Drug-induced heart failure

Heart failure is a clinical syndrome that is predominantly caused by cardiovascular disorders such as coronary heart disease and hypertension. However, several classes of drugs may induce heart failure in patients without concurrent cardiovascular disease or may precipitate the occurrence of heart failure in patients with preexisting left ventricular impairment. We reviewed the literature on drug-induced heart failure, using the MEDLINE database and lateral references. Successively, we discuss the potential role in the occurrence of heart failure of cytostatics, immunomodulating drugs, antidepressants, calcium channel blocking agents, nonsteroidal anti-inflammatory drugs, antiarrhythmics, beta-adrenoceptor blocking agents, anesthetics and some miscellaneous agents. Drug-induced heart failure may play a role in only a minority of the patients presenting with heart failure. Nevertheless, drug-induced heart failure should be regarded as a potentially preventable cause of heart failure, although sometimes other priorities do not offer therapeutic alternatives (e.g., anthracycline-induced cardiomyopathy). The awareness of clinicians of potential adverse effects on cardiac performance by several classes of drugs, particularly in patients with preexisting ventricular dysfunction, may contribute to timely diagnosis and prevention of drug-induced heart failure.     

Congenital heart disease and heart failure

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.     

心率减速力对肺心病心力衰竭患者的预警研究

目的 探讨心率减速力值对肺心病心力衰竭患者的预警作用.方法 应用24h动态心电图记录60例肺心病心力衰竭患者和60名健康者（对照组）的心率减速力值和心率加速力值,并进行预警分析.结果 60例肺心病心力衰竭患者心率减速力值≥4.5 ms,1年内死亡率为3.33％％,DC值2.6～4.4 ms为6.66％,DC值≤2.5ms为13.33％,P＜0.01;对照组心率减速力各值中无死亡病例,心率加速力值≤-7.0 ms.除肺心病患者组1年死病死率为1.66％外,余均无死亡.结论 心率减速力值测定能定量、单独分析和测定迷走神经作用的强度,对肺心病心力衰竭高危人群筛选与预警具有较强的实用价值.     

Platelets and heart failure.

Heart failure is associated with increased risk of venous thromboembolism, stroke, and sudden death. Platelet abnormalities have been well described in heart failure but the significance of platelets in contributing to the thromboembolic complications of heart failure remains uncertain. Furthermore, the role of antiplatelet agents in heart failure remains unclear. This review will focus on platelet activation and the role of platelet dysfunction in heart failure, with particular regard to pathophysiology and outcome. The effects of heart failure therapeutics on platelet function and antiplatelet therapy in heart failure will also be discussed.     

Epidemiology of heart failure

Of all persons aged over 40 years, approximately 1% have heart failure. The prevalence of heart failure doubles with each decade of life, and is around 10% in persons over 70 years of age. In Spain, heart failure causes nearly 80,000 hospital admissions every year. As in other developed countries, heart failure is the most frequent cause of hospitalization among persons 65 years of age and over, and is responsible for 5% of all hospitalizations. The incidence of heart failure increases with age, and reaches 1% per year in those over 65. Heart failure is a progressive, lethal disorder, even with adequate treatment. Five-year survival is around 50%, which is no better than that for many cancers. In Spain, heart failure is the third leading cause of cardiovascular mortality, after coronary disease and stroke. In 2000, heart failure caused 4% of all deaths and 10% of cardiovascular deaths in men; the corresponding figures for women were 8% and 18%. In recent decades the prevalence and number of hospitalizations due to heart failure have increased steadily in developed countries. Heart failure will probably continue to increase in coming years: although its incidence has not materially decreased, survival is increasing due to better treatment. The control of risk factors for hypertension and ischemic heart disease, the main causes of heart failure in Spain, is the only method to halt the foreseeable increase in heart failure in the near future.     

急性心力衰竭综合病因评分预计死亡率研究

目的 探讨急性心力衰竭病因评分在急性心力衰竭疾病中的应用价值.方法 采用APACHEⅡ评分、心力衰竭基础病因及诱因综合评分,在此评分基础上对42 例急性心力衰竭患者预计死亡率进行评估并建立预计死亡率模型,分层计算群体预计死亡率.结果 根据急性心力衰竭病因评分分值进行分组,随着分值逐渐升高,实际病死率和预计死亡率也逐渐升高,死亡组评分均值显著高于生存组(P＜0.05).结论 急性心力衰竭病因评分系统简易实用,可用于院前急救及急诊急性心力衰竭患者初步评估.     

