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Contemporary burden of illness of congestive heart failure in Canada.

BACKGROUND: Congestive heart failure (CHF) is associated with high morbidity and mortality; however, there is little contemporary Canadian data to quantify the burden of this illness. OBJECTIVE: To report the impact of CHF in Canada, as measured by hospitalizations. METHODS: Data were obtained from the Canadian Institute for Health Information on patients hospitalized with CHF as a most responsible, primary or complication diagnosis during fiscal year 2000/01. RESULTS: There were a total of 106,130 discharges for 85,679 CHF patients in the fiscal year 2000/01. Total in-hospital mortality was 15.8%. In terms of total discharges for CHF, 32.7% were readmissions. On an individual patient basis, 19.9% of patients were rehospitalized once or more during 2000. In terms of burden of illness of CHF compared with other major illnesses, CHF is associated with the second highest total number of hospital days and third highest number of patients affected. CONCLUSIONS: Hospitalization for CHF occurs frequently and accounts for a large number of hospital bed-days in Canada. These figures should signal a call to action for researchers, administrators and health care providers regarding the need for more efficacious therapies, better application of already-proven therapies and patient education.

Aged↗

Long-term automated peritoneal dialysis in patients with refractory congestive heart failure.

Patients with severe congestive heart failure (CHF), mainly class IV on the New York Heart Association (NYHA) scale, became refractory to standard medical therapy. The factor that favored that evolution was renal insufficiency with inadequate renal perfusion. Our objectives in the present study were to make a preliminary assessment of the usefulness of automated peritoneal dialysis (APD) for the treatment of volume overload in those patients. Our study was carried out in the peritoneal dialysis unit of the clinical hospital of Pontificia Universidad Católica de Chile. We studied 3 non uremic patients with refractory CHF secondary to ischemic cardiomyopathy, severe secondary lung hypertension (> 70 mmHg), and associated moderate renal insufficiency. The patients (2 women and 1 man) ranged in age from 55 years to 68 years. A Tenckhoff double-cuff peritoneal catheter was placed in each patient, and peritoneal dialysis was carried out using the nightly intermittent peritoneal dialysis (NIPD) modality. The treatment used was appropriate to obtain a gradual removal of fluids: dialysate dextrose at 1.5% and 2.5%, 4-5 cycles, and total volume of 10-12 L per night. All three patients were able to remain at home, with no signs of hypervolemia. The frequency and length of hospitalizations decreased on average from 59 days pre-APD to 37 days post-APD. No hospitalizations for cardiac problems occurred, and the mean survival was 11 months (range: 6-22 months). This preliminary observation suggests that APD could be offered as an effective treatment for helping to remove fluids in patients with refractory CHF, reducing the number and length of hospitalizations, and improving quality of life.

Aged↗

Congestive heart failure in the elderly.

Congestive heart failure is in large part a disease of patients with advancing age. As our population ages, the incidence and prevalence of this disorder will continue to rise. The etiology of CHF in the elderly is multifactorial and one must take into account normal changes associated with aging, the heterogeneity of the elderly population, and possible noncardiac as well as cardiac disorders. Therapy must be aimed at the primary pathophysiologic process affecting the heart. Despite a number of therapeutic advances with medical therapy, CHF usually signals a generally irreversible process with a high mortality, especially in those patients with advanced disease. Therefore preventive measures should assume a paramount role in this disorder. Modification of risk factors such as diabetes, smoking, obesity, sedentary life style, and hypercholesterolemia should be aggressively stressed and pursued in patients of all ages. These preventive measures may have a substantial impact on the incidence of CHF in the elderly.

Aged↗

Congestive heart failure: a current overview.

Congestive heart failure (CHF), a disease seen primarily in the older patient, can be due to either systolic or diastolic dysfunction. Management is quite different if the heart failure is due to a filling abnormality as compared to poor ventricular systole. The disorder also poses many diagnostic pitfalls in the elderly. Current understanding of CHF and its influence on diagnosis and management is the focus of this review.

