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PubMed2003

Beta-adrenergic Receptor Blockers in Heart Failure.

Congestive heart failure is a progressive disease with high morbidity and mortality if left untreated. Standard therapy for patients with systolic left ventricular dysfunction now includes angiotensin-converting enzyme inhibitors and beta blockers. beta Blockers have been demonstrated to decrease mortality, reduce hospitalizations, improve functional class, decrease left ventricular dimensions, and improve ejection fraction in several large-scale, randomized, placebo-controlled trials. In addition to reducing deaths due to progressive heart failure, beta blockers also reduce the incidence of sudden death. Therapy with beta blockers can successfully be initiated in most patients with heart failure if recommended titration schedules are followed. beta Blockers are an important component of medical therapy for all stages of heart failure.

Journal Article↗

PubMed2004

Gender and risk of adverse outcomes in heart failure.

Congestive heart failure (CHF) is the leading cause of hospitalization in the elderly, and these patients are at high risk for subsequent hospitalization. Whether gender affects the risk of rehospitalization in patients who have CHF is less well understood. We studied a random sample of 1,700 adults who had been hospitalized with CHF (from July 1, 1999 to June 30, 2000) and identified all readmissions through June 30, 2001. We used proportional hazards regression to evaluate whether gender affects the risk of all-cause and CHF-specific rehospitalization, after adjusting for differences in demographic characteristics, health-related behaviors, co-morbid conditions, left ventricular systolic function status, and use of CHF therapies. Among 1,591 adults who had confirmed CHF, 752 were women (47.3%). Women were older than men (73 vs 71 years, p <0.001) and more likely to have preserved systolic function (55.3% vs 40.9%, p <0.001), hypertension (83.1% vs 75.2%, p <0.001), and prior renal insufficiency (46.8% vs 34.6%, p <0.001). No significant differences existed between women and men with respect to crude rates of any readmission (144.7 vs 134.6 per 100 person-years, p = 0.36) or CHF-specific readmission (39.9 vs 37.4 per 100 person-years, p = 0.65). After adjusting for potential confounders, there was no significant difference between women and men with respect to risk of any readmission (adjusted hazard ratio 0.88, 95% confidence interval 0.76 to 1.02) or readmission for CHF (adjusted hazard ratio 0.89, 95% confidence interval 0.71 to 1.11). Among a contemporary, diverse population of patients who had CHF, rates of readmission overall and for CHF remained high, but gender was not independently associated with a differential risk of readmission.

Aged↗

PubMed2003

Surgical therapy in advanced heart failure.

Congestive heart failure (CHF) affects about 1% of adults in the United States and is a contributing factor in >250,000 deaths per year. In an increasingly elderly population, the surgical treatment of CHF made great progress during the past 3 decades, consuming enormous health care resources. Heart transplantation is still the most effective therapy for end-stage heart disease, with the 10-year survival rate after transplantation approaching 50%. Efforts to increase the supply of donor organs have failed to improve the shortage, underscoring the crucial need for alternatives to cardiac allotransplantation. Alternative surgical options to end-stage heart transplantation are rapidly evolving. Left ventricular assist devices have been used as a bridge to heart transplantation for patients who otherwise might die awaiting a new heart. There is also continued interest in the use of these devices either to bridge patients to full recovery or to destination therapy, without the need for heart replacement. Left ventricular reconstruction, including the Batista and Dor procedures, along with mitral valve repair, cardiomyoplasty, and extreme coronary artery bypass graft surgery, are now being increasingly performed as alternative options. The history, status, and personal experience of surgical treatment of end-stage heart disease are discussed.

Heart Failure↗

PubMed2004

A story of maladies, misconceptions and mishaps: effective management of heart failure.

Congestive heart failure (CHF) is a common chronic disease with effective therapy, yet interventions to improve outcomes have met with limited success. Though problems in self-management are suspected causes for deterioration, few efforts have been made to understand how self-management could be improved to enhance the lives of affected patients. We conducted semi-structured interviews of 19 patients with CHF treated at an urban United States hospital to elucidate their knowledge and beliefs about CHF and to understand what underlies their self-care routines. A comparison of the themes generated from these interviews with the common-sense model for self-management of illness threats, clarifies how patients' perceptions and understanding of CHF affected their behaviors. Patients had an acute model of CHF. They did not connect chronic symptoms with a chronic disease, CHF, and did not recognize that these symptoms worsened over time from their baseline of moderate, chronic distress, to a severe state that required urgent care. As a consequence, they often did not manage symptoms on a routine basis and did not, therefore, prevent or minimize exacerbations. When they worsened, many patients reported barriers to reaching their physicians and most reported seeking care primarily in an emergency room. These in depth responses elucidate how the interplay between acute and chronic models of a chronic illness effect self-management behaviors. These factors play a previously not understood role in patient's efforts to understand and manage the ever-present but symptomatically variable chronic illness that is CHF. These new concepts illustrate the tools that may be needed to effectively manage this serious and disabling illness, and suggest possible ways to enhance the self-management process and ultimately improve patients' lives.

