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PubMedDate not supplied

Cost-effectiveness analysis in clinical practice: the case of heart failure.

Heart failure is the leading cause of hospitalization in adults older than 65 years, and it is currently the most costly cardiovascular disorder in the United States, with estimated annual expenditures in excess of $20 billion. Recent studies have shown that selected pharmacological agents, behavioral interventions, and surgical therapies are associated with improved clinical outcomes in patients with heart failure, but the cost implications of these diverse treatment modalities are not widely appreciated. In this review, a brief outline of cost-effectiveness analysis is provided, and current data on the cost-effectiveness of specific approaches to managing heart failure are discussed. Available evidence indicates that angiotensin converting enzyme inhibitors, other vasodilators, digoxin, carvedilol, multidisciplinary heart failure management teams, and heart transplantation are all cost-effective approaches to treating heart failure; moreover, some of these interventions may result in net cost savings.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2001

Electrical modulation of cardiac contractility: clinical aspects in congestive heart failure.

Heart failure is a highly prevalent disease in western society. Drug therapies aimed at increasing myocardial contractility have been associated with decreased survival. Several short and mid term clinical studies have suggested adjuvant or alternative therapies to congestive heart failure using modified pacing techniques that were aimed to increase contractility (e.g. Paired pacing) or restore synchrony of contraction (biventricular pacing). While delivery of paired pacing was abandoned during the early 70's, biventricular pacing has recently emerged as an adjuvant treatment to limited group of congestive heart failure patients with aberrant left ventricular conduction. In this brief review, we describe our initial safety and efficacy experience in patients with heart failure using a novel non-stimulatory electrical approach to the delivery of positive inotropic therapy to the failing myocardium. The study suggests that unlike modified pacing techniques, delivery of the signal to the left ventricle during the refractory period resulted in a rapid increase in myocardial contractility and improved hemodynamic performance. The near instantaneous contractility improvement achieved by this type of stimulus was shown to be safe and effective independently of the primary cause of heart failure or the function of the conduction system. Unlike pharmacologic treatments, which have a relatively constant effect, use of electrical stimuli may prove useful as a new therapeutic modality in the treatment of heart failure with which contractility can be improved when and as needed.

Cardiac Pacing, Artificial↗
PubMedDate not supplied

Diagnosis and assessment in heart failure.

Heart failure is a common and growing problem. Its optimal and effective management and the evaluation of new therapies require assessment of underlying etiology, type of cardiac dysfunction, severity, prognosis, and response to therapy. Unfortunately, the lack of a universally agreed definition of heart failure and uniform criteria make an accurate and complete diagnosis of heart failure difficult. Currently, a wide range of investigations and assessments is available, including assessment of symptoms, exercise performance, and cardiac function. In particular, left ventricular (LV) ejection fraction (EF) is widely used and a good marker of the severity of LV dysfunction and prognosis. It is now being recognized that the early identification and treatment of patients with asymptomatic LV dysfunction may prevent subsequent progression to symptomatic heart failure. Recently, attention has focused on the neurohormonal activation that occurs early in heart failure, and especially increasing evidence suggests that plasma levels of neurohormones and brain natriuretic peptides, may be useful biochemical markers in the diagnosis and assessment of heart failure at an early stage. Further evaluation of this neurohormonal activation and treatments directed towards it may provide considerable benefits in improving patient morbidity and mortality. (c)1999 by CHF, Inc.

Journal Article↗
PubMedDate not supplied

Genetic polymorphisms and oxidative stress in heart failure.

Heart failure results from various known cardiovascular diseases, such as coronary artery disease, or can be the result of an idiopathic dilated cardiomyopathy. It is of utmost importance for diagnostic, preventive, and therapeutic purposes to understand the cellular events that trigger the cascade of functional and structural changes that result in the development and progression of heart failure. Progress in unraveling the genetic background in both ischemic and nonischemic cardiomyopathies has been slow compared with that for monogenic diseases, such as some forms of hypertrophic cardiomyopathy or familial dilated cardiomyopathies. It is likely that susceptibility to and risk of progression of heart failure are both influenced by many genes acting in concert or independently. Among the diverse subcellular mechanisms implicated in the pathogenesis and progression of heart failure, reactive oxygen species play a major role. The search for genetic polymorphisms in clinical association studies in order to identify genotypes susceptible to develop and affect the progression to heart failure has been the focus of many investigations over the past several years. In this review, the authors summarize the current data in support of the role of various polymorphisms of genes related to oxidative stress in the susceptibility to develop heart failure, and its progression.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed2001

Beta-blocker treatment in heart failure.

