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PubMed1980

Fulminant hepatic failure due to transient circulatory failure in patients with chronic heart disease.

Heart failure is a recognized, although uncommon, cause of massive liver cell necrosis, the clinical consequences of which are intermingled with those of cardiac insufficiency in most cases. We report the cases of six patients suffering from chronic heart failure in whom an episode of acute circulatory failure resulted in massive liver cell necrosis and fulminant hepatic failure. The manifestations of fulminant hepatic failure, ie, hepatic encephalopathy, jaundice, and marked increase in prothrombin time, developed after an interval of one to three days, after the episode of acute circulatory failure, while the patiens' hemodynamic condition had returned to the previous basal status.

Adult↗
PubMedDate not supplied

Thin myofilament proteins in norm and heart failure. I. Polymerizability of myocardial Straub actin in acute and chronic heart failure.

The reduced and intrinsic viscosities of myocardial Straub F-actin from the left ventricle of a practically healthy man were equal to 3.05 +/- 0.2 and 2.4 +/- 0.32 and from the right ventricle were 2.37 +/- 0.2 and 2.1 +/- 0.3 dl/g, respectively (the difference between ventricles was not significant). The average length of filaments measured by flow birefringence technique was equal to 1.3 +/- 0.04 micron, the number-average length (Ln), determined by the electron microscopy was 1.4 micron, the weight-average length (Lw), was 2 microns and the maximal one was 5.5 microns. The histograms showed that the most characteristic length was that of 0.8-1.2 micron. According to the flow birefringence data canine myocardial F-actin had a length similar to that of myocardial F-actin from a practically healthy man, though its reduced and intrinsic viscosities were higher. In acute and especially chronic congestive heart failure the actin polymerizability was sharply reduced. In consequence, in acute heart failure the number-average length of F-actin filaments was decreased by 43% and in congestive heart failure by 65.7%. The characteristic length in acute heart failure shifts to the range of 0.2-0.6 micron, while in congestive heart failure the range is 0.2-0.4 micron. This fact can possibly explain why during preparation of actin from the pathologically changed myocardium according to the methods including purification by the cycles of polymerization-sedimentation-depolymerization, the pathologically changed actin is discarded and the normal actin remains. A definite parallel was observed between the reduction of actin polymerizability and the ability of myocardial glycerinated fiber bundles (MBGF) to generate force. We conclude that the changes of actin properties in heart failure may cause a decrease in contractibility of the myocardial contractile protein system.

Actins↗
PubMed2006

Heart failure: a model of cardiac and skeletal muscle energetic failure.

Chronic heart failure (CHF), the new epidemic in cardiology, is characterized by energetic failure of both cardiac and skeletal muscles. The failing heart wastes energy due to anatomical changes that include cavity enlargement, altered geometry, tachycardia, mitral insufficiency and abnormal loading, while skeletal muscle undergoes atrophy. Cardiac and skeletal muscles also have altered high-energy phosphate production and handling in CHF. Nevertheless, there are differences in the phenotype of myocardial and skeletal muscle myopathy in CHF: cardiomyocytes have a lower mitochondrial oxidative capacity, abnormal substrate utilisation and intracellular signalling but a maintained oxidative profile; in skeletal muscle, by contrast, mitochondrial failure is less clear, and there is altered microvascular reactivity, fibre type shifts and abnormalities in the enzymatic systems involved in energy distribution. Underlying these phenotypic abnormalities are changes in gene regulation in both cardiac and skeletal muscle cells. Here, we review the latest advances in cardiac and skeletal muscle energetic research and argue that energetic failure could be taken as a unifying mechanism leading to contractile failure, ultimately resulting in skeletal muscle energetic failure, exertional fatigue and death.

Animals↗
PubMed1991

Parasympathetic withdrawal is an integral component of autonomic imbalance in congestive heart failure: demonstration in human subjects and verification in a paced canine model of ventricular failure.

