Frontiers in congestive heart failure: Congestive heart failure in the United States: is there more than meets the I(CD code)? The Corpus Christi Heart Project.
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Protocol: congestive heart failure.
Congestive heart failure is a serious pathological heart state which is manifested by cardiorespiratory signs and symptoms. It is present in the chronic state in many elderly people and in those with previously damaged hearts. An understanding of the pathophysiology and etiology of congestive heart failure along with the factors predisposing the elderly to congestive heart failure aids in the initial diagnosis and treatment. Management of the patient with chronic congestive heart failure and prevention of acute congestive heart failure requires very close followup and assessment of the patient for early signs and symptoms of congestive heart failure. Active involvement of the patient in the care plan along with ongoing education and counseling is essential for good management.
Digitalis Glycosides↗
Characteristics and prognosis of patients with acute myocardial infarction in relation to occurrence of congestive heart failure.
Congestive heart failure is one of the major symptoms accompanying acute myocardial infarction (AMI). The study aimed to describe the occurrence, characteristics and prognosis of congestive heart failure in AMI and to compare post-MI patients with and without congestive heart failure. The methods used included baseline characteristics, initial symptoms, electrocardiogram (ECG), mortality during hospitalization and one year follow-up in consecutive patients with AMI admitted to Sahlgrenska Hospital, Göteborg, Sweden. Congestive heart failure was observed in 51% of the cases. Patients with congestive heart failure were older, more frequently had a history of previous cardiovascular disease, and, less frequently had chest pain on admission to hospital. They had a higher occurrence of life-threatening ventricular arrhythmias during initial hospitalization, and their mortality during one year follow-up was 39% as compared to 17% in patients without congestive heart failure (P < 0.001). This difference remained significant when correcting for differences at baseline. Patients with severe congestive heart failure had a one year mortality of 47% vs 31% in patients with moderate congestive heart failure (P < 0.01). Signs and symptoms of congestive heart failure occur in every second patient admitted to hospital due to AMI, and indicate a bad prognosis, which is directly related to the severity of congestive heart failure.
Aged↗
Alterations of radial artery compliance in patients with congestive heart failure.
Congestive heart failure is accompanied by several hemodynamic alterations. To investigate whether these alterations include reduced arterial compliance, we studied 25 patients (age 57 +/- 2 years, mean +/- SE) with a mild or severe congestive heart failure based on clinical symptoms (New York Heart Association class II vs III or IV) and on echocardiographic alterations of left ventricular diastolic diameter and ejection fraction. Radial artery diameter and blood pressure were continuously measured by Doppler ultrasonography and a finger pressure device, respectively. Compliance was calculated by the Langewouters formula, and compliance values were derived throughout the systolic-diastolic pressure range. The area under the compliance-pressure curve normalized for pulse pressure was used to compare compliance values in the various groups. Data were obtained both in baseline condition and at the release from a 12-minute brachial artery occlusion. Fourteen healthy, age-matched subjects served as controls. Compared with the control group, patients with severe congestive heart failure showed a reduction of baseline compliance index (-48%, p < 0.01). Furthermore, while in control subjects compliance markedly increased after brachial artery occlusion (+43%, p < 0.01), in patients with severe congestive heart failure no increase occurred. No baseline compliance alteration was seen in patients with mild congestive heart failure in whom, however, the postischemic increase in compliance was also significantly blunted (-50% vs controls, p < 0.05). Thus, arterial compliance and arterial compliance modulation are impaired in congestive heart failure. Although more marked in severe congestive heart failure, the impairment is manifest in mild congestive heart failure as well.
Blood Pressure Determination↗
Considerations related to disability and exercise in elderly women with congestive heart failure.
