In‐hospital worsening heart failure

Acute worsening heart failure (WHF) is seen in a sizable portion of patients hospitalized for heart failure, and is increasingly being recognized as an entity that is associated with an adverse in‐hospital course. WHF is generally defined as worsening heart failure symptoms and signs requiring an intensification of therapy, and is reported to be seen in anywhere from 5% to 42% of heart failure admissions. It is difficult to ascertain the exact epidemiology of WHF due to varying definitions used in the literature. Studies indicate that WHF cannot be precisely predicted on the basis of baseline variables assessed at the time of admission. Recent data suggest that some experimental therapies may reduce the risk of development of WHF among hospitalized heart failure patients, and this is associated with a reduction in risk of subsequent post‐discharge cardiovascular mortality. In this respect, WHF holds promise as a endpoint for acute heart failure clinical trials to better elucidate the benefit of targeted novel therapies. Better understanding of the pathophysiology and a consensus on the definition of WHF will further improve our epidemiological and clinical understanding of this entity.     

Heart failure etiologies and clinical factors precipitating for worsening heart failure: Findings from BIOSTAT-CHF

BackgroundKnowledge on the association between heart failure (HF) etiologies, precipitant causes and clinical outcomes may help in ascertaining patient's risk and in selecting tailored therapeutic strategies.MethodsThe prognostic value of both HF etiologies and precipitants for worsening HF were analyzed using the index cohort of BIOSTAT-CHF. The studied HF etiologies were: a) ischemic HF; b) dilated cardiomyopathy; c) hypertensive HF; d) valvular HF; and e) other/unknown. The precipitating factors for worsening HF were: a) atrial fibrillation; b) non-adherence; c) renal failure; d) acute coronary syndrome; e) hypertension; and f) Infection. The primary outcome was the composite of all-cause death or HF hospitalization.ResultsAmong 2465 patients included in the study, 45% (N = =1102) had ischemic HF, 23% (N = =563) dilated cardiomyopathy, 15% (N = =379) other/unknown, 10% (N = =237) hypertensive and 7% (N = =184) valvular HF. Patients with ischemic HF had the worst prognosis, whereas patients with dilated cardiomyopathy had the best prognosis. From the precipitating factors for worsening HF, renal failure was the one independently associated with worse prognosis (adjusted HR (95%CI) = =1.48 (1.04–2.09), p < 0.001). We found no interaction between HF etiologies and precipitating factors for worsening HF with regard to the study outcomes (p interaction > 0.10 for all). Treatment up-titration benefited patients regardless of their underlying etiology or precipitating cause (p interaction > 0.10 for all).ConclusionsIn BIOSTAT-CHF, patients with HF of an ischemic etiology, and those with worsening HF precipitated by renal failure (irrespective of the underlying HF etiology), had the highest rates of death and HF hospitalization, but still benefited equally from treatment up-titration.     

NT-proBNP in heart failure: therapy decisions and monitoring

With increasing cardiac dysfunction, a complex neurohormonal response results in increasing circulating levels of an array of plasma hormones. Increments in plasma levels of atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) and their amino-terminal congeners are more closely related to cardiac structure and function and to cardiovascular prognosis than changes in other plasma neurohormones. Reports suggest that changes in plasma BNP levels in the course of treatment of acutely decompensated heart failure provide a more powerful prognostic indicator of the likelihood of survival or recurrent decompensation than symptomatic assessment. This observation requires a randomised controlled trial in which changes in peptide levels determine aggression and duration of in-patient therapy in order to establish whether this indicator can improve results from management of acute in-patient heart failure. Plasma BNP or NT-proBNP is a powerful independent predictor of mortality and morbidity in long-term follow-up of heart failure cohorts. In addition, it appears likely to be a good predictor of beneficial response to the addition of beta blockade to anti-heart failure pharmacotherapy. Finally, adjustment of therapy for heart failure according to serial measurements of NT-proBNP promises to improve outcomes in comparison with adjusting therapy according to unassisted clinical acumen.     

慢性心力衰竭患者肾功能恶化的危险因素分析

目的 研究慢性心力衰竭(心衰)患者肾功能恶化的危险因素及其对预后的影响.方法 采用病例对照研究方法,分析与肾功能恶化发生有统计学关联的独立危险因素,同时观察肾功能恶化对预后的影响.结果 住院心衰患者肾功能恶化发生率31%,入院肌酐水平及心功能分级与肾功能恶化的发生独立相关,OR值分别为2.248(95%CI1.088～4.647,P=0.029)和2.485(95%CI1.385～4.459.P＝0.002).发生肾功能恶化的患者住院期间病死率明显高于对照组(16.7%比2.1%,P=0.000),调整混杂因素后,肾功能恶化是死亡的独立危险因素,OR值3.824(95%CI2.452～5.137.P＜0.015).结论 肾功能恶化在住院心衰患者中发生率较高,与住院期间病死率明显相关.入院肌酐水平偏高及心功能差为发生肾功能恶化的独立危险因素.