Chronic Disease↗

PubMed2000

Management of advanced heart failure.

Congestive heart failure (CHF) due to progressive systolic dysfunction has become a modern-day epidemic. Despite the increased incidence and prevalence, significant progress has been made in the past 10 to 15 years in the treatment of CHF at all stages. The current outlook for patients with newly diagnosed, mild heart failure is encouraging. It should be noted, however, that most of the morbidity and health care expenditure is incurred by a minority of patients diagnosed with CHF who are in the advanced stages of their disease. The thrust of this article will be to provide practical advice beyond current guidelines on the management of advanced CHF.

Adrenergic beta-Antagonists↗

PubMed2002

Management of advanced heart failure.

Adrenergic beta-Antagonists↗

PubMed2004

Determinants of platelet responsiveness to nitric oxide in patients with chronic heart failure.

Congestive heart failure (CHF) is associated with oxidative stress. Platelet responsiveness to nitric oxide (NO) donors, are impaired in patients with angina pectoris, possibly by increasing oxidative stress. We investigated the occurrence of platelet resistance to NO in patients, with ischaemic or non-ischaemic cardiomyopathy compared with normal subjects. Anti-aggregatory effects of sodium nitroprusside (SNP), oxidative stress and whole blood superoxide anion content were determined, with correlates of responsiveness to SNP. Inhibition of platelet aggregation by SNP was 65.4+/-3.55% in controls and 59.3+/-4.1% in CHF (P=ns) despite increased oxidative stress and post-aggregation O2- in CHF patients. However, subsets of CHF patients have NO-resistant platelets: this is associated with increasing age and/or increased oxidative stress (both p<0.05).

Adult↗

PubMed2001

The role of inflammatory mediators in the failing heart: immunomodulation of cytokines in experimental models of heart failure.

Congestive heart failure may be produced by a variety of disorders, including dilated cardiomyopathy, hypertension, and ischemic heart disease. We have developed experimental models of these diseases, and found gene expressions of proinflammatory cytokines increased in the hearts of these animals. Various drugs for heart failure modulate the production of cytokines in experimental models of heart failure. Pimobendan, an inhibitor of phosphodiesterase III prolonged survival, attenuated inflammatory lesions, and decreased the production of cytokines and nitric oxide. Recent studies have shown that these inhibitory effects are due to inhibition of activation of NF-kappaB. In contrast, digitalis increased the production of cytokines and exacerbated myocarditis. Interleukin-10 prolonged survival, attenuated myocardial injury, and appears promising as a treatment of heart failure due to viral myocarditis. Endothelin-1 plays an important pathophysiological role in heart failure, and treatment with an endothelin antagonist had a cardioprotective effect in experimental models of heart failure.

Adjuvants, Immunologic↗

PubMed2002

Endothelin stimulates an endogenous nitric oxide synthase inhibitor, asymmetric dimethylarginine, in experimental heart failure.

