Heart failure monitor最新文献

Hypertrophy is the response of cardiac muscle to altered hemodynamic loads. The increase in ventricular wall thickness normalizes increased wall stress and, therefore, hypertrophy is initially beneficial. However, progressive hypertrophy is associated with deleterious long-term consequences that significantly increase the risk of mortality. This review outlines the events associated with hypertrophy and discusses how strategies can be aimed at preventing pathological hypertrophy. The fact that heart failure is one of the leading causes of death in the West demands a detailed understanding of the complexities underlying this response. Complete dissection of hypertrophy will aid the development of novel therapeutic approaches that could take advantage of its beneficial features while removing the deleterious consequences caused by hypertrophic growth of the heart. Heart Fail Monit 2008;5(4):112-8.

The rapidly evolving insights into the protective and modulatory function of neuregulin-1 (NRG-1) in the adult heart are discussed in this review. The actions of NRG-1 in the adult heart have begun to be elucidated following the unexpected clinical observation that trastuzumab can cause ventricular dysfunction and increases the risk of cardiomyopathy induced by anthracyclines. Trastuzumab is an inhibitory antibody against the NRG receptor erythroblastic leukemia viral oncogene homolog 2 (ErbB2) and is used in the treatment of breast cancer. In vitro studies have demonstrated that NRG-1 promotes growth and survival of isolated cardiomyocytes. Ventricular dysfunction following anti-ErbB2 treatment was initially explained by a loss of ErbB2-dependent cell survival pathways in the heart. However, in vivo studies in genetically modified mice did not uniformly confirm this finding. More recent studies have revealed that NRG-1 counterbalances the adrenergic inotropic response of the adult myocardium through an obligatory interaction with the muscarinic cholinergic system. In addition, it was demonstrated that cardiac NRG-1 synthesis and release from the cardiac endothelium, the principal source of NRG-1 in the heart, is dynamically controlled by neurohormonal and biomechanical stimuli, allowing adaptive tuning of ErbB signaling during cardiovascular stress. Cardiac NRG-1 is beginning to emerge as a cardioprotective factor implicated in the physiological regulation of myocardial performance and sympathovagal balances. Cardiac NRG-1/ErbB signaling has implications for the treatment of both cancer and heart failure. As novel ErbB inhibitors are currently being tested in broader oncological indications, there is a need to better understand their cardiovascular side effects. It is possible that pharmacological activation of ErbB signaling is an indirect, beneficial effect of the drugs currently used in heart failure, and this could be a promising therapeutic approach for prevention or reversal of myocardial dysfunction. Heart Fail Monit 2008;5(4):119-24.

At least half of patients with heart failure (HF) suffer from sleep apnea. Growing evidence suggests that there may be a strong pathophysiological link between chronic HF and sleep apnea due to nocturnal oxygen desaturation and sympathetic activation. It seems that sleep apnea contributes to systolic and diastolic HF, reduced left and right ventricular function, and arrhythmia (e.g. atrial fibrillation, bradycardia, or ventricular ectopy). Therefore, treatment of sleep apnea might alleviate cardiac symptoms and improve cardiac function. Nevertheless, the exact role of long-term treatment of sleep apnea in HF patients remains to be elucidated, as important clinical endpoints (e.g mortality) have been assessed in only a few studies. Heart Fail Monit 2008;5(4):106-11.

Diuretics have been the cornerstone of acute heart failure (AHF) therapy for >200 years, although the treatment of chronic heart failure has changed dramatically over the past decades with the introduction of angiotensin-converting enzyme inhibitors, angiotensin II receptor antagonists, beta-blockers, and aldosterone inhibitors. These treatment modalities were never tested prospectively in the acute setting. Furthermore, there is a significant lack of prospective data on the use of diuretics in both chronic (CHF) and AHF. Hence, despite lack of knowledge on their efficacy and safety, diuretics remain an essential component of the current management of AHF and CHF. In the present manuscript we will address the practical concerns regarding diuretic selection, dosage, combination regimens, and the importance of achieving clinical improvement with minimal changes to kidney function in patients with AHF. Heart Fail Monit 2008;6(1):9-19.