Heart failure treatment has markedly changed during the last few decades, with demonstration of benefit of afterload reduction by vasodilator therapy and introduction of the concept of the deleterious consequences of the neuro-hormonal compensatory stimulation. Blockade of beta-adrenergic receptors, initially contra-indicated in heart failure, provide a marked reduction of mortality and morbidity in combination with diuretics and angiotensin-converting enzyme inhibitors, as demonstrated in many clinical trials. We performed a review of all clinical trials that compare beta-blockers vs. placebo in chronic heart failure. Beta-blockers with different pharmacological profiles have been tested, mainly metoprolol, bisoprolol, bucindolol and carvedilol. With progressive dose increment, tolerance of such treatment was generally good, left ventricular function improved, hospitalisations for heart failure were less frequent and mortality was reduced. The meta-analysis of the 16 randomised trials, with at least one death in each treatment group, provides a 24% relative risk reduction for such hospitalisations (95% CI=19%-29%) and 22% reduction for mortality (95% CI=16%-28%). Heterogeneity of beta-blocker effect for mortality was found and related to the non-significant benefit obtained in the BEST trial with bucindolol. When such a trial is excluded, the effect model analysis shows that relative risk reduction (beta-blocker induced benefit) is constant whatever the severity of the disease. The mechanism of beta-blocker induced benefit remains unclear, but is at least partly related to left ventricular function improvement and prevention of severe ventricular arrhythmias. In conclusion, beta-blocker treatment has become an established therapy for heart failure, in combination with diuretics and ACE inhibitors. Complementary informations will be needed to clarify the mechanism of benefit and to define the best therapeutic strategy according to the individual characteristics of patients with heart failure.

Adrenergic beta-Antagonists↗
PubMed1995

Pathophysiologic aspects of end-stage heart failure.

Heart failure is not a distinct disease, but rather a complex clinical syndrome that can result from virtually any form of heart disease. The so-called "end stages" of heart failure do not respect etiologic boundaries. Patients are characterized clinically by extreme cardiomegaly, breathlessness, and fluid retention. Despite recent advances in the pharmacologic management of congestive heart failure, it remains a highly lethal and disabling disorder. Only through an improved understanding of the basic biology of the early stages of the syndrome can heart failure be prevented or at least forestalled. There is now intense interest in understanding the mechanisms operative in early left ventricular remodeling, which has the potential to culminate in end-stage heart failure. The study of animal models has been particularly useful in this regard, as have clinical studies performed in the early stages of acute myocardial infarction. The remodeling process is characterized by myocyte loss and segmental scarring, interstitial fibrosis, myocardial slippage, and myocyte hypertrophy. Although the mechanisms responsible for these topographic changes are as yet unclear, the net result is progressive enlargement of the heart, culminating in severe left ventricular dysfunction. A long-held view that cardiomegaly is a necessary adaptive process that maintains stroke volume in the presence of a falling ejection fraction has been challenged, although undoubtedly the early responses to myocardial injury in the form of myocyte hypertrophy and maintenance of wall stress are useful adaptations. However, as the left ventricle continues to dilate and hypertrophy over time, a form of overadjustment occurs that perhaps is an important contributory factor toward end-stage failure.

Cardiomegaly↗
PubMed1981

Normal left ventricular ejection fraction in systemic arteriovenous fistula. Implications for the use of noninvasive methods in differential diagnosis of heart failure.

Heart failure is frequently a result of impaired systolic ventricular performance. We describe a patient with heart failure and a systemic arteriovenous fistula who had left ventricular enlargement and a normal left ventricular ejection fraction, demonstrated by gated cardiac blood pool scanning. The heart failure was relieved by surgical repair of the fistula, but the left ventricular ejection fraction did not change. These observations show that volume overload rather than impaired systolic function was the mechanism by which heart failure occurred in this patient with a systemic high output state and illustrate the value of gated cardiac blood scanning in noninvasively elucidating the mechanism of heart failure.

Arteriovenous Fistula↗
PubMed2003

Sex differences in the causes and natural history of heart failure.

Heart failure is a clinical syndrome of increasing prevalence in the United States, with significant morbidity and mortality. Although men have a higher annual mortality rate, more women than men die from heart failure each year. Optimal disease management is critical in limiting the impact of heart failure on life quality, quantity, and health care expenditures. Women have a unique risk-factor profile and different clinical manifestations of heart failure than men. Understanding inherent sex differences in heart failure epidemiology, pathophysiology, and natural history is imperative in determining whether the optimal therapy for this prevalent and important syndrome is affected by sex.

Aged↗
PubMedDate not supplied

Genetic polymorphisms and heart failure.