Aged↗

Monitored long-term treatment with ibopamine in patients suffering from severe congestive heart failure.

50 patients with congestive heart failure underwent monitored long-term treatment aimed at evaluating the effect of ibopamine (SB-7505), the 3,4-diisobutyryl ester of N-methyldopamine, on their condition. Ibopamine was administered alone or in combination with traditional therapy mainly at a dose of 100 mg t.i.d. Clinical scores and NYHA (New York Heart Association) functional classes improved. Biochemical parameters showed no adverse modifications. Mild transient side-effects probably related to ibopamine occurred in two patients.

Adult↗

[Current aspects of drug treatment of patients with congestive heart failure].

Patients with advanced congestive heart failure are high cost users of medical care, are limited by severe symptoms and have a poor prognosis. Medical treatment should therefore not be based on tradition but on pathophysiological considerations. A rational treatment program should give priority to the principle of unburdening rather than stimulating the failing heart. Unburdening the heart by use of diuretics and vasodilators is most effective in patients with hypertensive heart disease and valvular incompetence, and in acute heart failure. Digoxin remains the basic treatment in patients with tachyarrhythmias, and is valuable additive treatment in most instances. Guidelines are given for a stepwise treatment scheme including diuretics, vasodilators and digoxin.

Blood Pressure↗

ACE inhibitors: myocardial infarction and congestive heart failure.

Myocardial infarction and congestive heart failure are associated with high morbidity and mortality rates. The results of recent clinical trials support a beneficial role for angiotensin-converting enzyme (ACE) inhibitors in attenuating mortality from myocardial infarction and left ventricular dysfunction. Large-scale survival studies provide practical evidence that the addition of an ACE inhibitor to conventional therapy with diuretics and digoxin can significantly reduce the number of hospital admissions and the risk of death related to progressive heart failure.

Angiotensin-Converting Enzyme Inhibitors↗

Role of vasodilator therapy in congestive heart failure. Effects on mortality.

Congestive heart failure is associated with a considerable reduction in survival with only about 50% of patients alive within 5 years of its diagnosis. Recent trials have demonstrated that vasodilator therapy can improve survival in this condition. Agents that have been shown to be effective in well-designed double-blind clinical trials include the combination of hydralazine-isosorbide dinitrate (in V-HeFT) and the angiotensin converting enzyme inhibitors (in SOLVD, SAVE, and CONSENSUS).

Clinical Trials as Topic↗

Beta-blockers in congestive heart failure. A Bayesian meta-analysis.

PURPOSE: Congestive heart failure is an important cause of patient morbidity and mortality. Although several randomized clinical trials have compared beta-blockers with placebo for treatment of congestive heart failure, a meta-analysis quantifying the effect on mortality and morbidity has not been performed recently. DATA SOURCES: The MEDLINE, Cochrane, and Web of Science electronic databases were searched from 1966 to July 2000. References were also identified from bibliographies of pertinent articles. STUDY SELECTION: All randomized clinical trials of beta-blockers versus placebo in chronic stable congestive heart failure were included. DATA EXTRACTION: A specified protocol was followed to extract data on patient characteristics, beta-blocker used, overall mortality, hospitalizations for congestive heart failure, and study quality. DATA SYNTHESIS: A hierarchical random-effects model was used to synthesize the results. A total of 22 trials involving 10 135 patients were identified. There were 624 deaths among 4862 patients randomly assigned to placebo and 444 deaths among 5273 patients assigned to beta-blocker therapy. In these groups, 754 and 540 patients, respectively, required hospitalization for congestive heart failure. The probability that beta-blocker therapy reduced total mortality and hospitalizations for congestive heart failure was almost 100%. The best estimates of these advantages are 3.8 lives saved and 4 fewer hospitalizations per 100 patients treated in the first year after therapy. The probability that these benefits are clinically significant (>2 lives saved or >2 fewer hospitalizations per 100 patients treated) is 99%. Both selective and nonselective agents produced these salutary effects. The results are robust to any reasonable publication bias. CONCLUSIONS: beta-Blocker therapy is associated with clinically meaningful reductions in mortality and morbidity in patients with stable congestive heart failure and should be routinely offered to all patients similar to those included in trials.

