Treatment of heart failure with beta-blockaders]

Since 1975 several studies have indicated that treatment with beta-adrenergic blocking drugs has a positive effect on prognosis in patients with left ventricular dysfunction. After myocardial infarction, treatment with timolol and propranolol improves prognosis in patients with symptoms of cardiomegaly and heart failure. In patients with idiopathic dilated cardiomyopathy, treatment with metoprolol improves the left ventricular ejection fraction and symptoms of heart failure, and may have a positive effect on prognosis. Recent studies of patients with chronic congestive heart failure also indicate that carvedilol has a positive effect on mortality and morbidity. The authors review some relevant studies, to stimulate the use of beta-adrenergic blocking drugs to treat certain types of heart failure.     

Therapeutic strategy of chronic heart failure]

Considerable advances have been made in the management of heart failure during the past decade, with the development of new pharmacological agents. Now the therapeutic goals are not only to reduce symptoms but also to decrease the occurrence of acute heart failure, hospitalizations and to delay death. Prevention plays a key role: by correcting predisposing factors, and by slowing the process which leads from asymptomatic left ventricular dysfunction to overt heart failure. The range for therapeutic action is broad: general and dietetic advices, pharmacological agents, surgical procedures which are reserved for the end-stage patient. Angiotensin converting enzyme inhibitors remain the cornerstone of treatment at almost all stages of the disease.     

Mechanical circulatory support in heart failure]

Heart transplantation is an established therapy for end-stage cardiac disease. The number of organ donors is limited, and the mortality on the waiting list is increasing. To give these patients a chance to survive their waiting time, chronic mechanical circulatory support, especially left ventricular assist devices have been clinically established. The results with this therapy are encouraging. Because of these results trials using these devices as an alternative for cardiac transplantation are initiated. Due to the further development and miniaturization of such devices this indication will become more important. The most interesting patients are the one, in which devices could be explanted after chronic support, because their myocard has recovered. If we can find a way to identify such patients a new form of therapy for end-stage heart disease could be established.     

Aggressive therapy in patients with heart failure]

The potential role of genetic factors in the etiology of posttraumatic and alcohol-associated seizures was studied in 289 male patients with recurrent seizures and in 174 individuals who had never experienced a seizure. The incidence of seizures in first-degree relatives of probands was compared with that in relatives of unaffected individuals. Relatives of patients with alcohol-associated seizures had a rate ratio of 2.45 [95% confidence interval (CI) 1.41-4.25], whereas no excess incidence was noted among relatives of posttraumatic epilepsy patients (rate ratio 1.20, 0.64-2.25 CI). Relatives of probands with both antecedents showed an intermediate rate ratio of 1.72 (0.92-3.20 CI). Among probands with alcohol-associated seizures, the rate ratio of 2.05 for patients with alcohol-related seizures (i.e., spontaneously occurring seizures in association with chronic alcohol abuse) was slightly higher than that of 1.85 for probands with alcohol withdrawal seizures. Trauma severity had a slight impact on the incidence of affected relatives; patients with severe head injuries had a rate ratio of 0.73 and probands with milder trauma had a rate ratio of 0.99. The results indicate a limited, if any, role of genetic predisposition in development of posttraumatic seizures. Alcohol-related seizures, however, showed familial aggregation of unprovoked seizures, suggesting an involvement of genetic factors in the origin of such seizures.     

Aspirin, oral anticoagulants, and heart failure]

This study tests the hypothesis that myocardial blood flow and coronary microvascular dilator capacity vary as a function of time after orthotopic heart transplantation in humans. Positron emission tomography measurements of myocardial blood flow were obtained at rest and during adenosine in 24 patients between 1 and 86 months after heart transplantation. At the time of the study all patients were clinically well and had angiographically normal epicardial coronary artery vessels. Patients were divided into 3 groups based on time from transplant to positron emission tomography measurement of myocardial blood flow: group 1 to 12 months (n = 9); group 13 to 34 months (n = 8); and group > or = 37 months (n = 7). Basal myocardial blood flow in group 1 to 12 months (1.86+/-1.01 ml/min/g) exceeded (p <0.05) that of group 13 to 34 months (1.17+/-0.73) and group > or = 37 months (0.98+/-0.34). In group 13 to 34 months, basal myocardial blood flow and maximal dilator capacity (minimal coronary vascular resistance with adenosine 36+/-12 mm Hg/ml/min/g) were comparable to that of normal volunteers (1.01+/-0.20 and 37+/-, respectively). In group > or = 37 months, maximal flow response to adenosine was reduced (2.54+/-1.25 vs 3.16+/-0.52, respectively, p = 0.06). Maximal dilator capacity in group > or = 37 months (60+/-34) was impaired versus group 1 to 12 months (36+/-10) and group 13 to 34 months (36+/-12; both p <0.05) as well as normals (37+/-9, p <0.05). During the first year after cardiac transplantation basal myocardial blood flow is elevated out of proportion to external determinants of myocardial oxygen demand, but maximal dilator capacity of the coronary microcirculation is normal. Between 1 and 3 years both basal myocardial blood flow and microvascular function tend to normalize. After 3 years, although basal myocardial blood flow is normal, microvascular dilator capacity is impaired.     