Treatment of chronic systolic heart failure secondary to Chagas heart disease in the current era of heart failure therapy

The treatment of chronic heart failure secondary to Chagas disease has been based on extrapolation of data achieved in the treatment of non-Chagas disease heart failure. Because beta-blockers decrease the incidence of sudden cardiac death in non-Chagas disease heart failure and sudden cardiac death occurs preferentially in patients with mild Chagas disease heart failure, beta-blockers may be administered first to class I/II patients with Chagas disease heart failure. In advanced Chagas disease heart failure, angiotensin-converting enzyme inhibitor and diuretics may be given at first to compensate for congestive symptoms. After clinical status improvement, beta-blockers should be given at targeted doses, if necessary reducing angiotensin-converting enzyme inhibitor doses. Primary and secondary prevention of sudden cardiac death may be accomplished with implantable cardioverter defibrillators because of the high recurrence of life-threatening arrhythmias despite amiodarone administration. In refractory heart failure, heart transplantation is the treatment of choice.     

Congenital heart disease: the original heart failure syndrome.

Heart failure is characterised by a triad comprising cardiac abnormality, exercise limitation and neurohormonal activation. The 2% of the adult population who suffer with heart failure are known to derive both symptomatic and prognostic benefit from exercise and pharmacologic neurohormonal antagonism. The existence of heart failure has traditionally been considered in the context of ischaemic, hypertensive, valvular and myopathic disease but in this article we develop the argument that patients with congenital heart disease also manifest all the pathophysiological criteria that constitute the chronic heart failure syndrome. We discuss the inherent limitations to a purely anatomical approach to congenital heart disease, bring attention to the large and rapidly growing population of adults with this condition and conclude by calling for a therapeutic approach to congenital heart disease that is based on the heart failure paradigm.     

Therapy for diastolic heart failure

There is little objective to guide the therapy of patients with diastolic heart failure. Because of the similarities of pathophysiology abnormalities in diastolic and systolic heart failure, it is a reasonable inference to suggest that the proven therapy for systolic heart failure may also be of benefit in patients with diastolic heart failure. Treatment of underlying or exacerbating conditions in diastolic heart failure, such as hypertension, left ventricular hypertrophy, ischemia, diabetes, anemia, obesity and pulmonary disease is an important means of managing diastolic heart failure. Control of systolic blood pressure is effective in improving and preventing the development of diastolic heart failure. Treatment of diastolic heart failure is most effective when it is associated with hypertension. Production of systolic arterial pressure acutely reduces pulmonary congestion, ischemia, and chronically may lead to regression of left ventricular hypertrophy. Patients with diastolic heart failure in the absence of hypertension are very difficult to treat.     

Beta blockers in heart failure

The rationale for beta blockade in heart failure is now well established. Heart failure mortality, which is predicted by neurohormonal activation, remains high despite modern treatment, including angiotensin-converting enzyme (ACE) inhibition, and additional neurohormonal blockade has further therapeutic potential. Previous clinical trial experience in heart failure, most of which has been in patients with idiopathic cardiomyopathy, indicates consistent improvement in ventricular function, although variable changes in symptoms and exercise performance. However, the major burden of heart failure occurs in patients with ischemic heart disease, and in this respect it is notable that beta blockade following myocardial infarction confers a significant mortality benefit in subgroups with heart failure. An overview of all currently available randomized clinical trials of beta blockade in heart failure, which includes more than 1600 patients, indicates a mortality risk reduction of approximately 20%, but with wide confidence intervals. A large scale trial with several thousand patients is required to confirm reliably a plausible 20% mortality reduction with beta blockade in heart failure. The dissociation of clinical and mortality effects demonstrated with other heart failure treatments indicates the necessity for an appropriately powered mortality study that could define a major improvement in heart failure therapy for the future. The response to beta blockade will vary according to heart failure severity. A cautious dosetitration approach is required in all cases. In severe heart failure, symptomatic improvement may result, but for the large group of patients with moderate and stable heart failure, the principal aim of treatment is improved longevity.     

Towards defining heart failure in adults with congenital heart disease

Injury to the myocardium disrupts geometric integrity and results in changes to intracardiac pressure, wall stress and tension, and the pattern of blood flow through the heart. Significant disruption to pump function results in heart failure which is defined in terms of symptoms: breathlessness and fatigue, signs of salt and water retention, and neurohormonal activation. This syndrome most commonly occurs in the context of injury due to ischaemic heart disease and dilated cardiomyopathy but because patients with congenital heart disease (CHD) are born with sometimes gross distortions of cardiac anatomy they too are subject to the forces that drive heart failure. This paper explores the available data relating to the clinical and neurohormonal manifestations of heart failure in patients with congenital heart disease and describes how, by additionally exploring events at a cellular level, we may be able to arrive at a definition of heart failure relevant to this population.     

