in hospitalized patients with decompensated congestive heart failure (CHF), where secondary aldosteronism is expected, and who were either untreated or treated medically. METHODS: In 9 consecutive patients (7 males, 2 females; 8 African-American, 1 Caucasian; 33-60 yrs) admitted to the Regional Medical Center during a 28-day period with chronic left ventricular systolic dysfunction (EF<35%) and decompensated CHF (5 untreated; 4 treated with an angiotensin converting enzyme inhibitor, furosemide, and small-dose spironolactone), we measured: plasma parathyroid hormone (PTH); serum calcium corrected for albumin, magnesium, and phosphorus; serum creatinine and calculated creatinine clearance. RESULTS: Plasma PTH was elevated above the normal range (6-65 pg/mL) in both untreated and treated patients with CHF (204+/-60 and 134+/-14 pg/mL, respectively). Serum corrected calcium was normal (8.4-10.2 mg/dL) in both untreated and treated CHF (9.7+/-0.l and 9.1+/-0.2 mg/dL, respectively) as were serum magnesium and phosphorus. Calculated creatinine clearance did not differ between untreated and treated patients (74+/-15 and 83+/-21 mL/min, respectively). CONCLUSIONS: Secondary HPT was found in 5 untreated and 4 treated patients consecutively hospitalized over a 28-day period with decompensated CHF. Corrected serum calcium was normal. Plasmaionized calcium, a determinant of PTH secretion, was not measured. Although vitamin D levels were not assessed, the presence of hypovitaminosis D in these housebound patients with symptomatic CHF cannot be discounted. HPT may contribute to the systemic illness that accompanies CHF, including bone wasting.

Adult↗
PubMed1996

The identification of contributory mechanisms for the development and progression of congestive heart failure in animal models.

Congestive heart failure is a clinical syndrome which results from left ventricular pump dysfunction. Animal models of congestive heart failure have been developed to better understand the complex mechanisms which contribute to the clinical syndrome of heart failure. The species and lesions used to create chronic left ventricular dysfunction in animals are as varied as the etiologic factors which cause congestive heart failure in human beings. However, a central issue to the animal models of congestive heart failure is how closely they mimic the human syndrome of congestive heart failure. The findings derived from the study of an animal model of left ventricular dysfunction should be carefully interpreted, keeping in mind the complexity of the human disease process. With careful interpretation of the results, important insights into the pathogenesis of congestive heart failure in patients can be realized. For example, the rat coronary artery ligation model provided fundamental information on the role of the angiotensin-converting enzyme system on left ventricular function and survival. Chronic pressure and volume overload, as well as rate overdrive (rapid pacing), models have provided temporal and mechanistic information on left ventricular remodeling and the transition to left ventricular dysfunction and, subsequently, congestive heart failure. Preclinical studies using animal models of heart failure are needed to investigate the effects of pharmacologic interventions in the progression of congestive heart failure. Animal models which have been produced with specific gene product deletions or over-expression will increase our ability to identify potential contributory mechanisms for the progression of left ventricular dysfunction. Animal models of congestive heart failure are clearly helpful to define the mechanisms responsible for this syndrome and to develop effective strategies to slow or better reverse its progress.

Animals↗
PubMed1978

The role of the central nervous system in chronic congestive heart failure.

Even though congestive heart failure is extremely common, the mechanisms responsible for the clinical manifestations remain a puzzle. The central and autonomic (sympathetic) nervous systems are responsible for a large part of the clinical manifestations. The role of the nervous system in CHF is discussed briefly. It is evident that there are many gaps in knowledge that remain concerning the role of the central, peripheral, and autonomic nervous systems in congestive heart failure. The peripheral vascular constriction, increase in venous tone and pressure, tachycardia, sweating, dermal pallor, and tension and anxiety in patients with CHF reflect generalized sympathetic nervous system activity and the influence of the central and autonomic nervous systems on the clinical syndrome of CHF.

Adrenal Cortex Hormones↗
PubMed1986

Why are the angiotensin converting enzyme inhibitors rational in the treatment of congestive heart failure?

In chronic congestive heart failure, there is stimulation of the renin-angiotensin-aldosterone system, in addition to other homeostatic mechanisms. In addition to increased tone in the arteriolar and venous beds, there is salt and water retention by the kidney and excitation of the central nervous system by angiotensin. Interference with the generation of angiotensin reduces preload and afterload without a reflex tachycardia as the effects of angiotensin on the central nervous system are reduced. ACE inhibition is, therefore, a logical approach to the management of chronic congestive heart failure.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Reduction in mortality by pharmacological therapy in congestive heart failure.

Mortality in congestive heart failure remains high. In analysis of heart failure in the perspective of pathophysiological mechanisms, some approaches to treatment to improve survival become particularly interesting. The concept of unloading myocardial performance by reducing systemic vascular resistance has received general acceptance. This approach was associated with improved survival with nitrates and hydralazine in the V-HeFT I study. Stimulation of the myocardium in excess of what is achieved by endogenous stimulation might be dangerous. Long-term therapy with positive inotropic agents, therefore, is not an appropriate approach at present. However, addition of beta-blockers may protect the myocardium from the intense endogenous sympathetic stimulation in congestive heart failure. There are favorable trends with this approach in several small trials. An ongoing trial in idiopathic dilated cardiomyopathy may help to clarify this question. Counteraction of neuroendocrine activation may also be obtained by the addition of an angiotensin converting enzyme inhibitor. The CONSENSUS I study demonstrated a clear improvement in survival among very compromised patients by addition of enalapril. A positive effect was significantly associated with the degree of neuroendocrine activation at baseline. Two recent large-scale trials have emphasized the importance of adding an angiotensin converting enzyme inhibitor to other treatments in patients with mild to moderate symptoms and left ventricular dysfunction. These trials also support the importance of myocardial protection from neuroendocrine stimulation with symptomatic or asymptomatic myocardial failure. Antiarrhythmic agents have not been documented to improve survival. On the contrary, class I agents are deleterious in some patients with left ventricular dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMedDate not supplied

Quantification of interventions and outcomes in an outpatient telemanagement and care management congestive heart failure program.

The congestive heart failure continuum was developed in collaboration with the medical management committee of our hospital in response to a need to decrease readmissions for this chronic and progressive disease. This is accomplished via a multidisciplinary team that provides education and long-term telemanagement, as well as care management to assist these patients in maintaining an optimum level of functioning and the ability to remain in their homes for as long as possible. Since October 1996 there have been 375 patients referred with a decrease in the 31-day readmission rate from 21% to an average of 5%. Costs are presently $55.00 per month per patient. Evaluation of the congestive heart failure phone management tool revealed a strong 77% positive correlation between the patient's score and the number of interventions needed to stabilize the patient. Care management visits, when necessary, help reduce the need for hospitalization. (c)2000 by CHF, Inc.

Journal Article↗