Although enhanced sympathetic tone is a well recognized component of the autonomic profile characteristic of congestive heart failure, the contribution of parasympathetic withdrawal to this autonomic imbalance is less well described. The technique of spectral analysis of heart rate variability provides a dynamic map of sympathetic and parasympathetic tone and was thus used to define the nature of sympathetic-parasympathetic interactions in humans with idiopathic dilated cardiomyopathy and in a paced canine model of congestive heart failure. Humans with cardiomyopathy were found to have an augmentation of the sympathetically mediated low frequency area of the power density spectrum. Parasympathetic withdrawal was demonstrated by significant reductions in the parasympathetically mediated high frequency area (p less than 0.05) and the ratio of high to low frequency areas (p less than 0.01). Administration of atropine to normal subjects resulted in a significant reduction in the high frequency area (p less than 0.05) and the high/low frequency area ratio, both of which decreased within the range noted in patients with congestive heart failure. Administration of isoproterenol in normal subjects led to an augmentation of the low frequency area but to only a small decrease in the high/low frequency area ratio. Induction of congestive heart failure in a paced canine model resulted in alterations in the autonomic profile that resembled those seen in humans with ventricular failure. The prominent high frequency region of the spectrum at baseline, indicating a predominance of parasympathetic tone, was absent after the evolution of congestive heart failure, and there was a marked augmentation of the low frequency region of the spectrum.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2004

The expanding national burden of heart failure in the United States: the influence of heart failure in women.

BACKGROUND: Although some studies have shown that hospital admissions for heart failure doubled between 1973 and 1995, other data suggest that the heart failure hospitalization epidemic has stabilized in the United States. We sought to describe trends in heart failure hospitalizations over the past decade using data from the National Hospital Discharge Survey (NHDS). METHODS: The NHDS provides annual estimates of hospitalization discharges from a sample of hospitals in the United States. We combined the heart failure hospitalization frequencies with census estimates to calculate age and gender-specific annual hospitalization rates. RESULTS: Hospitalizations with a primary diagnosis of heart failure among adults (age > or =35) increased from 810,624 in 1990 to 989,500 in 1995 (annual increase 36,088, R2 = 0.816, P =.014), and to 1,088,349 in 1999 (annual increase 31,091, R2 = 0.780, P =.047). The age-adjusted hospitalization rate (per 1000 persons) increased from 7.186 in 1990 to 8.554 in 1999 for women (annual increase 0.14/year, R2 = 0.731, P =.002) and from 6.892 in 1990 to 7.372 in 1999 for men (annual increase 0.011/year, R2 = 0.008, P = 0.80). For women, the annual hospitalization rate increased from 1990 to 1999 in each age group (35-64, 65-74, 75-84, and > or =85), while the age-specific rates did not change in men. CONCLUSIONS: Heart failure hospitalizations have continued to increase from 1990 to 1999. Although aging and growth of the US population contribute to this trend, the increases are substantially influenced by changes in hospitalization rates in women.

Age Distribution↗
PubMed2004

Patterns of beta-blocker utilization in patients with chronic heart failure: experience from a specialized outpatient heart failure clinic.

BACKGROUND: Beta-blockers have been shown incontrovertibly to improve morbidity and survival in patients with heart failure. However, there is limited information regarding their use in clinical practice settings, and reasonable utilization targets for quality improvement initiatives have not been established. METHOD: We identified 500 consecutive patients with chronic heart failure seen at a specialized outpatient heart failure clinic from March 2001 to May 2001, and retrospectively extracted clinical and drug information from an electronic medical record. RESULTS: In this cross-sectional analysis, the rate of beta-blocker utilization was 69%. Seventy-five percent of patients had at least tried a beta-blocker. Among those with beta-blockers initiated, 16% experienced side effects that led to drug discontinuation (9.1%) or down-titration (6.9%) that was similar across all NYHA classes. A lower utilization rate of beta-blockers was observed in patients of advanced age and those with diabetes mellitus, concomitant antiarrhythmic therapy, and preserved left ventricular ejection fraction (P <.05). Respiratory disease remained the most common reason for withholding beta-blocker therapy, especially with severe obstructive (rather than restrictive) physiology. CONCLUSION: It appears that about 70% of patients with chronic heart failure can be successfully treated with a beta-blocker in a specialized heart failure outpatient setting where physicians are committed to beta-blocker use in heart failure. It is possible that subgroups with lower utilization rates can be targeted for quality improvement initiatives.