Novel drugs for heart rate control in heart failure

In patients with heart failure, increased sympathetic activity is associated with a positive chronotropic stimulation leading to accelerated resting heart rate. Elevated heart rate (HR) is a risk factor for cardiovascular events, both in the general population and in patients with heart failure. Ivabradine is a pure HR-lowering agent, and it does not affect myocardial contractility, blood pressure, intracardiac conduction, or ventricular repolarization. In clinical trials such as BEAUTIFUL, CARVIVA HF, SHIFT, and INTENSIFY in patients with systolic left ventricular dysfunction, heart rate reduction with ivabradine brought positive outcomes. However, the results of the recent meta-analysis are rather neutral. In a diabetes mouse model of heart failure with preserved ejection fraction (HFpEF), selective heart rate reduction by I_f inhibition improved vascular stiffness, left ventricular (LV) contractility, and diastolic function. However, EDIFY (Effect of ivabradine in patients with heart rate with preserved ejection fraction) trial show that the use of ivabradine in patients with HFpEF is not supported. The further clinical trials investigating the use of ivabradine in heart failure should be carried out.     

Pediatric heart failure

Heart failure is a clinical syndrome which presents similarities and differences between children and adults; in pediatric age the spectrum of causes of heart failure is wide and congenital heart defects are the most common etiology. Volume and pressure overload on a 'normal myocardium' is the classical physiological pattern while myocardial contractile dysfunction of different etiology is much less observed in the pediatric population. However there are some peculiarities in clinical presentation of heart failure in infants and small children. The medical therapy cornerstones still remain loop diuretics, angiotensin-converting enzyme inhibitors, beta-blockers and digitalis. There are also some reported experiences with new inotropics drugs in acute heart failure. In pediatric cardiology there are few prospective studies on pharmacology of heart failure and the data are often extrapolated from adult large trials. Non pharmacological treatment with autonomic implantable cardioverter defibrillators and resynchronization therapy as well as the surgically implant of ventricular assist devices are increasingly employed in children. Cardiac transplantation is currently the treatment option with good outcome and long-term survival in pediatric patients with end-stage or refractory heart failure.     

The effects of heart rate control in chronic heart failure with reduced ejection fraction

Elevated heart rate has been associated with worse prognosis both in the general population and in patients with heart failure. Heart rate is finely modulated by neurohormonal signals and it reflects the balance between the sympathetic and the parasympathetic limbs of the autonomic nervous system. For this reason, elevated heart rate in heart failure has been considered an epiphenomenon of the sympathetic hyperactivation during heart failure. However, experimental and clinical evidence suggests that high heart rate could have a direct pathogenetic role. Consequently, heart rate might act as a pathophysiological mediator of heart failure as well as a marker of adverse outcome. This hypothesis has been supported by the observation that the positive effect of beta-blockade could be linked to the degree of heart rate reduction. In addition, the selective heart rate control with ivabradine has recently been demonstrated to be beneficial in patients with heart failure and left ventricular systolic dysfunction. The objective of this review is to examine the pathophysiological implications of elevated heart rate in chronic heart failure and explore the mechanisms underlying the effects of pharmacological heart rate control.     

Management of acute heart failure in adult patients with congenital heart disease

Heart failure is an increasing reason for hospitalization and the leading cause of death in patients with adult congenital heart disease (ACHD). Recently, the European Society of Cardiology and the American Heart Association published consensus documents on the management of chronic heart failure in ACHD patients. However, little data and/or guidelines are available for the management of (sub)acute heart failure. The ACHD population is heterogeneous by definition and often has complex underlying anatomy, which could pose a challenge to the physician confronted with the ACHD patient in (sub)acute heart failure. Recognizing the underlying anatomy and awareness of the possible complications related would result in better treatment, avoid unnecessary delays, and improve outcomes of the ACHD patient with (sub)acute heart failure. This review focuses on the management of (sub)acute heart failure in ACHD with specific attention to lesion-specific issues.     

合并心脏病的住院孕产妇发生心力衰竭危险因素的分析

目的探讨合并心脏病的孕产妇发生心力衰竭的危险因素。方法回顾分析2008年1月至2013年12月于内江市第一人民医院住院的340例合并心脏病的孕产妇（以下简称＂心脏病孕产妇＂）的临床资料,以孕产期发生心力衰竭患者为观察组,同期未发生心力衰竭的心脏病孕产妇为对照组。采用单因素和多因素Logistic逐步回归法分析心脏病孕产妇发生心力衰竭的危险因素。结果 340例心脏病孕产妇中先天性心脏病132例（38.8%）、风湿性心脏瓣膜病86例（25.3%）、心律失常63例（18.5%）、高血压心脏病33例（9.7%）、围生期心肌病26例（7.6%）。65例（19.1%）患者发生心力衰竭,4例（1.2%）患者死亡。多因素Logistic逐步回归分析：年龄≥35岁、孕前NYHA心功能分级≥Ⅱ级、肺动脉压力〉50 mmHg（1 mmHg=0.133 kPa）、基础心率〉100次/min、孕前发生心脏事件是心脏病孕产妇发生心力衰竭的独立危险因素,而孕前咨询和产前规律检查是其保护性因素。结论心脏病孕产妇发生心力衰竭受多种因素影响,在临床工作中应针对相应危险因素给予积极的干预措施,以减少心力衰竭的发生。     