Heart failure is a complex clinical syndrome. There is evidence for a genetic contribution to the pathophysiology of heart failure. Considering the fundamental role of neurohormonal factors in the pathophysiology and progression of cardiac dysfunction and hypertrophy, variants of genes involved in this system are logical candidate genes in heart failure. In this report, genetic polymorphisms of the major neurohormonal systems in heart failure will be discussed. Studies on polymorphisms of the renin-angiotensin-aldosterone system (RAAS), adrenergic receptor polymorphisms, endothelin (receptor) polymorphisms, and a group of miscellaneous polymorphisms that may be involved in the development or phenotypic expression of heart failure will be reviewed. Research on left ventricular hypertrophy is also included. The majority of genetic association studies focused on the ACE I/D polymorphism. Initial genetic associations have often been difficult to replicate, mainly due to problems in study design and lack of power. Promising results have been obtained with genetic polymorphisms of the RAAS and sympathetic system. Considering the evidence so far, a modifying role for these polymorphisms seems more likely than a role of these variants as susceptibility genes. Besides the need for larger studies to examine the effects of single nucleotide polymorphisms and haplotypes, future studies also need to focus on the complexity of these systems and study gene-gene interactions and gene-environment interactions.

Heart Failure↗
PubMed1997

Management of atrial fibrillation in the setting of heart failure.

Heart failure is often complicated by atrial fibrillation. Once atrial fibrillation has started it further enhances heart failure due to uncontrolled rate with shortened filling time and provocation of tachycardiomyopathy. Absent atrial kick and irregularity of the ventricular rhythm also contribute. Considering these mechanisms, restoration of sinus rhythm is most beneficial but is associated with frequent recurrences. Before cardioversion heart failure must be treated. ACE inhibition, initiated before cardioversion, may enhance maintenance of sinus rhythm by reducing neurohumoral activation. As a consequence, arrhythmogenic factors diminish and ventricular function may improve. beta-blockade and amiodarone may have similar effects. If cardioversion fails, adequate rate control is mandatory to prevent progressive ventricular dysfunction. Digitalis is the treatment of first choice, but when the heart rate remains uncontrolled low-dose beta-blockade should be given. If the ventricular rate remains uncontrolled despite drugs, atrioventricular node ablation with implantation of a pacemaker may be considered. Not only patients with idiopathic heart failure and atrial fibrillation, but also those with significant underlying heart disease may benefit from this intervention. In atrial fibrillation patients undergoing cardiac surgery for heart failure due to valvular disease, additional arrhythmia surgery may be contemplated.

Adult↗
PubMed2002

Prevention of heart failure.

Heart failure carries a sizeable health burden. Efforts to prevent this condition are not generally well studied. Most of the interventions that have demonstrated benefit address cardiac risk factors such as hypertension and hyperlipidemia. The results of the HOPE study have recently expanded the indications for angiotensin converting enzyme inhibitors in the prevention of heart failure. Once heart failure occurs, a variety of interventions can prevent recurrent episodes of congestion. Biventricular pacing, left ventricular assist devices, and disease-specific management clinics join more standard medical therapies such as angiotensin converting enzyme inhibitors, beta-blockers, diuretics, digoxin, and spironolactone in improving outcomes for patients with this disorder.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

Crosstalk of the heart and periphery: skeletal and cardiac muscle as therapeutic targets in heart failure.

Heart failure syndrome is initiated as the body's metabolic needs temporarily exceed the pumping capacity of the heart. In most cases, this phenomenon tends to occur during physical exercise. Although not always subjectively recognized, limited exercise capacity remains the clinical hallmark of congestive heart failure. It can be measured objectively as reduced skeletal muscle performance and maximal whole-body oxygen uptake, which are not necessarily explained by central haemodynamic abnormalities. In fact, the initial cardiac condition sets forth a series of peripheral adaptations that are potentially life-saving during acute decompensation but become disadvantageous and symptom-generating in stable heart failure. Inodilator drugs were theoretically ideal to revert the adverse haemodynamic crosstalk between the heart and periphery. However, these drugs failed to improve prognosis in congestive heart failure, whereas drugs that did so showed typically unimpressive haemodynamic effects. Exercise therapy has recently emerged as a safe and effective way to enhance physical performance and subjective well-being in congestive heart failure. A dual therapeutic approach is suggested, consisting of exercise training to improve the periphery and the use of cardioprotective drugs to limit cardiac cellular damage from neurohormonal activation.

Adrenergic beta-Antagonists↗
PubMed1993

[Electrocardiogram in heart failure].