Congestive heart failure is one of the most common diagnoses in older women. This article reviews physiologic and pathophysiologic factors that contribute to disability in older women with normal left ejection fraction congestive heart failure; the possibility that aerobic exercise training may be an effective means to reduce the disability experienced by these women is examined. Most literature has dealt with low-output ejection fraction congestive heart failure. Comparisons between low-output ejection fraction congestive heart failure and normal left ejection fraction congestive heart failure can help to clarify beneficial interventions. A physiologic model is proposed that includes peripheral and cardiac factors caused by heart disease, and factors caused by aging, that may account for increasing the disabling consequences and reducing exercise tolerance of older women with normal left ejection fraction congestive heart failure. The potential impact of exercise training on these factors is discussed. Directions for practice and further research are included.
Age Factors↗
Update on digoxin therapy in congestive heart failure.
Congestive heart failure is a progressive disease with significant morbidity and mortality. Despite advances in the prevention and treatment of cardiovascular diseases, the incidence and prevalence of congestive heart failure have increased in recent years. Contributing factors include increased survival in patients with coronary artery disease (especially myocardial infarction), an aging population and significant advances in the control of other potentially lethal diseases. New and existing agents, including angiotensin-converting enzyme inhibitors, beta blockers and, more recently, spironolactone, are being used increasingly to prolong life in patients with heart failure. Although digoxin has been used to treat heart failure for more than 200 years, its role in patients with congestive heart failure and sinus rhythm is still debatable. Over the past decade, digoxin has received renewed attention because of recognition of its neurohormonal effect and the successful use of lower dosages. In recent trials, digoxin has been shown to reduce morbidity associated with congestive heart failure but to have no demonstrable effect on survival. The goal of digoxin therapy in patients with congestive heart failure is to improve quality of life by reducing symptoms and preventing hospitalizations.
Cardiotonic Agents↗
Angiotensin-converting enzyme inhibition and radial artery compliance in patients with congestive heart failure.
Congestive heart failure is characterized by a clear-cut impairment of arterial compliance of medium-sized arteries, but whether this alteration is irreversible or can be favorably affected by cardiovascular drugs currently used in congestive heart failure treatment is unknown. We studied 9 congestive heart failure patients (New York Heart Association class II; age, [mean +/- SEM] 60.7 +/- 3.3 years) receiving diuretic and digitalis treatment in whom arterial compliance was assessed at the level of the radial artery by an echotracking device capable of measuring the arterial diameter along the entire cardiac cycle. Beat-to-beat arterial blood pressure was concomitantly measured by a Finapres device that allowed diameter-pressure curves and compliance-pressure curves (Langewouters' formula) to be calculated for the entire systolic-diastolic blood pressure range. Arterial compliance was expressed as the area under the compliance-pressure curve normalized for pulse pressure (compliance index). Data were collected before and after 4 and 8 weeks of oral administration of benazepril (10 mg/day). Ten healthy subjects were studied before and after an observational period of 4 weeks (5 subjects) or 8 weeks (5 subjects), and 9 age-matched mildly essential hypertensive subjects studied before and after 4 to 12 weeks of benazepril administration served as control subjects. In congestive heart failure patients, baseline compliance index was significantly less than in normotensive and hypertensive subjects. However, the compliance index showed a marked increase after 4 weeks of benazepril administration (+95.7 +/- 24.9%, P < .05); the increase was also marked after 8 weeks of angiotensin-converting enzyme inhibitor treatment (+77.7 +/- 4.2%, P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)
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Current trends in the primary care management of chronic congestive heart failure.
Congestive heart failure affects over 2.3 million Americans; approximately 400,000 new cases are diagnosed yearly in this country. Congestive heart failure is a complex disorder with a poor long-term prognosis. The major causes of congestive heart failure are ischemia, infarction, and idiopathic cardiomyopathy. Patients often present with dyspnea and a low exercise tolerance. In congestive heart failure there may be an alteration in preload, afterload, and contractility of the heart. Many compensatory mechanisms occur to support the failing heart. Cardiac symptoms slowly develop and eventually systemic symptoms develop. The cornerstones of pharmacologic therapy are cardiac glycosides, diuretics, and angiotensin-converting enzyme inhibitors.