Acute heart failure

OBJECTIVE: The purpose of this study was to determine whether arthrosis begins at an unusually early age in professional dancers; if there is an association between hypermobility and osteoarthrosis in dancers; and if osteoarthrosis is a contributing factor to retirement from a professional career in this population. DESIGN: Dance and injury history; physical examinations of back, lower extremities, and ligamentous laxity; and radiographs of lower extremity joints were performed in retired dancers. The dancers' radiographs were compared to those of age-matched nondancers. The radiologist was blinded to the origin of the radiographs. PARTICIPANTS: Fourteen retired dancers aged 27 to 46 years who had performed professionally for a minimum of 10 years were included in the study. Thirty-six age-matched nondancers with injuries or pain in various lower extremity joints were used as controls. MAIN OUTCOME MEASURES: This study measured radiographic findings of osteoarthrosis, including sclerosis, joint space narrowing, osteophytes, and subchondral cysts; hypermobility (after Klemp) as manifested by > 3 of 5 tests being positive; and the dancers' reasons for retirement. RESULTS: Changes of arthrosis were found in 34 of 56 joints in 14 dancers and in 3 of 36 joints in 36 nondancers. Hip calcifications were found in 10 hips in 7 dancers and in 1 nondancer's hip. None of the participants in this study was hypermobile or had retired because of arthrosis. CONCLUSIONS: The prevalence of arthrosis in knees, ankles, and first metatarsophalangeal joints in young dancers was increased when compared to that of nondancers in the same age group. Arthrosis does not necessarily cause retirement from a performance career.     

Prevention of acute renal failure

Acute renal failure (ARF) induced by therapeutic agents that are nephrotoxic (e.g., gentamicin, cisplatin, amphotericin, and nonsteroidal anti-inflammatory drugs) or hypotension associated with anesthesia and surgery unfortunately occur with some regularity in small animal practice. Several clinical conditions have been identified that can increase the risk of hospital-acquired ARF in dogs. Recognition of these risk factors allows the clinician to assess the risk/benefit ratio for various drugs and/or procedures. Additionally, initiating protective measures and increasing the monitoring of renal function in those patients that require potentially harmful treatment may decrease the incidence of hospital-acquired ARF.     

Congestive heart failure

The differentiation between systolic and diastolic CHF is clinically important because it allows one to formulate an appropriate therapeutic regimen. As a rule, ACE inhibitors have become a major component in the treatment of systolic heart failure; diuretics, digoxin, and other vasodilators are used in conjunction with them. Optimal therapy for diastolic heart failure remains to be defined. Further research is required for this subset of patients. Numerous other support measures, such as counseling, activity, diet, patient knowledge of medications, and compliance, all affect the patient's outcome.     

Treatment of heart failure

Heart failure is a disease which involves not only the heart but the entire circulatory system. Progression is directly related to interactions between myocardial disorders and neurohormonal and circulatory phenomena. Advances in treatment have resulted more from the development of vasodilator drugs with neurohormonal effects than from drugs with a direct effect on the myocardium. Diuretics are essential due to their rapid functional effect and the reduction in pressure on the ventricle wall. The effectiveness of digitalics is recognized not only in patients with atrial fibrillation, but also in those in sinus rhythm with ischemic heart disease. Conversion enzyme inhibitors are useful in all stages of heart failure, improving both quality of life and life expectancy as well as limiting myocardial and vascular remodeling and retarding progression of ventricular dysfunction. As current progress in the treatment of heart failure has not greatly reduced mortality, prevention is the major challenge facing all physicians. Treatment of asymptomatic ventricular function is one rational approach.     

Abdominal aortic thrombosis mimicking aortic coarctation in a newborn with heart failure]

The case of a neonate in heart failure with the classical signs of coarctation of the aorta is described. Two dimension and Doppler echocardiography ruled out coarctation of the aorta and an abdominal ultrasonography detected a large thrombotic formation in the abdominal aorta, confirmed at necropsy.     

Preventing congestive heart failure

The morbidity, mortality and health care costs associated with congestive heart failure make prevention a more attractive public health strategy than treatment. Aggressive management of etiologic factors, including hypertension, coronary artery disease, valvular disease and excessive alcohol intake, can prevent the left ventricular remodeling and dysfunction that lead to heart failure. Early intervention with angiotensin converting enzyme inhibitors in patients with chronic left ventricular dysfunction can prevent, as well as treat, the syndrome. Several intervention strategies in patients with acute myocardial infarction can slow or prevent the left ventricular remodeling process that antedates congestive heart failure. The primary care physician must be alert to the need for aggressive intervention to reduce the burden of heart failure syndrome on the patient and on society.     