Adrenergic beta-Antagonists↗

Myocardial myoglobin deficiency in various animal models of congestive heart failure.

Myoglobin is known to protect the mechanical function of the heart from hypoxia by acting as a sarcoplasmic oxygen reservoir and shuttle. We postulated a role for myoglobin in the pathogenesis of congestive heart failure. Several models of congestive heart failure were employed to test the hypothesis, including spontaneous inherited dilated cardiomyopathy in Doberman Pinschers, and heart failure produced by rapid ventricular pacing in dogs, volume overload in chickens and furazolidone toxicity in turkeys. Myocardial myoglobin was decreased by approximately 50% for all models (P less than 0.05). In Doberman Pinschers dogs which are predisposed to the development of dilated cardiomyopathy and have mild subclinical depression of cardiac performance, myocardial myoglobin (1.05 +/- 0.22 mg/g) is approximately 50% decreased compared to healthy mongrel dogs (2.15 +/- 0.52 mg/g), approximately twice as much as dobermans with heart failure (0.47 +/- 0.25 mg/g) but similar to the concentration found in dogs paced to heart failure (1.09 +/- 0.34 mg/g). Myocardium from poultry had remarkably decreased myoglobin compared to mammals (34 +/- 4 micrograms/g) with heart failure produced either by furazolidone or salt toxicity causing a further 50% reduction. In the canine models of heart failure, myocardial myoglobin concentration was demonstrated to be correlated with biochemical and physiological indicators of myocardial performance, namely, mitochondrial and sarcoplasmic reticular ATPase activities, and cardiac output, systemic vascular resistance, pulmonary capillary wedge pressure and mean arterial pressure, respectively. Our data implicates a role for myoglobin deficiency in the pathogenesis of congestive heart failure and in the predisposition of doberman pinschers to dilated cardiomyopathy.

Animals↗

Circulating cardiac troponin I in severe congestive heart failure.

BACKGROUND: Spontaneous progression of severe congestive heart failure is structurally characterized by cellular degeneration and multiple foci of myocardial cell death. The cardiac muscle isoform of troponin I is uniquely expressed in the adult human myocardium, and an increase in its circulating levels is highly indicative of myocardial injury. Accordingly, we addressed the usefulness of cardiac troponin I as a sensitive and specific molecular marker of congestive heart failure in patients with severely reduced left ventricular performance. METHODS AND RESULTS: A new generation single-step immunoenzymoluminometric assay with high analytical sensitivity was used to assess cardiac troponin I in patients with severe congestive heart failure, healthy blood donors, and hospitalized control subjects without known cardiac disease. The cardiac troponin I concentration (mean+/-SEM) was 72.1+/-15.8 pg/mL in heart failure patients and 20.4+/-3.2 and 36.5+/-5.5 pg/mL in healthy and hospitalized control subjects, respectively (P<.01 versus heart failure patients). When both control groups were considered, the mean cardiac troponin I level was 25.4+/-2.9 pg/mL (P<.01 versus heart failure patients). Creatine kinase MB mass and myoglobin concentrations remained within the normal range in all groups. CONCLUSIONS: These data (1) provide the first evidence for ongoing myofibrillar degradation and increased cardiac troponin I levels in patients with advanced heart failure and (2) show potential usefulness of cardiac troponin I as a specific and sensitive new serum marker molecule in severe congestive heart failure.

Blood Donors↗

Tissue iron storage patterns in fetal hydrops associated with congestive heart failure.