Cardiovascular Agents↗
Pathophysiology of edema in congestive heart failure.
Congestive heart failure is one of the most important causes of peripheral edema seen in clinical practice. Edema in congestive heart failure is the result of the activation of a series of humoral and neurohumoral mechanisms that promote sodium and water reabsorption by the kidneys and expansion of the extracellular fluid. These mechanisms, in concert with abnormal Starling forces such as increased venous capillary pressure and decreased plasma oncotic pressure, promote fluid extravasation and edema formation. The management of edema in congestive heart failure is designed to improve cardiac function and to inhibit the hormonal and neurohumoral pathways that promote edema. The combination of diuretics and vasodilators or angiotensin converting enzyme inhibitors and, in some cases, cardiac inotropic agents is highly effective in achieving these goals and providing significant symptomatic improvement in patients with edema secondary to congestive heart failure.
Angiotensin-Converting Enzyme Inhibitors↗
Myocardial Na,K-ATPase: the molecular basis for the hemodynamic effect of digoxin therapy in congestive heart failure.
Congestive heart failure may be deemed the epidemic of cardiology in the 21st century in the industrialized part of the world. Although new therapies improving morbidity and mortality from chronic heart failure have emerged it is likely that there is a growing role for digoxin. Thus, digoxin treatment is known to control symptoms of congestive heart failure when added to standard therapy. In this setting, we review the prevailing knowledge of the Na,K-ATPase, the cellular receptor for the inotropic action of digitalis glycosides, in relation to the hemodynamic effect of digoxin. It is concluded that if improvement of hemodynamics is needed in congestive heart failure, this knowledge should be taken into account and in many cases digoxin should be added to standard therapy. Digoxin is still the only safe inotropic drug for oral use that improves hemodynamics. Digoxin should be used to heart failure patients in sinus rhythm when they after institution of mortality reducing treatment still have heart failure symptoms, and to patients intolerant to heart failure mortality reducing drugs. Digoxin should probably in heart failure patients with sinus rhythm be given in the lowest possible dose that relieves symptoms sufficiently.
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Total-body and myocardial substrate oxidation in congestive heart failure.
Congestive heart failure is a condition associated with increased plasma norepinephrine levels, which have been demonstrated to impair glucose handling. In the present study, 10 patients suffering from congestive heart failure and 10 healthy age- and body mass index-matched subjects were submitted to a hyperinsulinemic (insulin infusion rate, 0.5 mU/kg.min-1) glucose clamp, while simultaneous D-3H-glucose infusion and indirect calorimetry allowed for determination of glucose turnover parameters and substrate oxidation, respectively. On a separate day, basal local (myocardial) indirect calorimetry was also performed. Our data demonstrate that in congestive heart failure, fasting myocardial glucose oxidation (Gox) was inhibited with a simultaneous increase in lipid oxidation (Lox). In our patients, a significant decrease in total-body insulin-stimulated glucose metabolism (31.0 +/- 0.5 v 20.3 +/- 0.4 mumol/kg.min-1, P < .01) and nonoxidative glucose metabolism (18.9 +/- 1.1 v 11.0 +/- 0.5 mumol/kg.min-1, P < .05) was also found. Such latter changes were also associated with a simultaneous overdrive of Lox (0.4 +/- 0.2 v 1.9 +/- 0.2 mumol/kg.min-1, P < .02) that was correlated with an enhanced availability of plasma free fatty acids (FFAs).
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Uric acid--a marker for systemic inflammatory response in patients with congestive heart failure?