Congestive heart failure (CHF) is characterized by increased peripheral vascular resistance. Endothelin-1 (ET-1), a potent endothelium-derived vasoconstrictor, is present at increased concentrations in the plasma and contributes to the regulation of vascular tone in CHF. An endothelium-derived relaxing factor, nitric oxide (NO), also regulates vascular tone, but endothelium-dependent NO-mediated vasodilation is blunted in CHF. An endogenous NO synthase inhibitor, asymmetric dimethylarginine (ADMA), which inhibits NO production and endothelium-dependent relaxation, is present at increased levels in the plasma and plays a role in impaired endothelial function in CHF. However, at present, the relationship between ET-1 and impaired vascular relaxation in CHF is not well known. We hypothesized that ET-1 inhibits NO-mediated vasodilation via increased ADMA production in CHF, and that an endothelin receptor antagonist can prevent this increase in plasma ADMA levels. In the present study, we first examined whether circulating ADMA levels were increased in a dog model of CHF induced by 3 weeks of rapid ventricular pacing (n=5; 270 beats/min) compared with normal dogs (n=5). After 3 weeks of pacing, cardiac output had decreased significantly (1.56+/-0.16 compared with 2.93+/-0.25 litres/min; P<0.01) and systemic vascular resistance had increased (4653+/-374 compared with 3227+/-396 dyn.s.cm(-5); P<0.01) in dogs with CHF compared with normal dogs. Plasma levels of both ET-1 (4.95+/-0.83 compared with 2.12+/-0.39 pg/ml; P<0.05) and ADMA (3.27+/-0.49 compared with 1.91+/-0.25 nmol/ml; P<0.05) were significantly increased in CHF dogs. A significant positive correlation was observed between plasma ET-1 and ADMA levels (r=0.72, P<0.05). Secondly, we chronically administered an ET(A) receptor antagonist, TA-0201 (0.3 mg/kg; n=5), to paced CHF dogs. Drug administration started on day 8 of pacing and continued throughout the experiment. TA-0201 significantly increased cardiac output (2.58+/-0.24 litres/min; P<0.01) and suppressed the increases in plasma ADMA levels and systemic vascular resistance (2.36+/-0.30 nmol/ml and 2423+/-188 dyn.s.cm(-5) respectively; P<0.05 for each) compared with CHF dogs without TA-0201 treatment. In conclusion, ET-1 contributes to the regulation of vascular tone due, in part, to increased levels of an endogenous NO synthase inhibitor in CHF, and an ET(A) receptor antagonist can prevent the inhibition of NO production and the increased peripheral vascular resistance observed in CHF.

Animals↗

PubMed2005

Gene therapy for heart failure.

Congestive heart failure (CHF) remains a leading cause of morbidity and mortality in the United States and in many other countries. Current heart failure therapies, including multidrug treatment regimens, biventricular pacing, and mechanical support such as left ventricular assist devices, are often hindered by limited benefits or significant associated procedural complications or side effects. Therefore, new forms of treatment, which could ideally target the underlying biological processes affecting the ailing cardiomyocyte, would be of significant potential benefit to the population of individuals with CHF. Gene transfer strategies, including modification of cellular contractile signaling and regulatory pathways, represent a promising new form of such biologic therapy for heart disease.

Adenylyl Cyclases↗

PubMed2006

Adaptation of renal function in heart failure.

Congestive heart failure is the only major cardiovascular disease with an increasing incidence and prevalence in industrialized countries. Despite considerable progress in the clinical management of heart failure during the last 20 years, the prognosis is still worse than in many common types of cancer. The kidney is the main organ affected when cardiac function is compromised. In addition, the kidney significantly contributes to the development of the clinical syndrome of heart failure. Specific hemodynamic and neurohormonal abnormalities define the pathophysiology, clinical presentation, and prognosis of this disorder. In this setting, the kidney plays a dual role: the activation of the renin-angiotensin-aldosterone system and the regulation of sodium and water excretion. The kidney is generally intact in heart failure, but extrarenal stimuli alter its function to a point where mechanisms that are initially homeostatic become maladaptive. In this review article, the mechanisms involved in renal adaptation to heart failure are presented.

Acclimatization↗

PubMed1996

Heart failure.

Congestive heart failure (CHF) affects more than 2 million Americans and requires greater than 900,000 hospitalizations each year. The incidence of CHF is increasing because of the increasing age of the American population and the use of newer medications and technologies that have increased survival at the expense of increased morbidity. Physical therapists are treating many patients who have varying degrees of CHF. Recent research has demonstrated the importance of exercise conditioning in patients with CHF. This article will review the pathophysiology, compensatory mechanisms, and signs and symptoms of CHF as well as provide a discussion of physical therapy in the treatment of patients with CHF.

Activities of Daily Living↗

PubMed1996

The cellular pathophysiology of progression to heart failure.