Apoptosis in heart failure

A characteristic feature of heart failure is the progressive worsening of ventricular function over months or years despite the absence of clinically apparent intercurrent adverse events. The mechanism or mechanisms responsible for this hemodynamic deterioration are not known but may be related to progressive intrinsic contractile dysfunction of residual viable cardiac myocytes, or to ongoing degeneration and loss of myocytes, or both. This report will address the concept of ongoing cardiac myocyte loss that may occur during the course of evolving heart failure viewed from the perspective of apoptosis or "programmed cell death" as the potential mediator of cardiac muscle cell loss. In recent years, several studies have shown that constituent myocytes of failed explanted human hearts and hearts of animals with experimentally induced heart failure undergo apoptosis. Recent studies have shown that cardiac myocyte apoptosis also occurs after acute myocardial infarction, as well as in the hypertrophied heart and the aging heart, conditions frequently associated with the development of heart failure. Considerable work has also been conducted and novel concepts advanced to explain potential molecular triggers of cardiac myocyte apoptosis in heart failure. Although available data support the existence of myocyte apoptosis in the failing heart, questions essential to our understanding of the importance of myocyte apoptosis in this disease process remain unanswered. Lacking are studies aimed at identifying physiological factors inherent to heart failure that trigger myocyte apoptosis. Also lacking are studies that address the importance of myocyte apoptosis in the progression of left ventricular dysfunction. If loss of cardiac myocytes through apoptosis can be shown to be an important contributor to the progression of heart failure, and if factors that trigger apoptosis in the heart can be identified, such knowledge can potentially lead to the development of novel therapeutic modalities aimed at preventing, or at the very least retarding, the process of progressive ventricular dysfunction and the ultimate transition toward end-stage, intractable heart failure.     

Hypercoagulability in heart failure

Thromboembolism is an important complication in patients with heart failure. A variety of factors associated with heart failure predispose to thrombosis. These include vascular pathology, increased coagulability, and impaired flow. The focus of this review is to summarize data on platelet function and coagulation indices in heart failure. Several studies have shown that patients with heart failure have increased plasma concentrations of beta-thromboglobulin, a marker of platelet activation. Increased plasma concentrations of fibrinopeptide A and thrombin activation have also been demonstrated. In addition, plasma concentrations of endothelial procoagulants, von Willebrand factor, fibrinolytic products, and D-dimer are also increased during heart failure. If platelet activation and hypercoagulability are a surrogate for clinical events, treatment with antiplatelet or anticoagulant therapy can potentially reduce thromboembolism and mortality in heart failure.     

Pacing and heart failure

Conventional dual-chamber cardiac pacing with the right ventricular pacing catheter positioned at the apex of the right ventricle was proposed eight years ago by Hochleitner as primary treatment of refractory cardiac failure. Although the preliminary results were encouraging, those at long-term and subsequent studies were less favourable in this indication. Biventricular pacing is now a technical possibility and allows at least partial correction of the electromechanical abnormalities observed in dilated cardiomyopathy. The preliminary results of biventricular pacing in patients with refractory cardiac failure due to dilated cardiomyopathy with major intraventricular conduction defects are very encouraging. This new therapeutic approach should now be validated by controlled, randomised therapeutic trials.     

Nitrates in heart failure

Organic nitrates have been used widely in the treatment of chronic congestive heart failure. These drugs have been shown to have beneficial hemodynamic effects both at rest and during dynamic and isometric exercise. In combination with hydralazine, nitrates have been shown to improve exercise tolerance, enhance left ventricular ejection fraction, and prolong survival. The potential limitations of nitrate therapy are related to dose-related nitrate resistance and the development of nitrate tolerance. More information is needed regarding the usefulness of nitrate therapy without hydralazine and the additional benefits of these drugs in patients already treated with angiotensin converting enzyme inhibitors.     

Management of chronic heart failure

Throughout the last years the concept and methods of treatment of chronic heart failure have considerably changed. The objective of the treatment is not only the relief of the symptoms, but also prevention of the onset and progression of the disease. The emphasis of treatment aims to moderate the increased neuroendocrine activity and thus to prevent myocardial damage. This review summarizes our knowledge concerning the treatment of chronic heart failure due to left ventricular dysfunction. It is based on former American guidelines and especially on the guideline of the Task Force of the European Society of Cardiology. The treatment of systolic and diastolic dysfunction of left ventricle are separately discussed. Emphasis is laid on the non pharmacologic treatment of heart failure. The treatment with ACE-inhibitors, diuretics, betablockers, digitalis, calcium antagonists and other drugs as well as the invasive procedures are also discussed.