Adrenergic beta-Antagonists↗
PubMed2004

Multinational economic evaluation of valsartan in patients with chronic heart failure: results from the Valsartan Heart Failure Trial (Val-HeFT).

BACKGROUND: The Valsartan Heart Failure Trial (Val-HeFT) compared valsartan versus placebo in 5010 patients taking prescribed background therapy for New York Heart Association class II to IV heart failure. Valsartan reduced the risk of heart failure hospitalization and improved clinical signs and symptoms of heart failure. We sought to compare resource use, costs, and health outcomes among patients taking prescribed therapy for heart failure and randomly assigned to receive valsartan or placebo. METHODS: Measures of resource use were based on data collected during the trial. Unit cost estimates were collected from individual countries and converted to 1999 US dollars. Total costs were estimated for hospitalizations, inpatient and outpatient physician services, ambulance transportation, deaths outside the hospital, and outpatient cardiovascular medications. RESULTS: Mean follow-up was 23 months. Mean costs for heart failure hospitalizations were 423 dollars lower among patients receiving valsartan (95% CI, -706 to -146). Mean total costs were 9008 dollars for patients receiving valsartan and 8464 dollars for patients receiving placebo, a net incremental cost of 545 dollars (95% CI, -149 to 1148), including the cost of valsartan. There was an overall reduction in total costs of 929 dollars (95% CI, -3243 to 1533) among patients not receiving an ACE inhibitor at baseline but a slight increase in costs of 334 dollars (95% CI, -497 to 1199) among those receiving an ACE inhibitor without a beta-blocker and a 1246 dollars increase (95% CI, 54 to 2230) in patients receiving both an ACE inhibitor and a beta-blocker at baseline. CONCLUSIONS: Valsartan provided clinical benefits at a mean incremental cost of 285 dollars per year during the trial. In patients not taking ACE inhibitors, valsartan was economically attractive, increasing survival while reducing or marginally increasing overall costs.

Adrenergic beta-Antagonists↗
PubMed2005

Why do patients fail to receive beta-blockers for chronic heart failure over time? A "real-world" single-center, 2-year follow-up experience of beta-blocker therapy in patients with chronic heart failure.

BACKGROUND: The longitudinal pattern of beta-blocker use in a heart-failure practice setting has not been explored. Previous studies have not specifically addressed the use of beta-blockers over time to determine the rate of use and reasons for discontinuation. The long-term compliance rate for beta-blocker drugs outside the context of a clinical trial has not been established. METHODS: We prospectively followed a cohort of 500 consecutive patients between March and May 2001, with a clinical diagnosis of chronic heart failure seen in a specialized heart failure clinic and determined the longitudinal pattern of beta-blocker use and clinical outcomes over a 2-year period. RESULTS: The final cohort consists of 340 patients with a complete 2-year follow-up data (mean age 61 +/- 14 years, 69% men, 53% with ischemic etiology, mean ejection fraction 27.6 +/- 15%). At 6, 12, and 24 months, beta-blocker utilization rates were maintained in 69%, 70%, and 74% of patients, respectively. Of the 120 confirmed initial non-beta-blocker users, 28 (23%) were subsequently started on beta-blocker, despite suspected relative contraindications in 53% of patients. Over a period of 2 years, the discontinuation rate was 10%, with failure to restart a beta-blocker after hospitalization as the most common reason for beta-blocker discontinuation. CONCLUSION: Utilization rates of beta-blockers in our heart failure clinic have remained constant at approximately 70% throughout a 2-year follow-up. Of those who discontinued beta-blockers (10%), the most common documented cause was failure to restart beta-blockers after hospitalization.

Adrenergic beta-Antagonists↗
PubMed2004

N-terminal proBNP and mortality in hospitalised patients with heart failure and preserved vs. reduced systolic function: data from the prospective Copenhagen Hospital Heart Failure Study (CHHF).