Congestive heart failure is the final common pathway of diverse etiologies that result in impaired systolic and diastolic function, deleterious activation of neurohumoral pathways, and high morbidity and mortality. Many studies published in 1995 significantly added to our understanding of the pathophysiologies of heart failure at the cellular level. Because a common accompaniment to all forms of low output heart failure are hypertrophy and contractile dysfunction of the cardiomyocyte, applications of the techniques of molecular and cell biology to animal models that demonstrate this phenomenon are providing new insights into the mechanisms responsible for this important clinical problem. In the past year, critical information was derived from animal models that mimic human cardiac hypertrophy and failure. Likewise, genetically engineered mice in which a gene product of interest is overexpressed or eliminated provided critical information, in particular regarding the roles of phospholamban and beta-adrenergic receptor kinase 1 in mediating the contractile responses of the heart to beta-adrenergic stimulation. Furthermore, study of human myocardial tissue from patients with end-stage cardiomyopathy continues to provide insight into the diverse etiologies of heart failure. The recent applications of the techniques of molecular and cell biology to this clinical problem are likely to accelerate our understanding of the complex mechanisms responsible for this syndrome.

Action Potentials↗

PubMed2000

Advances in the molecular mechanisms of heart failure.

Congestive heart failure is a common clinical problem resulting in significant morbidity and mortality. Although considerable progress has been made in elucidating the pathophysiologic mechanisms that lead to the development of this process, much remains unknown. The techniques of modern molecular biology now allow a detailed and systematic analysis of this disease. Recent data linking cardiac hypertrophy, aberrant signaling, or cytoskeletal abnormalities to the development of heart failure have provided new insights into this process. These studies have confirmed the importance of many classical pathways but also revealed novel pathways. This review will focus on the recent advances that have been made and will highlight the importance they have had in our understanding and treatment of heart failure.

Angiotensins↗

PubMed2001

Endothelial function in patients with chronic heart failure.

Congestive heart failure is characteristically associated with systemic vasoconstriction and impaired vasodilatory capacity, leading to decreased peripheral perfusion. Factors identified as possible causes of reduced vasodilatory capacity include activation of the sympathetic nervous system and the renin-angiotensin system, vascular stiffness due to increased sodium and fluid retention, and structural vascular changes. More recently, the role of the endothelium as a mediator of vasoregulation and tissue perfusion has been recognized.

Endothelium, Vascular↗

PubMedDate not supplied

Advances in the management of acute and chronic decompensated heart failure.

Congestive heart failure (CHF) is a pervasive and insidious disease that affects almost 5 million, mostly elderly, Americans. Significant therapeutic advances in the management of heart failure (HF) have resulted in striking decrements in mortality rates, but hospitalization use is ever increasing, now at over 1 million hospitalizations per year with a cost of >15 billion dollars-a cost that is largely borne by Medicare and Medicaid. One of the most historically challenging factors facing case managers who work with the CHF population is how to minimize treatment costs while enhancing clinical outcomes for those with this highly prevalent and clinically challenging chronic disease. To date the typical treatment of acute decompensation has been based in the hospital and woefully inadequate in promoting any long-term medical stability.

Acute Disease↗

PubMedDate not supplied

Advances in the management of acute and chronic decompensated heart failure.

Congestive heart failure (CHF) is a pervasive and insidious disease that affects almost 5 million, mostly elderly, Americans. Significant therapeutic advances in the management of heart failure (HF) have resulted in striking decrements in mortality rates, but hospitalization use is ever increasing, now at over 1 million hospitalizations per year with a cost of > $15 billion--a cost that is largely borne by Medicare and Medicaid. One of the most historically challenging factors facing case managers who work with the CHF population is how to minimize treatment costs while enhancing clinical outcomes for those with this highly prevalent and clinically challenging chronic disease. To date the typical treatment of acute decompensation has been based in the hospital and woefully inadequate in promoting any long-term medical stability.

Acute Disease↗

PubMedDate not supplied

The pharmacologic treatment of heart failure.

Congestive heart failure is common, affecting 4-5 million American's with more than 500,000 new cases each year. A number of therapies have been proposed for the treatment of CHF; some have been found useful and some not. Digoxin therapy long a mainstay of therapy has been found beneficial, but lower doses and caution with its use in women has been recently advised based on new information. Converting enzyme inhibitors and beta blockers both add benefit when used in combination. The addition of aldosterone antagonists to the digoxin, diuretic, ACE, and beta-blocker combination appears to offer benefit and the use of the new less toxic eplerone will become more frequently employed in selected patients. Sudden death is also an important contributor to mortality in CHF patients. Use of a amiodarone and ICD's have both been reported to offer benefit. Selecting the optimum cost effective therapy is a challenge to those treating heart failure patients. ICD's are recommended in class II, III CHF with EF < 30 and amiodarone may be the therapy of choice in selected class IV patients and in patients with EF > 30%.

Age Factors↗