To learn whether fetal congestive heart failure causes a characteristic tissue iron storage pattern, we selected 15 neonatal autopsy cases of hydrops fetalis in which both the clinical and gross autopsy findings suggested intrauterine congestive heart failure. The latter appeared to be due to functional causes in 10 (3 nonhemolytic anemia, 4 cardiac dysrhythmia, 3 dilated cardiomyopathy) and was associated with cardiac malformation in 5. We graded the amount of hepatocellular siderosis, reticuloendothelial siderosis, and renal tubular siderosis in Perls-stained microscopic sections of liver, spleen, and kidney and compared the iron storage pattern with that in 15 normally developed neonatal autopsy controls (4 preterm, 11 term) and a further 7 with hemolytic anemia (5 alpha-thalassemia, 2 parvovirus B19 infection). Liver cell siderosis was absent in the three cases with nonhemolytic anemia. It was increased in 11 of the remaining 12 cases, as in hemolytic anemia controls. Among the five cardiac malformation cases, three had proximal renal tubular siderosis (as in hemolytic anemia controls) attributed to turbulent blood flow through the heart. Among the five, hydrops appeared to be due to prenatal closure of the foramen ovale in one and to prenatal constriction of the ductus arteriosus in another. In one of the five, and despite complex malformation of the heart, hydrops appeared to be due to complete heart block. We concluded that, although clinical information and morphologic assessment of the heart were basic to identifying a cardiac cause of fetal hydrops, histologic assessment of the pattern of iron storage helped confirm the pathologic diagnosis. Analysis of the pathologic findings led to a scheme for categorizing cardiogenic fetal hydrops.

Female↗

Correlation between the demethylation rate of 14C-aminopyrine (breath-test) and haemodynamic parameters in congestive heart failure.

In 18 patients with congestive heart failure, the 14C-aminopyrine demethylation rate was studied by the breath-test, 24 hours after the measurement of haemodynamic parameters. In the 12 patients with a cardiac index higher than 2.2 l/m2/min, the half life of 14CO2 specific activity in breath was found to be significantly correlated (p less than 0.001, r = 0,82) with the telediastolic pressure of the right ventricle. On the other hand, in the 6 patients with a cardiac index below 2.2 l/m2/min the 14C-aminopyrine half life was higher than the value predicted by this correlation. Congestive heart failure probably reduces hepatic demethylation of aminopyrine through altered hepatic microsomal function associated with congestion and possibly hypoxia.

Aged↗

Outpatient dobutamine infusion using a totally implantable infusion pump for refractory congestive heart failure.

A patient with refractory congestive heart failure was treated, on an outpatient basis, with intermittent dobutamine using a totally implantable infusion pump. Dobutamine was infused for 48 hours every week and resulted in sustained clinical improvement. Symptoms and signs of congestive heart failure remained well controlled until his death from a stroke eight months after implantation of the pump.

Aged↗

Treatment of congestive heart failure. Pathophysiologic and pharmacologic concepts.

Congestive heart failure is a serious health problem in Western society. Understanding of both the basic pathophysiology and the design of rational and effective treatment of this syndrome has increased dramatically in the last ten years. However, congestive heart failure remains a highly lethal disease, which kills at a rate exceeding that of most cancers. Prevention is therefore of the utmost importance and has to come primarily from a reduction in the incidence and damage done from myocardial infarction. Improved understanding of the pathophysiology of idiopathic dilated cardiomyopathy is also needed. Through understanding of pathophysiologic principles, effective therapy based on interference with known mechanisms that are operative in the disease is now available but can be refined in the future.

Angiotensin-Converting Enzyme Inhibitors↗

Propranolol treatment of congestive heart failure in infants with congenital heart disease: The CHF-PRO-INFANT Trial. Congestive heart failure in infants treated with propanol.

