Sex differences in response to chronic heart failure therapies

Sex-related differences in clinical and laboratory characteristics, course and prognosis are well documented in patients with heart failure. However, most information regarding heart failure therapies has been obtained from studies conducted primarily in men. Reviewing the existing literature indicates that the recommendations regarding pharmacological and device therapies should apply similarly to men and women. One possible exception, however, is the possibility of more benefit derived from angiotensin receptor blockers in women, and from angiotensin converting enzyme inhibitors in men. Future clinical trials should be conducted either exclusively in women or have a larger representation of women to insure the adequate assessment of the potential benefit versus risk in women.     

Sex differences in response to chronic heart failure therapies

Sex-related differences in clinical and laboratory characteristics, course and prognosis are well documented in patients with heart failure. However, most information regarding heart failure therapies has been obtained from studies conducted primarily in men. Reviewing the existing literature indicates that the recommendations regarding pharmacological and device therapies should apply similarly to men and women. One possible exception, however, is the possibility of more benefit derived from angiotensin receptor blockers in women, and from angiotensin converting enzyme inhibitors in men. Future clinical trials should be conducted either exclusively in women or have a larger representation of women to insure the adequate assessment of the potential benefit versus risk in women.     

Future therapies for heart failure

The treatment of heart failure has changed as the understanding of the disease evolves. Heart failure remains the only cardiovascular disease that continues to rise in both incidence and prevalence, despite recent advances in treating symptoms and thwarting disease progression. Many opportunities exist for improving patient outcomes with pharmaceutical agents and technologies available now or in the near future. This article discusses recently approved drugs and devices and clinical trials that may affect the management of this challenging disease.     

Upcoming therapies for heart failure

Treatment of maladaptive neurohormonal activation in congestive heart failure (CHF) has been successful because basic cardiovascular science findings have been confirmed or dismissed through the use of well-controlled, large-scale clinical trials. It should be no surprise that this exciting approach is evolving toward novel agents and devices directed toward other pathways involved in CHF neurohormonal/cytokine activation. Several of these are in advanced clinical development and are likely to play prominent roles in CHF therapy in the near future.     

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.     

The use of inotropic agents in acute and chronic congestive heart failure

This article reviews our current understanding of the physiology of myocardial contraction; recent research into its mechanical, macromolecular, and biochemical foundations; and its role in the clinical syndromes of congestive heart failure. This review serves as a background for discussing the mechanism of action and pharmacology of currently available and experimental inotropic agents. The clinical applications of these drugs are discussed and the successes and failures of the pharmacologic approach to patients with congestive heart failure analyzed.     

米力农治疗慢性心力衰竭急性加重期临床疗效观察

目的观察米力农治疗慢性心力衰竭急性加重期的临床疗效。方法 92例慢性心力衰竭患者随机分为两组。A组使用洋地黄、ACEI、利尿剂、硝酸脂类等药物常规治疗;B组在A组基础上,加用米力农静脉滴注,观察疗程2周。对比两组左室射血分数(LVEF)、左室舒张末期内径(LVDd)、心率、血压、临床心功能NYHA分级的改变及药物不良反应。结果两组患者治疗2周后心功能均有显著改善,治疗前后差异具有统计学意义(P<0.05),B组与A组相比,患者心率减慢,血压、LVDd降低,LVEF升高的幅度更显著(P<0.05),差别有显著性。结论米力农治疗慢性心力衰竭急性加重期,临床疗效显著且安全可靠。     

急性心力衰竭的诊治进展：2016 ESC 急慢性心力衰竭诊断和治疗指南

根据《中国心血管病报告2015》,目前我国心血管病死亡占城乡居民总死亡原因的首位,心血管病的病死率仍处于持续上升阶段［1］。心力衰竭（简称心衰）是所有心脏病患者自然病程的归宿,目前对于心衰的治疗仍困难重重。全球心血管病专家一直致力于这一领域的研究,取得了许多重要的进展,进一步完善了心血管重症领域的防治策略。     

Valsartan in chronic heart failure

OBJECTIVE: To evaluate the evidence for valsartan in the treatment of heart failure and determine its need for formulary inclusion. DATA SOURCES: OVID and PubMed databases were searched (1983-June 2004) using the key words angiotensin-receptor blocker, heart failure, valsartan, Diovan, and angiotensin-converting enzyme inhibitor. Only English-language literature was selected. STUDY SELECTION AND DATA EXTRACTION: Pharmacology and pharmacokinetic evaluations for valsartan were selected. Prospective, randomized clinical trials investigating the use of valsartan and other angiotensin-receptor blockers (ARBs) in chronic heart failure were evaluated. DATA SYNTHESIS: Valsartan, a selective antagonist for angiotensin receptor subtype 1, is the first ARB to be approved for use in chronic heart failure. Clinical trial data support valsartan as an alternative to angiotensin-converting enzyme (ACE) inhibitors in ACE inhibitor-intolerant patients with chronic heart failure. Valsartan is generally well tolerated, with renal impairment, elevated serum creatinine and potassium levels, and dizziness being the most common adverse effects; consequently, patients experiencing those adverse events while taking ACE inhibitors are likely to experience them with valsartan. Although further study is needed, differences in effectiveness among races may exist with use of valsartan; however, at this time, valsartan is recommended as an alternative to ACE inhibitors regardless of race. Candesartan and losartan have been studied in similar settings. Candesartan's data support its use in heart failure; however, losartan's data have been less consistent. CONCLUSIONS: Valsartan is a safe and effective alternative for heart failure patients intolerant of ACE inhibitors. Valsartan has not been shown to be safe and effective when used in combination with ACE inhibitors.     