Heart failure is basically a manifestation of mechanical disturbances of the heart, but not of electrical abnormalities and is not associated with specific ECG patterns. Several ECG findings are, however, experienced in cases with heart failure as a result of cardiac chamber enlargement and other related changes. Left atrial enlargement is known to cause characteristic P wave changes, which sometimes show parallel course with the clinical state. ECG criteria for atrial enlargement are critically reviewed. In cases with cardiac enlargement, which was improved in a relatively short period of time, R wave height often showed first increase and then decrease. Tissue edema was thought to be the major reason for the initial increase and the distance between the recording electrode and the heart for the later decrease, although other factors can contribute and modify the findings. Minor conduction disturbances due to myocardial stretch and other reasons may also contribute to changes of QRS complex. Analysis of RR intervals offers another possibility to characterise heart failure. A decrease in variability of the RR intervals and in high frequency components on frequency spectrum has been reported in cases with heart failure.

Electrocardiography↗
PubMed2001

[New pharmacological agents in heart failure].

Heart failure is a common and growing public health problem, with increasing incidence and prevalence over the last 2 decades. Despite improvements in its current management, heart failure is still associated with significant morbidity and mortality. This has motivated the search for newer therapeutic modalities, which are based on a better understanding on the pathophysiologic events that lead to heart failure. This review summarizes the potential role of new pharmacological agents in the treatment of heart failure. These potential new agents can be classified according to their role in the modulation of the main pathophysiologic abnormalities that characterized heart failure, that include: cellular-extracellular abnormalities, endothelial dysfunction, neurohormonal and immunologic activation.

Cardiovascular Agents↗
PubMed2001

Pathophysiology of sodium and water retention in heart failure.

Heart failure is a leading cause of morbidity and mortality. In the United States, there are more than 5 million patients with heart failure and over 500,000 newly diagnosed cases each year. Numerous advances have been made in our understanding of the pathophysiologic mechanisms contributing to sodium and water retention in this condition. Important alterations in the sympathetic nervous system and the renin-angiotensin-aldosterone system have been described in heart failure, allowing the use of mechanism-specific treatments such as beta-adrenergic receptor antagonism and angiotensin-converting enzyme inhibition. As our understanding of the roles of the natriuretic peptides and the arginine vasopressin-aquaporin-2 system in the pathophysiology of heart failure evolves, treatments directed toward the alterations in these systems in heart failure can be further developed.

Adrenergic beta-Antagonists↗
PubMed2001

[Drug-induced heart failure].

Heart failure is a clinical syndrome caused mainly by cardiovascular diseases such as coronary heart disease, hypertension and valvular disease, but several categories of drugs may potentially induce heart failure in patients without previous heart disease or precipitate revealing of heart failure symptoms in patients with preexisting left ventricle impairment. Pathophysiologically drugs that increase preload, afterload or have negative inotropic properties may be able to cause this adverse reaction. In the article the potential role in the occurrence of heart failure of cytostatics, immunomodulating drugs, nonsteroidal anti-inflammatory drugs, calcium channel blockers, beta-adrenoceptor antagonists, antiarrhythmics, anesthetics and antidepressants is reviewed.

Adrenergic beta-Antagonists↗
PubMed2006

[Surgical strategy for severe heart failure].

Heart transplantation had been an only effective treatment for severe congestive heart failure secondary to dilated or ischemic cardiomyopathy. Recently, mitral valve repair and left ventricular reconstruction have been introduced to restore their own cardiac function. These operations can be one of treatment options for relatively stable congestive heart failure patients. For those with severer heart failure complicated with cardiogenic shock or end-organ dysfunction, use of mechanical assist device should be included in the treatment strategies. Perioperative problems of implantation of left ventricular assist device include right heart failure, multi-organ failure, infection and anti-coagulation. Implantable LVAS, which provides potent circulatory assist is useful to overcome organ dysfunction and render good QOL during long waiting period for heart transplantation.

Cardiac Surgical Procedures↗
PubMed1996

ACE inhibitors before or after heart failure?

Heart failure is a progressive disease and once the process has started it continues with further deterioration of cardiac function or ends in sudden death. In many patients changes within the heart start to develop long before clinical symptoms occur. The left ventricle goes through a number of adaptions-remodelling-to compensate for increased pressure or volume load or subsequent myocardial infarction. Several of these compensatory changes have prognostic implications and indicate increased risk of clinical heart failure or cardiac events. Thus, increased left ventricular dimensions, volume and mass together with reduced systolic function are all markers of poor prognosis. Treatment with angiotensin-converting enzyme (ACE) inhibitors before the onset of clinical heart failure has been shown to improve prognosis. Identification of individuals at high risk is difficult since signs and symptoms of heart failure are often lacking. A strategy to find these patients must use objective methods to characterise the state of the left ventricle. It is likely that not only patients with significant reduction of systolic function but also other signs of impaired left ventricular dysfunction will benefit from treatment with ACE inhibitors. Only by preventive treatment may we be able to decrease the number of patients with new onset of clinical heart failure.

Angiotensin-Converting Enzyme Inhibitors↗