Congestive heart failure is associated with hyperuricemia and elevations in the levels of circulating markers for inflammation. The purpose of this study was to assess the relationship between levels of serum uric acid, activity of the renin-angiotensin-aldosterone system and TNF-alpha in heart failure patients with respect to the extent of left ventricular dysfunction. Circulating uric acid, TNF-alpha, plasma renin activity and concentrations of aldosterone were measured in 30 patients with congestive heart failure, divided into subgroups according to their NYHA class (II-IV). We found a significant step-by-step increase in TNF-alpha among the subgroups. Significant differences among the subgroups were found for the values of uric acid and the values of plasma renin and aldosterone. Serum uric acid correlated significantly with TNF-alpha concentrations (r = 0.36, P < 0.05) leukocytes (r = 0.38, P = 0.03) and ejection fraction (r = 0.64, P < 0.01). No significant correlation was found between the activity of the renin-angiotensin-aldosterone system and uricemia (r = 0.34). In a multivariate model, uric acid concentration was predicted significantly by the ejection fraction and blood leukocytes, this relationship being independent of serum creatinine, treatment modality, age and gender. We conclude that serum uric acid may reflect the severity of systolic dysfunction and the activation of an inflammatory reaction in patients with congestive heart failure.
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Altered connexin expression in human congestive heart failure.
Congestive heart failure is associated with a high risk of life-threatening ventricular re-entrant arrhythmias. Down-regulation of the principal gap-junctional protein of the ventricular myocytes, connexin43, has previously been implicated in arrhythmia in ischaemic heart disease, but it is not known whether connexin43 is similarly reduced in heart failure due to idiopathic dilated cardiomyopathy, whether disease-related connexin43 down-regulation occurs at the level of transcription or translation, or whether the expression of other connexin isotypes is altered in congestive heart failure. We therefore investigated the expression of the four connexins expressed in the heart-connexins 43, 40, 45 and 37-at the mRNA and protein levels in explanted hearts from transplant patients with end-stage heart failure (NYHA class 4) by immunoconfocal analysis, and northern and western blotting. Connexin43 mRNA and protein were markedly downregulated in the left ventricle in end-stage heart failure due both to ischaemic cardiomyopathy and idiopathic dilated cardiomyopathy. Connexin43 content was spatially heterogeneous in the diseased ventricle. Connexin40 mRNA was increased in the ischaemic group, more so in the left ventricle than the right. This correlated with an increased depth of connexin40 protein expression in myocytes at the endocardial surface. Connexin45 mRNA and protein, present only in very low quantities, followed a similar trend to connexin43, while connexin37 (exclusively expressed in endothelium) showed no change. Our findings show that congestive heart failure is associated with significantly reduced levels of the principal gap junction protein, connexin43, in the left ventricle, potentially contributing to enhanced arrhythmogenicity and contractile dysfunction. This down-regulation is due predominantly to a reduced transcript steady-state level. Elevated connexin40 may represent a compensatory response that improves the spread of depolarization in the otherwise compromised ischaemic ventricle.
Adult↗
Comparative trial of quinapril versus captopril in mild to moderate congestive heart failure. Quinapril/Captopril Congestive Heart Failure Study Group.
OBJECTIVE: To compare the efficacy and safety of captopril twice a day with quinapril once a day for the treatment of mild to moderate congestive heart failure in a multicentre, double-blind, randomly allocated, parallel-group, 12-week study. METHODS: Exercise capacity, M-mode echocardiographic left ventricular measurements and clinical signs and symptoms were evaluated. After a 2-week, single-blind, placebo washout period, the patients were randomly allocated to double-blind treatment with either captopril twice a day or quinapril once a day; the initial doses of 12.5 and 5 mg, respectively, were increased to 25 and 10 mg, respectively, in the first month, and 50 and 20 mg in the second and third months, as required to achieve adequate blood pressure control. Baseline diuretic and/or digitalis therapy was allowed during the study, so that the patients were maintained in a stable condition. RESULTS: Data from 70 captopril- and 76 quinapril-treated patients were analysed. Both angiotensin converting enzyme inhibitors displayed comparable efficacy. Both drugs were well tolerated, with a low drop-out rate (11.4% for captopril and 10.5% for quinapril). CONCLUSION: Treatment with 20 mg quinapril once a day was as effective and safe for the treatment of congestive heart failure as 100 mg captopril administered twice a day.