Abstract：

Objective To investigate the risk factors of worsening renal function (WRF) in patients with chronic heart failure ( CHF) and WRF influence on prognosis. Methods A case-control study were undertaken to analyze independent risk factor statistically related to incidence of WRF, and to assess the influence of WRF on prognosis. Results The independent predictors of WRF were creatinine level at admission (OR 2.248,95% CI 1.088-4.647, P = 0.029) and NYHA class on admission ( OR 2.485, 95% CI 1.3854. 459, P = 0.002). The mortality of patient with WRF was obviously higher than that of control group during hospitalization( OR 3. 824,95% CI 2. 452-5. 637 ,P ＜0.015). Conclusions WRF is a common complication among patients hospitalized for CHF, and is obviously associated with mortality during hospitalization. Higher creatinine level and weak heart function are independent risk factors for incidence of WRF of patients with CHF.     

Elevated intra-abdominal pressure in acute decompensated heart failure: a potential contributor to worsening renal function?

OBJECTIVES: This study sought to determine whether changes in intra-abdominal pressure (IAP) with aggressive diuretic or vasodilator therapy are associated with improvement in renal function in acute decompensated heart failure (ADHF). BACKGROUND: Elevated IAP (>or=8 mm Hg) is associated with intra-abdominal organ dysfunction. There is potential for ascites and visceral edema causing elevated IAP in patients with ADHF. METHODS: Forty consecutive patients admitted to a specialized heart failure intensive care unit for management of ADHF with intensive medical therapy were studied. The IAP was measured using a simple transvesical technique at time of admission and before removal of the pulmonary artery catheter. RESULTS: In our study cohort (mean age 59 +/- 13 years, mean left ventricular ejection fraction 19 +/- 9%, baseline serum creatinine 2.0 +/- 0.9 mg/dl), the mean baseline IAP was 8 +/- 4 mm Hg, with 24 (60%) patients having elevated IAP. Elevated IAP was associated with worse renal function (p = 0.009). Intensive medical therapy resulted in improvement in both hemodynamic measurements and IAP. A strong correlation (r = 0.77, p < 0.001) was observed between reduction in IAP and improved renal function in patients with baseline elevated IAP. However, changes in IAP or renal function did not correlate with changes in any hemodynamic variable. CONCLUSIONS: Elevated IAP is prevalent in patients with ADHF and is associated with impaired renal function. In the setting of intensive medical therapy for ADHF, changes in IAP were better correlated with changes in renal function than any hemodynamic variable.     

Exploring symptoms in chronic heart failure

Symptoms in patients with chronic heart failure (CHF) are the cry for help, reflecting not only the physical aspects of the disease but the impact on lifestyle, anxiety, depression and expectations of the patient. Studies consistently show a difference in patients' self-assessed functional classification compared to investigator reported NYHA classification. Moreover, patient self-assessed symptoms have recently been shown to independently predict hospitalisation and mortality over 5 years. Recognition of symptoms and appreciation of their importance justifies the use of a structured assessment in order to provide optimal medical care for patients with CHF. A model of how to structure symptom assessment equally with signs is presented in this paper.     

A qualitative study of chronic heart failure patients' understanding of their symptoms and drug therapy

OBJECTIVES: To explore patients' understanding of their symptoms and the treatment of their heart failure. DESIGN: Qualitative analysis of in-depth interviews, using a constant comparative approach. SUBJECTS: 27 patients identified by Cardiology and Care of the Elderly physicians as having (a) symptomatic heart failure (New York Heart Association functional classes II, III and IV) and (b) a hospital admission for heart failure in the previous 20 months. RESULTS: Patients were aged between 38-94 years (mean 69), 20 were in NYHA functional class III or IV. All had at least one concurrent illness. Analysis of the data identified four key areas: patients had little understanding of the purpose of their medications, were concerned about both the quantity and combination of drugs they were prescribed, had difficulties in differentiating between the side effects of drugs and symptoms of heart failure, and had little knowledge to help them interpret and/or treat changing symptoms. CONCLUSION: Providing patients with relevant information about their medications may help to reduce anxiety about the drugs they are taking. Acknowledging the symptoms associated with heart failure and the likely side effects of treatments might improve patients' ability to interpret, treat or relieve symptoms.     