UNLABELLED: Preserved systolic function among heart failure patients is a common finding, a fact that has only recently been fully appreciated. The aim of the present study was to examine the value of NT-proBNP to predict mortality in relation to established risk factors among consecutively hospitalised heart failure patients and secondly to characterise patients in relation to preserved and reduced systolic function. MATERIAL: At the time of admission 2230 consecutively hospitalised patients had their cardiac status evaluated through determinations of NT-proBNP, echocardiography, clinical examination and medical history. Follow-up was performed 1 year later in all patients. RESULTS: 161 patients fulfilled strict diagnostic criteria for heart failure (HF). In this subgroup of patients 1-year mortality was approximately 30% and significantly higher as compared to the remaining non-heart failure population (approx. 16%). Using univariate analysis left ventricular ejection fraction (LVEF), New York Heart Association classification (NYHA) and plasma levels of NT-proBNP all predicted mortality independently. However, regardless of systolic function, age and NYHA class, risk-stratification was provided by measurements of NT-proBNP. Having measured plasma levels of NT-proBNP, LVEF did not provide any additional prognostic information on mortality among heart failure patients (multivariate analysis). CONCLUSION: The results show that independent of LVEF, measurements of NT-proBNP add additional prognostic information. It is concluded that NT-proBNP is a strong predictor of 1-year mortality in consecutively hospitalised patients with heart failure with preserved as well as reduced systolic function.

Adult↗
PubMed2004

Rationale and design of the GISSI heart failure trial: a large trial to assess the effects of n-3 polyunsaturated fatty acids and rosuvastatin in symptomatic congestive heart failure.

BACKGROUND: The GISSI Heart Failure project is a large-scale, randomized, double-blind study designed to investigate the effects of n-3 polyunsaturated fatty acids and rosuvastatin on mortality and morbidity in patients with symptomatic heart failure. METHODS AND RESULTS: Patients with New York Heart Association classes II to IV heart failure, already receiving optimized recommended therapy, will be recruited in a nation-wide network of more than 300 cardiology and internal medicine services to be randomly allocated to treatment with n-3 polyunsaturated fatty acids (1 g daily) or the corresponding placebo. Patients with no clear indication or contraindication to cholesterol-lowering therapy will be further randomized to receive low-dose rosuvastatin (10 mg daily) or placebo. According to data available in heart failure registries, it is expected that 70% of the patients will be suitable to enter both components of the trial, which assume the same co-primary endpoints: (a) 15% reduction of all-cause mortality and (b) 20% reduction of all-cause mortality or cardiovascular hospitalizations. The trial is event-driven and will continue either until at least 1252 deaths have been recorded or a reduction of all-cause mortality will satisfy the significance boundaries, which have been established to stop the study. The recruitment of the planned sample size of approximately 7000 patients randomized in the n-3 PUFA trial is expected to be completed within 18 months from the trial start. As of February 29, 2004, 4624 heart failure patients have been included in the trial. CONCLUSION: The GISSI-HF project, with its protocol articulated into two independent randomization schemes, has the aim and the power to verify the hypothesis that n-3 polyunsaturated fatty acids and rosuvastatin can favorably modify the prognosis of patients with symptomatic heart failure.

Fatty Acids, Omega-3↗
PubMed2006

Disease management programs for heart failure: not just for the 'sick' heart failure population.

The development of disease management programs has been a major advance in heart failure care, bringing about significant improvements for the heart failure population, with reduction in readmission, better use of guideline therapy and improved survival. However, at present, the majority of such programs focus their attention only on the sicker segment of this population, with little application of this important service to the broader heart failure population, where potentially benefits may be even more impressive. This has led to an imbalance in the care of patients with heart failure, where aspects of management such as regular structured review and education are preferentially given to the group at the later stages of the natural history of the syndrome. This paper argues for a far wider application of the disease management program concept in heart failure care so as to bring the benefits of specialist care, patient education and follow-up to patients at an earlier stage in the natural history of heart failure.

Diffusion of Innovation↗
PubMed2005

Clinical presentation, management, and in-hospital outcomes of patients admitted with acute decompensated heart failure with preserved systolic function: a report from the Acute Decompensated Heart Failure National Registry (ADHERE) Database.