Aged↗
The role of norepinephrine in exercise impairment in congestive heart failure.
Congestive heart failure is a disorder that includes a multitude of neurohormonal responses that become maladaptive over time. Chronic sympathetic stimulation adversely affects the well-being and survival of heart failure patients and contributes to the exercise intolerance frequently seen in these patients. Norepinephrine levels have been correlated with poorer survival in heart failure patients. Administration of norepinephrine has been shown to impair exercise responses in those with congestive heart failure, and the recent effort to incorporate beta blocker therapy into the standard management of heart failure patients addresses this abnormal neurohormonal process. Studies with central-acting sympatholytics have shown mixed results. The use of drugs such as clonidine has been suggested as potentially useful therapy in the long-term management of patients with heart failure, but definitive conclusions await further study. Regular exercise has been shown to reduce resting norepinephrine levels in heart failure subjects. This may serve as an additional rationale to recommend chronic exercise for these patients.
Blood Flow Velocity↗
Epidemiologic patterns, clinical evaluation, and long-term prognosis in chronic congestive heart failure.
Congestive heart failure affects more than 2,000,000 Americans and is likely to increase in prevalence as our population ages. Clinical congestive heart failure should not be equated with cardiac dysfunction, as indexes of cardiac performance do not correlate with clinical manifestations. The clinical signs and symptoms of heart failure often lack sufficient sensitivity and specificity to permit accurate diagnosis. Objective tests, such as echocardiography and radionuclide angiography, are usually needed to establish the presence of left ventricular dysfunction, and exercise testing may be needed to quantitate symptomatic severity. Indexes of cardiac function do not correlate well with symptomatic status, and clinical assessment of severity of symptoms is often inaccurate. Therefore, exercise testing may be very useful in assessing symptomatic severity and in following patient progress. Prognosis in heart failure is very poor, with fewer than 50 percent of patients surviving five years from the time of initial diagnosis. Survival appears to relate more to the degree of cardiac dysfunction and less to the degree of symptomatic severity. Early recognition of heart failure in a latent stage and development of strategies aimed at preventing or delaying the onset of overt heart failure appear to offer the best chance of reducing mortality from heart failure.
Angiography↗
[Pathophysiologic aspects and modern treatment of congestive heart failure].
Congestive heart failure is a clinical syndrome with inadequate cardiac output and increased venous pressure, characterized by hyperfunction of the sympatho-neuro-endocrine system, favoring maximal vasoconstriction in non-essential organs and retention of salt and water. Identification of the cause of heart failure and its correction is the best treatment. The suppression of precipitant factors is also essential. Traditionally the treatment of congestive heart failure is based on diuretics, restriction of salt intake, and digitalis. The conventional vasodilators are effective in the short term, but they have a marked tendency to tachyphylaxis. The inhibitors of angiotensin-converting enzyme are, through their specific action on neuro-endocrine dysregulation, the most important advance in recent years. Of the non-glycosidic inotropic agents used in severe heart failure, the new inhibitors of phosphodiesterase need further testing. In certain cases, permanent synchronous pacing has to be considered.
Angiotensin-Converting Enzyme Inhibitors↗
The kidney in congestive heart failure.
Congestive heart failure (CHF) is characterized by activation of (i) vasopressor and antinatriuretic influences (ii) and by counter-activation of vasodilator natriuretic systems. The former comprise the sympathoadrenal, renin-angiotensin-aldosterone and arginine vasopressin systems, and possibly endothelin and withdrawal of endothelium dependent relaxing factor respectively. The latter include the prostaglandins (PGE-2, PGI-2), dopamine and atrial natriuretic factor. The response of the kidney to chronic heart failure, i.e. vasoconstriction and antinatriuresis, resembles the renal reaction to volume depletion. The adverse renal effects of ACE inhibitors in some patients with advanced congestive heart failure may be explained by lowering of renal perfusion pressure and dependence of glomerular filtration rate on angiotensin II.
Angiotensin-Converting Enzyme Inhibitors↗