Prognostic value of worsening renal function in outpatients with chronic heart failure

Introduction and objectivesRenal function impairment predicts poor survival in heart failure. Attention has recently shifted to worsening renal function, based mostly on serum creatinine and estimated glomerular filtration rate. We assessed the prognostic effect of worsening renal function in ambulatory heart failure patients.MethodsData from 306 ambulatory patients were abstracted from medical files. Worsening renal function was based on the change in estimated glomerular filtration rate, serum creatinine and urea within 6 months of referral. Prognosis was assessed by the composite endpoint all-cause death or heart failure hospitalization, censored at 2 years. Hazard ratios were estimated for worsening renal function, adjusted for sex, age, diabetes, New York Heart Association class, left ventricular systolic dysfunction, medications and baseline renal function.ResultsThe agreement among definitions was fair, with kappa coefficients generally not surpassing 0.5. Worsening renal function was associated with poor outcome with adjusted hazard ratios (95% confidence interval) of 3.2 (1.8–5.9) for an increase of serum creatinine > 0.3 mg/dl; 2.2 (1.3–3.7) for an increase in serum urea > 20 mg/dl and 1.9 (1.1–3.3) for a decrease in estimated glomerular filtration rate > 20%, independent of baseline renal function. The 2-year risk of death/heart failure hospitalization was approximately 50% in patients with an increase in serum creatinine or in serum urea; this positive predictive value was higher than for decreasing estimated glomerular filtration rate.ConclusionsIn conclusion, worsening renal function was significantly associated with a worse outcome. Different definitions identified different patients at risk and increasing creatinine/urea performed better than decreasing estimated glomerular filtration rate.     

An integrative review of the literature on in-hospital worsening heart failure

A subset of patients hospitalized for acute exacerbation of chronic heart failure develop in-hospital worsening heart failure. The objective of this paper is to present an integrative review of in-hospital worsening heart failure, including definitions, incidence, prevalence, mechanisms, treatments, outcomes, and early identification by providers. A search of electronic databases was conducted from January 2000-August 2017 using multiple search terms. Papers were reviewed for relevance; retained papers were abstracted and data were reported in a narrative synthesis. Twenty papers were selected. Many papers were observational data from in-hospital events that occurred during research trials. There was great variability in in-hospital worsening heart failure definition, incidence, prevalence, and treatments offered. Despite rescue therapies, in-hospital worsening heart failure was associated with increased risk for longer hospital stays, higher readmission rates, and death. To date, there are no therapies that target the underlying mechanisms or minimize its occurrence.     

Origin of symptoms in chronic heart failure

Skeletal muscle abnormalities are highly prevalent in chronic heart failure and are associated with an increase in the ergoreflex, a muscle reflex stimulated by work done. Stimulation of the ergoreflex results in increased ventilation and contributes to the increased sympathetic activation of the heart failure syndrome. The origin of the skeletal myopathy is related to a chronic imbalance between catabolic and anabolic processes, presumably as a consequence of chronic haemodynamic stress. Symptoms arise from the skeletal myopathy, causing the sensation of fatigue and contributing to the sensation of breathlessness as the myopathy affects respiratory muscle. Ergoreflex activation causes a greater ventilatory response to exercise than normal, contributing to the sensation of breathlessness.     

Role of left atrial booster pump function in a worsening course of congestive heart failure.

We evaluated changes in left ventricular (LV) preload and the Doppler-derived transmitral late to early diastolic peak velocity ratio (A/E ratio) during the exercise in 27 patients with ischemic heart disease. After the exercise, A/E ratio decreased in 16 patients with a remarkable elevation in LV preload, and increased in 11 with a mild elevation. Further, Doppler transmitral flow in conjunction with pulmonary venous flow and hemodynamic parameters were analyzed in 11 dogs during a worsening course of heart failure induced by dextran infusion. The relationship of A/E ratio to LV end-diastolic pressure showed a quadratic curve concave to the pressure axis. A/E ratio, an index expressing left atrial (LA) contribution to LV filling, returned to that seen before volume loading under the condition of cardiac dysfunction. Pulmonary venous reflux fraction determined as the ratio of peak velocity of pulmonary venous reflux during LA systole to the sum of systolic and diastolic peak velocities of pulmonary venous antegrade flow, did not increase here. In this situation, blood could not be ejected from the left atrium into the left ventricle and even into the pulmonary veins during LA contraction. Finally, LV filling was not compensated by the left atrium, and LA booster pump function itself was deteriorated.