Chronic heart failure (HF) is a major cause of morbidity and mortality, and is the reason for more than one in five of all hospital admissions in patients aged >65 years. Major advances in the diagnosis and treatment of HF over the last two decades have proven effective in reducing morbidity and mortality among both men and women, but with less improvement for women and elderly patients. Women and men with HF differ in several respects. Women tend to be older and more often hypertensive, but are less likely to demonstrate any clinical evidence of coronary heart disease (CHD) and more often have preserved ventricular function. Conversely, hypertension plays a greater role in the development of HF in women than in men. Sex differences in systolic and diastolic function in patients with hypertension have been demonstrated. Although men have higher incidence of HF at all ages, lifetime risk is similar in men and women because women live longer. Intervention studies have included far more men than women but in patients with reduced ventricular function there is no evidence to suggest that women benefit less than men from evidence-based treatments, and current guidelines do not differentiate between men and women. There is no consistent recent evidence that women receive poorer quality of care than men. Women with HF have better survival rates than men, which may be due to better systolic function or less CHD among women; however, mortality rates for HF are still very high regardless of sex. As most trials have been targeted towards patients with left ventricular systolic dysfunction, which is less typical for women than for men with HF, more research is needed to help define treatment aimed at improving prognosis for patients with HF and preserved systolic function. In light of these differences and ongoing uncertainties, future European guidelines should incorporate gender issues. Heart Fail Monit 2008;6(1):34-40.

The syndrome of heart failure in adult non-congenital heart disease patients includes myocardial disease and ventricular dysfunction. In the presence of congenital abnormalities the cause of heart failure is often multi-factorial and can be a result of the underlying anomaly, surgical intervention, or ventricular dysfunction. Despite the possible clinical similarities, the two conditions are fundamentally different. In congenital heart disease the neurohormonal system is already abnormal even in the absence of clinical manifestations of heart failure and, in many cases, exercise intolerance is related to cyanosis. The approach to heart failure management in the two etiologies might be similar. Preventative attempts to preserve ventricular function in coronary or valve disease parallels early reparative therapy in congenital heart disease Pharmacological therapy is common for the two conditions, despite the limited number of evidence-based recommendations for congenital diseases. In drug-resistant patients, cardiac electrical resynchronization is an established therapy for treating ventricular asynchrony in non-congenital heart failure sufferers, but has only recently been adopted in selected congenital cases. Due to this, congenital heart disease patients are managed in highly specialized unites in close cooperation with cardiologists and surgeons. The ideal follow-up protocol for such patients remains to be determined, particularly in those individuals with subclinical signs of residual cardiac dysfunction. Heart Fail Monit 2008;6(1):2-8.

The treatment of heart failure (HF) commonly requires a complex pharmacological regimen. Currently HF polypharmacy consists of drugs that target different factors for disease progression, such as altered hemodynamics and elevated neurohumoral factors. Even though a significant improvement of HF has been achieved by combination treatment with regard to morbidity and mortality rate, the increasing numbers and daily doses of drugs bare the risk of potential and sometimes unavoidable drug interactions. Furthermore, comorbidities can be a complication of polypharmacy treatment in HF patients. A pharmacological rationale behind polypharmacy in HF will be discussed on the basis of current treatment recommendations by the American Heart Association and the European Society of Cardiology. Finally, difficulties in polypharmacy regarding the major adverse drug effects and interactions will be outlined. Heart Fail Monitor 2008;6(1):20-27.

Anemia is frequently observed in patients with chronic heart failure (CHF) and is related to an impaired outcome. The origin of anemia in CHF is diverse and is associated with several factors including renal failure, resistance of the bone marrow to erythropoietin (EPO), hematinic deficiencies, and medication use. Recently, several small-scale clinical trials have shown that EPO treatment might improve clinical parameters in anemic heart failure patients. In addition, several preclinical studies have shown that EPO possesses non-hematopoietic effects. This current review focuses on the etiology, consequences, and treatment of anemia in heart failure patients. The pleiotropic effects of EPO in an experimental setting will also be discussed. Heart Fail Monit 2008;6(1):28-33.

Acute heart failure (HF) is characterized by the rapid onset or progression of symptoms and signs secondary to abnormal cardiac function, and remains a common disease associated with high morbidity and mortality rates. Angiotensin-converting enzyme inhibitors (ACEi) are an effective pharmacological option in the treatment of chronic HF, but their effect in acute HF is less well known. This review attempts to summarize the current understanding of acute HF and the pharmacological effects of ACEi in the treatment of acute HF.