UNLABELLED: Approximately 50% of patients hospitalized for heart failure have preserved systolic function. These patients are more likely to be older, women, and hypertensive. Their duration of hospitalization is similar to that of heart failure patients with systolic dysfunction, but their in-hospital mortality risk is lower. This mortality risk is increased in the setting of renal insufficiency, and the two most important risk predictors are elevated blood urea nitrogen and systolic blood pressure < or = 125 mm Hg. Medical treatment strategies for patients with preserved systolic function are inconsistent and reflect the need for efficacious evidence-based treatment regimens. OBJECTIVES: The aims of this analysis were to describe the clinical characteristics, management, and outcomes of patients hospitalized for acute decompensated heart failure (HF) with preserved systolic function (PSF). BACKGROUND: Clinically meaningful characteristics of these patients have not been fully studied in a large database. METHODS: Data from >100,000 hospitalizations from the Acute Decompensated Heart Failure National Registry (ADHERE) database were analyzed. RESULTS: Heart failure with PSF was present in 50.4% of patients with in-hospital assessment of left ventricular function. When compared with patients with systolic dysfunction, patients with PSF were more likely to be older, women, and hypertensive and less likely to have had a prior myocardial infarction or be receiving an angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker. In-hospital mortality was lower in patients with PSF compared with patients with systolic dysfunction (2.8% vs. 3.9%; adjusted odds ratio [OR]: 0.86; p = 0.005), but duration of intensive care unit stay and total hospital length of stay were similar. Serum creatinine >2 mg/dl was associated with increased in-hospital mortality in both systolic function groups (PSF: 4.8%; systolic dysfunction: 8.4%; p < 0.0001), and the most powerful predictors of in-hospital mortality in both groups were blood urea nitrogen >37 mg/dl (OR: 2.53; 95% confidence interval [CI]: 2.22 to 2.87) and systolic blood pressure < or =125 mm Hg (OR: 2.58; 95% CI: 2.33 to 2.86). CONCLUSIONS: Heart failure with PSF is common and is characterized by a unique patient profile. Event rates are worrisome and reflect a need for more effective management strategies.

Aged↗
PubMed1995

Effects of fosinopril on exercise tolerance and clinical deterioration in patients with chronic congestive heart failure not taking digitalis. Fosinopril Heart Failure Study Group.

A total of 241 men and women with mild to moderately severe chronic heart failure (New York Heart Association functional class II [90%] or III) and a mean (+/- SD) left ventricular ejection fraction of 25 +/- 7%, entered a 24-week, prospective, double-blind, placebo-controlled trial of 10 or 20 mg/day of fosinopril, a phosphinic acid angiotensin-converting enzyme inhibitor. Patients received concomitant diuretic therapy but not digitalis. Primary end points were mean change in maximal treadmill exercise time and occurrence of prospectively defined clinical events indicative of worsening heart failure (most to least severe): death, withdrawal for worsening heart failure, hospitalization for worsening heart failure, need for supplemental diuretic or emergency room visit for worsening heart failure, and no event. At study end point, treadmill exercise time had improved in the fosinopril versus the placebo group (+28.4 vs -13.5 seconds, p = 0.047). New York Heart Association functional class had improved at end point more frequently (24% vs 13%) and deteriorated less frequently (18% vs 32%) in the fosinopril group (p = 0.003). More patients treated with fosinopril (66% vs 50%) remained free of clinical events indicative of worsening heart failure, and fosinopril-treated patients had less severe clinical events (p = 0.004). Dyspnea, fatigue, and paroxysmal nocturnal dyspnea improved more often and worsened less often in this group (p < or = 0.002), and edema showed a trend toward improvement (p = 0.088). These clinical benefits did not require concomitant digitalis therapy. Fosinopril was associated with an acceptable safety profile.

Aged↗
PubMed2003

The EuroHeart Failure Survey programme--a survey on the quality of care among patients with heart failure in Europe. Part 2: treatment.