Novel biomarkers for heart failure

Heart failure (HF) has proven to be a major burden on the health system. The continuing prevalence of the condition and its rising associated costs and care, has amplified the need for earlier diagnosis, better risk stratification and cost-effective treatment to cut rates of hospitalization. Biomarkers seem poised to undertake such tasks, with biomarker management of patients with HF quickly evolving over the past several years. Biomarker guided diagnosis and treatment has become vital, especially during the acute setting in which the majority of patients with HF, were initially present. An adequate assessment of risk requires a multi-marker approach to a given HF patient. Established markers including brain natriuretic peptide and NT-proBNP are a significant clinical aid to physicians, though their utility is limited. In the past few years, momentous effort has been put into the discovery of new biomarkers. These endeavors have led to the emergence of several capable and promising biomarkers for HF management including troponins, mid-regional pro-adrenomedullin, GDF-15, C-reactive protein, Galectin-3, IL-6, ST-2, neutrophil gelatinase-associated lipocalin, copeptin and procalcitonin. This review will offer an insight into the novel biomarkers considered as the cutting-edge in the diagnosis and management of HF.     

Clinical and echocardiographic correlates of serum copper and zinc in acute and chronic heart failure

Aim

Emerging evidence suggests a pathophysiological role of micronutrient dyshomeostasis in heart failure, including promotion of adverse remodeling and clinical deterioration. We sought to evaluate serum copper (Cu) and zinc (Zn) levels in acute (AHF) and chronic (CHF) heart failure.

Methods

We studied 125 patients, 71 % male, aged 69 ± 11 years, 37 % with preserved left ventricular ejection fraction (LVEF ≥40 %) (HFPEF), including 81 with AHF and 44 with CHF; 21 healthy volunteers served as controls. Serum Cu and Zn levels were determined using air–acetylene flame atomic absorption spectrophotometry.

Results

Serum Cu levels were significantly higher in AHF (p = 0.006) and CHF (p = 0.002) patients compared to controls after adjusting for age, gender and comorbidities, whereas they did not differ between AHF and CHF (p = 0.840). Additionally, serum Cu in patients with LVEF <40 % was significantly higher compared to both controls (p < 0.001) and HFPEF patients (p = 0.003). Serum Zn was significantly lower in AHF (p < 0.001) and CHF (p = 0.039) compared to control after adjusting for the above-mentioned variables. Moreover, serum Zn was significantly lower in AHF than in CHF (p = 0.015). In multiple linear regression, LVEF (p = 0.033) and E/e ratio (p = 0.006) were independent predictors of serum Cu in total heart failure population, while NYHA class (p < 0.001) and E/e ratio (p = 0.007) were independent predictors of serum Zn.

Conclusion

Serum Cu was increased both in AHF and CHF and correlated with LV systolic and diastolic function. Serum Zn, in contrast, was decreased both in AHF and CHF and independently predicted by clinical status and LV diastolic function.     

Low-frequency electromyostimulation and chronic heart failure

Low-frequency electromyostimulation (EMS) acts on the skeletal muscle abnormalities that aggravate intolerance to effort in patients with chronic heart failure (CHF). It improves the oxidative capacity of muscles and thus enhances aerobic performance and physical capacity to almost the same degree, as does conventional physical training. No local or hemodynamic intolerance has been reported, even in cases of severe CHF. However, the presence of a pacemaker is one of the relative contra-indications (prior evaluation of tolerance is required), while that of an implanted defibrillator is one of the absolute contra-indications. EMS is an alternative to physical effort training when the latter is impossible due to a high degree of deconditioning or because there is a contra-indication, which may be temporary, due to the risk of acute decompensation and/or rhythm troubles. EMS can also be used in patients waiting for a heart transplant or in CHF patients who are unwilling to engage in physical activities. As EMS is not expensive and easy to set up, its use is likely to develop in the future.     

Cardiac remodeling in chronic heart failure

Left ventricular remodeling plays an important role in the progression of chronic heart failure. The early remodeling is an adaptive response to the increased load(i.e. hypertension) and/or the loss of contractile component (i. e. myocardial infarction) in order to maintain the pumping capacity. This process includes cardiac hypertrophy associated with myocyte hypertrophy and myocardial fibrosis. However, the persistence of the inadequate overload results in the decompensation of the adaptive mechanism. Finally, left ventricle is enlarged and the systolic function is impaired.     

Reversing chronic remodeling in heart failure

Chronic heart failure is a debilitating condition with significant morbidity, mortality and an increasing economic burden. The past 20 years have witnessed great strides in both medical and device-based therapies for heart failure. Central to these developments has been the ability to favorably reverse the chronic processes by which the failing heart remodels. In addition to pharmacotherapies, such as beta-blockade, and inhibition of the renin-angiotensin-aldosterone system, surgical remodeling, containment devices and new methods to restore synchronous contraction have been added to the armamentarium, in some instances, providing clear improvement to both symptoms and mortality. In more advanced stages of heart failure, left ventricular-assist devices provide marked unloading of the failing ventricle and such therapy has provided unique insights into the molecular and cellular mechanisms underlying reverse remodeling, given the immediate access to cardiac tissue. Genetic and cellular approaches, as well as new small molecule targets, may provide future avenues for reverse remodeling of the failing heart, improving symptoms and disease outcome.