AIM: Infants with congenital heart disease and left-to-right shunts may develop significant clinical symptoms of congestive heart failure in spite of therapy with digoxin and diuretics. We investigated the effects of beta-blockade in infants with severe heart failure. METHODS AND RESULTS: We performed a prospective, randomized, open monocenter trial in infants treated with digoxin and diuretics (n=10) in comparison to 10 infants receiving additional beta-blocker therapy. After 17 days on average beta-blocker treated infants (propranolol:1,6 mg/kg/day) improved significantly with respect to Ross heart failure score (3.3+/-2.3 vs. 8.3+/-1.9, P=0.002), lower renin levels (338+/-236 vs. 704+/-490 microU/l, P=0.008) and lower mean heart rates in Holter ECG (118+/-10 vs. 142+/-11 beats/min, P<0.001). While digoxin and diuretic treated infants had unchanged mean heart rate (149+/-8 vs. 148+/-10 beats/min), less decrease of symptoms (Ross Score: 8.5+/-1.7 vs. 6.8+/-2.3, P=0.02) but a significant increase of renin levels (139+/-102 vs. 938+/-607 microU/l, P=0.001). CONCLUSION: Additional propranolol treatment but not digoxin and diuretics alone can effectively reduce clinical symptoms of heart failure in infants with congenital heart disease, who suffer from increased neurohormonal activation.

Adrenergic beta-Antagonists↗

The mind of a failing heart: a systematic review of the association between congestive heart failure and cognitive functioning.

BACKGROUND: Congestive heart failure (CHF) is a frequent complication of most diseases of the heart. CHF is associated with impairment in several aspects of the quality of life of patients, including mood and cognitive performance. Early reports indicated that patients with CHF display deficits in memory and other intellectual abilities, although the clinical relevance of these findings remains unclear. AIM: We reviewed systematically the medical literature with the aim of clarifying the association between CHF and cognitive functioning. METHODS: Systematic review of Medline database for studies published between 1966 and June 2000 using the following key words: congestive heart failure, cognition, cognitive disorders, memory, memory disorders, short-term memory, attention. RESULTS: Thirteen studies reported cognitive information on patients with CHF, but only five met inclusion criteria for systematic review. Three reports described attention (total number of subjects = 369 patients and 882 controls) and memory scores (total number of subjects = 247 patients and 748 controls), two studies reported measures of general cognitive functioning (total number of subjects = 203 patients and 704 controls) and one reported the rate of cognitive impairment (total number of subjects = 88 patients and 987 controls). Pooled analysis indicated that CHF is associated with a pattern of generalized cognitive impairment that includes memory and attention deficits. CONCLUSIONS: The results of the present review highlight the enormous paucity of systematic information about the association between CHF and cognitive functioning, with only five studies reporting data suitable for analysis. We expect that new case-control and cohort studies will be designed to confirm the presence of cognitive impairment in patients with CHF and trust that this information will improve the management of CHF patients and our understanding of the mechanisms associated with cognitive decline in later life.

Attention↗

[Drug therapy of chronic congestive heart failure: the why and how].

As the prevalence of congestive heart failure is steadily increasing correct treatment becomes more and more important. In pathophysiology, clinical signs once believed to express the effort of the body to "compensate" for the failure (hypervolaemia, tachycardia, sympathetic stimulation) have been recognized as sort of a physiological error: to a primary signal which still remains not fully understood, the body responds in a similar way as to dehydration. As late as the mid-sixties, "function curves" represented a framework for our conceptual thinking and digitalis the essential treatment. Since then, we had to realize that the function of the failing ventricle is not determined just by filling and contractility-the way it is in the healthy ventricle is-but also by aortic impedance. Vasodilators have become the cornerstone of therapy. At present, diuretics are the most important drugs for congestive heart failure treatment. Thiazides, given together with loop diuretics, ameliorate extracellular fluid volume in all treated patients, but their effect is accompanied by potassium losses due to increased aldosterone levels. Angiotensin converting enzyme (ACE) inhibitors are unique in not only decreasing ventricular afterload and improving haemodynamics but, also, in decreasing circulating norepinephrine levels, protecting kidneys from inappropriate efferent arteriolo-constriction and suppression of aldosterone secretion. In other words, ACE inhibitors change the essential physiological set-up: they turn a high-perfusion-pressure body into a low-perfusion-pressure one. Furthermore, they convincingly improve life expectancy. Combination of diuretics and ACE inhibitors is the best we can do for our patients today. Although useful in some patients, the definite value of digitalis, and particularly its effect on longevity, remains an unresolved question.

Heart Failure↗