BACKGROUND: National surveys suggest that treatment of heart failure in daily practice differs from guidelines and is characterized by underuse of recommended medications. Accordingly, the Euro Heart Failure Survey was conducted to ascertain how patients hospitalized for heart failure are managed in Europe and if national variations occur in the treatment of this condition. METHODS: The survey screened discharge summaries of 11304 patients over a 6-week period in 115 hospitals from 24 countries belonging to the ESC to study their medical treatment. RESULTS: Diuretics (mainly loop diuretics) were prescribed in 86.9% followed by ACE inhibitors (61.8%), beta-blockers (36.9%), cardiac glycosides (35.7%), nitrates (32.1%), calcium channel blockers (21.2%) and spironolactone (20.5%). 44.6% of the population used four or more different drugs. Only 17.2% were under the combination of diuretic, ACE inhibitors and beta-blockers. Important local variations were found in the rate of prescription of ACE inhibitors and particularly beta-blockers. Daily dosage of ACE inhibitors and particularly of beta-blockers was on average below the recommended target dose. Modelling-analysis of the prescription of treatments indicated that the aetiology of heart failure, age, co-morbid factors and type of hospital ward influenced the rate of prescription. Age <70 years, male gender and ischaemic aetiology were associated with an increased odds ratio for receiving an ACE inhibitor. Prescription of ACE inhibitors was also greater in diabetic patients and in patients with low ejection fraction (<40%) and lower in patients with renal dysfunction. The odds ratio for receiving a beta-blocker was reduced in patients >70 years, in patients with respiratory disease and increased in cardiology wards, in ischaemic heart failure and in male subjects. Prescription of cardiac glycosides was significantly increased in patients with supraventricular tachycardia/atrial fibrillation. Finally, the rate of prescription of antithrombotic agents was increased in the presence of supraventricular arrhythmia, ischaemic heart disease, male subjects but was decreased in patients over 70. CONCLUSION: Our results suggest that the prescription of recommended medications including ACE inhibitors and beta-blockers remains limited and that the daily dosage remains low, particularly for beta-blockers. The survey also identifies several important factors including age, gender, type of hospital ward, co morbid factors which influence the prescription of heart failure medication at discharge.

Adrenergic beta-Antagonists↗
PubMed1997

Safety and efficacy of carvedilol in severe heart failure. The U.S. Carvedilol Heart Failure Study Group.

BACKGROUND: Many patients remain markedly symptomatic despite optimal current therapy for heart failure. Beta-blockers have often been viewed as contraindicated in this group because of their potential adverse short-term effects on cardiac function. METHODS AND RESULTS: One hundred thirty-one patients with severe congestive heart failure were enrolled into a double-blind, placebo-controlled study of the vasodilating beta-blocker carvedilol. All patients had symptomatic, advanced heart failure while on standard triple therapy, as evidenced by a mean ejection fraction of 0.22, marked reduction in distance traveled in a 6-minute corridor walk test, and severe impairment in quality of life measured by the Minnesota Living With Heart Failure Questionnaire. After a 2-week, open-label test of 6.25 mg twice daily carvedilol, 105 patients were randomized (2:1) to receive either carvedilol (up to 25 mg twice daily, n = 70) or matching placebo (n = 35) for 6 months while background therapy with digoxin, diuretics, and an angiotensin-converting enzyme inhibitor remained constant. Ten patients (8%) did not complete the open-label period because of adverse events and 11.4% in both the carvedilol and placebo groups dropped out in the double-blind phase. The study was terminated early by the Data Safety and Monitoring Board and follow-up evaluation was therefore aborted before the projected number of patients and follow-up time was achieved. Quality of life, which was the primary endpoint, improved similarly in the carvedilol and placebo groups, whereas the global assessment by the physicians and the patient exhibited a better response to carvedilol (P < .05). Hospitalization and mortality rate were too low to evaluate a difference, and exercise time and New York Heart Association classification did not change significantly in response to the drug. Left ventricular ejection fraction rose significantly (+0.09) in the carvedilol group compared with the placebo group (+0.02, P = .004). CONCLUSION: The beta-blocker carvedilol can be safely employed in patients with severe heart failure. Improved left ventricular function with a trend for some improvement in symptoms combined with the experience with the drug in the larger population of less severe patients in this multicenter trial suggests that carvedilol may have a favorable long-term effect in heart failure of diverse severity.

Adrenergic beta-Antagonists↗
PubMed1999

Patient preferences for heart failure treatment: utilities are valid measures of health-related quality of life in heart failure.