Diagnosing diastolic heart failure

BACKGROUND: increasing evidence supports the existence of left ventricular diastolic dysfunction as an important cause of congestive heart failure, present in up to 40% of heart failure patients. AIM: to review the pathophysiology of LV diastolic dysfunction and diastolic heart failure and the currently available methods to diagnose these disorders. RESULTS: for diagnosing LV diastolic dysfunction, invasive hemodynamic measurements are the gold standard. Additional exercise testing with assessment of LV volumes and pressures may be of help in detecting exercise-induced elevation of filling pressures because of diastolic dysfunction. However, echocardiography is obtained more easily, and will remain the most often used method for diagnosing diastolic heart failure in the coming years. MRI may provide noninvasive determination of LV three-dimensional motion during diastole, but data on correlation of MRI data with clinical findings are scant, and possibilities for widespread application are limited at this moment. CONCLUSIONS: in the forthcoming years, optimal diagnostic and therapeutic strategies for patients with primary diastolic heart failure have to be developed. Therefore, future heart failure trials should incorporate patients with diastolic heart failure, describing precise details of LV systolic and diastolic function in their study populations.     

舒张性心力衰竭的细胞生物学机制

舒张性心力衰竭主要指舒张功能异常的充血性心力衰竭.舒张性心力衰竭十分常见,且预后也接近于收缩性心力衰竭.舒张性心力衰竭的发生机制比较复杂,钙超载为导致舒张性心力衰竭的主要因素,围绕其细胞生物学发病机制的研究渐成为热点.     

Epidemiology of heart failure

The heart failure syndrome has first been described as an emerging epidemic about 25 years ago. Today, because of a growing and ageing population, the total number of heart failure patients still continues to rise. However, the case mix of heart failure seems to be evolving. Incidence has stabilized and may even be decreasing in some populations, but alarming opposite trends have been observed in the relatively young, possibly related to an increase in obesity. In addition, a clear transition towards heart failure with a preserved ejection fraction has occurred. Although this transition is partially artificial, due to improved recognition of heart failure as a disorder affecting the entire left ventricular ejection fraction spectrum, links can be made with the growing burden of obesity‐related diseases and with the ageing of the population. Similarly, evidence suggests that the number of patients with heart failure may be on the rise in low‐income countries struggling under the double burden of communicable diseases and conditions associated with a Western‐type lifestyle. These findings, together with the observation that the mortality rate of heart failure is declining less rapidly than previously, indicate we have not reached the end of the epidemic yet. In this review, the evolving epidemiology of heart failure is put into perspective, to discern major trends and project future directions.     

Increased circulating calcitonin gene-related peptide in congestive heart failure caused by congenital heart disease

Calcitonin gene-related peptide has potent vasodilatory and inotropic actions. The aim of this study was to characterize the changes in this peptide in children with varying degrees of heart failure secondary to congenital heart disease with left to right shunt and to assess its relationship to systolic pulmonary arterial pressure. Plasma calcitonin gene-related peptide levels were measured in 131 children including 13 healthy ones, 43 with various degrees of heart failure secondary to congenital heart disease, and 75 with congenital heart disease without heart failure. In patients with heart failure, calcitonin gene-related peptide concentrations were markedly elevated (15.8 +/- 2.1 pg/mL) as compared with healthy control subjects (7.0 +/- 0.8 pg/mL, P < 0.05) or patients with congenital heart disease but without heart failure (18.6 +/- 1.2 pg/mL, P < 0.01). Compared with the controls, there were highly significant stepwise increases in the calcitonin gene-related peptide levels in the mild (n = 15), moderate (n = 12), and severe (n = 16) heart failure subgroups by 1.5, 1.7 and 3.4 fold, respectively. The plasma calcitonin gene-related peptide levels also correlated directly with the pulmonary arterial systolic pressure (r = 0.515, P < 0.0001). The results of this study indicate that congestive heart failure secondary to congenital heart disease with increased pulmonary flow is associated with elevated levels of calcitonin gene-related peptide that are related to disease severity. Pulmonary overcirculation may play a role in upregulation of calcitonin gene-related peptide in congestive heart failure.