BACKGROUND: Current standards hold that cost-effectiveness analyses should incorporate measures of both quantity and quality of life, and that quality of life in this context is best measured by a utility. We sought to measure utility scores for patients with heart failure and to assess their validity as measures of health-related quality of life (HRQL). METHODS AND RESULTS: We studied 50 patients with heart failure. We measured utilities with the time trade-off technique, exercise capacity with a 6-minute walk test, and HRQL with the Minnesota Living With Heart Failure questionnaire, the Medical Outcomes Study Short Form-36 (SF-36) questionnaire, and a visual analogue score. Validity was assessed by establishing correlation between utilities and these other measures. Mean utility score was 0.77 +/- 0.28. There were significant (P < .05) curvilinear relationships between utility score and visual analogue score, the physical function summary scale of the SF-36, 6-minute walk distance, and the Living With Heart Failure score. Utility scores on retest at 1 week were unchanged in a subset of 12 patients. Utilities did not vary systematically with age, sex, or ethnicity. CONCLUSION: Utilities are valid measures of HRQL in patients with heart failure, and cost-effectiveness analyses of heart failure treatments incorporating utilities in the outcome measure can be meaningful.

Adult↗
PubMed1997

Combination drug therapy in chronic heart failure: is treatment part of the problem in heart failure?

Despite advances in medical treatment, the annual mortality associated with severe heart failure remains over 40%, and even in mild heart failure the associated mortality is 40% over 4 years. Once it has been demonstrated that the morbidity and mortality to heart failure can be adequately addressed by combinations of drug therapy, then it is logical to attempt to strip out redundant components of these therapeutic regimes. In the meantime, however, combination therapy is required to counter many of the pathophysiological facets of the heart failure syndrome, including fluid retention, neuroendocrine activation, progressive ventricular dysfunction, and sudden cardiac death. Diuretics and ACE inhibitors are well-established drug treatments. Digoxin appears to lessen the rate of progression of heart failure without altering survival. New evidence suggests that beta-blockers may be useful additions to the heart failure therapeutic armamentarium, although whether all beta-blockers are equally effective remains to be established.

Adrenergic beta-Antagonists↗
PubMed1997

Tissue expression of components of the renin-angiotensin system in experimental post-infarction heart failure in rats: effects of heart failure and angiotensin-converting enzyme inhibitor treatment.

1. It has been suggested that local tissue renin-angiotensin systems may be activated in heart failure and that effects on such systems may, at least partially, explain the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors in this syndrome. To investigate these hypotheses, we examined expression of renin-angiotensin system components in several tissues in a rodent model of post-myocardial infarction (MI) heart failure, and analysed whether such expression is modified by ACE inhibitor treatment. 2. Four groups of rats (n = 8 - 12 per group) were studied 30 days after surgery: (A) sham-operated rats with no treatment, (B) rats with post-MI heart failure induced by ligation of the left coronary artery, (C) sham-operated rats treated with the ACE inhibitor perindopril (1.5 mg day-1 kg-1), and (D) rats as per B, but treated with perindopril. Expression of renin, angiotensinogen, ACE and angiotensin subtype 1 receptor was assessed by quantification of their respective mRNAs by Northern blotting. 3. Renal renin mRNA increased 2-fold in animals with MI (group B) compared with controls (group A) (P < 0.05) and between 50 and 100-fold after ACE inhibitor treatment (P < 0.001). No change in renin gene expression was found in any extra-renal site either following MI or after ACE inhibitor treatment. Hepatic angiotensinogen mRNA level was similar in all groups, but kidney angiotensinogen mRNA level was increased 1.6-fold (P < 0.01) in the groups receiving perindopril. ACE mRNA level in the lung was not affected by ACE inhibitor treatment but decreased by 50% following MI (groups B and D, P < 0.01). This was associated with a similar (50%, P < 0.01) fall in lung ACE activity and was correlated with the severity of heart failure. Angiotensin subtype 1 receptor mRNA level was not affected in any tissue by either MI or ACE inhibitor treatment. 4. We did not find a systematic activation of tissue renin-angiotensin systems, as assessed by steady-state mRNA levels of key components of the system in experimental post-MI heart failure, or a major effect of ACE inhibitor treatment on expression of these components. However, we observed tissue-specific changes in expression of selected components of the renin-angiotensin system in the kidney and the lung in post-MI heart failure and after ACE inhibitor treatment, which may be of relevance to the pathophysiology of the syndrome and the effects of ACE inhibition.

Angiotensin-Converting Enzyme Inhibitors↗