Portrait of the patient with intermediate ejection fraction of the left ventricle on the background of acute decompencation of heart failure

Recent Trends in the Incidence, Treatment, and Prognosis of Patients With Heart Failure and Atrial Fibrillation (the Worcester Heart Failure Study)

Rafael Correo, de izquierdas, y Alvaro Noboa, magnate conservador, vencieron con un discurso clientelista en el pais mas inestable de America Latina.

Increased left ventricular filling pressure is a hallmark of heart failure (HF) caused by left ventricular dysfunction (LVD). Within the closed hemodynamic system, increased LV filling pressure results in elevated pressures in the left atrium and pulmonary venous vasculature. When pulmonary hypertension (PH, defined by mean pulmonary artery pressure [mPAP] >25 mm Hg) is associated with an abnormally elevated pulmonary capillary wedge pressure (PCWP >15 mm Hg) or left ventricular end-diastolic pressure (LVEDP >18 mm Hg),1 it has been variably termed World Health Organization (WHO) Group 2 PH,1 pulmonary venous hypertension,2 “postcapillary PH,”3 or “passive PH.”4 Article see p 644 Patients with LVD also have a propensity to develop a precapillary pulmonary arterial contribution to PH, reflected by an increased transpulmonary gradient (TPG, defined as mPAP-PCWP that exceeds 12 to 15 mm Hg) or an elevated pulmonary vascular resistance (PVR, defined as TPG/cardiac output that exceeds 2.5 to 3 Wood units [WU]).5,6 This type of PH, which is “out of proportion” to underlying left-sided disease in the setting of normalized volume status, has been termed “mixed PH,” given both precapillary and postcapillary contributions to elevated PAP.7 PH in HF can be simplistically organized along 2 sequential dyads: (1) the presence or absence of a significant precapillary contribution to elevated PAP (ie, mixed PH as opposed to purely passive PH) and (2) if present, the relative fixed (ie, nonreversible with lowering left-sided filling pressures) or reactive (ie, reversible with reduction of left-sided filling pressures) character of the precapillary contribution to PH (Figure). Figure. Diagnostic framework for pulmonary hypertension in heart failure (HF). mPAP indicates mean pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; PVR, pulmonary vascular resistance; and PH, pulmonary hypertension. There are no widely established cut-points to define PVR and transpulmonary …

16512 Background: Little is known regarding management or treatment of cardiac failure after bone marrow transplantation. We investigated the management, treatment and outcome of new onset acute decompensated heart failure (ADHF) after bone marrow transplantation (BMT) with beta blockers, ace-inhibitors and adjuvant intravenous immune globulin (IVIG) therapy. Methods: We retrospectively examined 25 patients with ADHF. Eleven of these patients developed congestive heart failure within 100 days of BMT. Baseline echocardiograms were normal prior to admission and all patients were hospitalized and evaluated for left ventricular ejection fraction (LVEF), and New York Heart Association (NYHA) class. Patients with acute heart failure were treated with standard heart failure medications and patients post-BMT were treated with standard heart failure therapy plus adjuvant (IVIG) (500mg/Kg/day) for 48 hours. Baseline LVEF and NYHA class of 11 patients pre- and post-BMT were compared with LVEF and NYHA class of 14 patients with ADHF that did not receive a BMT. Results: The baseline diagnosis for all patients in the BMT group was NYHA class 4 and post-therapy improved to class 1.2. The baseline diagnosis for all patients in the non-BMT group were NYHA class 3.7 and improved to class 1.2 with medical therapy. The mean LVEF in the BMT group at diagnosis of ADHF was 27.5% and the mean post-therapy with IVIG was 57.6%. The mean baseline LVEF in the group not undergoing BMT and at diagnosis of ADHF was 28.2% and improved post-therapy to 45.2%. Conclusions: Acute decompensated heart failure in the cancer patient is highly treatable with aggressive medical management. Patients with ADHF after BMT and treated with IVIG may have potential clinical benefits with IVIG and standard medical therapy. Significant improvement in LVEF and NYHA were present in the BMT group versus the non-BMT group. These data suggest that BMT outcomes may be improved with routine heart failure management. Further randomized studies should be conducted. [Table: see text] No significant financial relationships to disclose.

Renal dysfunction is a common and progressive complication of chronic heart failure, with a clinical course that typically fluctuates with the patient’s clinical status and treatment. Despite growing recognition of the frequent presentation of combined cardiac and renal dysfunction, or “cardiorenal syndrome,” its underlying pathophysiology is not well understood, and no consensus as to its appropriate management has been achieved. Because patients with heart failure are surviving longer and dying less frequently from primary arrhythmia, we expect that the cardiorenal syndrome will become more common. Against this background, the article by Wang and colleagues1 in the present issue of Circulation is particularly significant because it is the first prospective, controlled therapeutic trial in patients with this condition. To place the findings and implications of this study in context, we first briefly review what is currently known about the cardiorenal syndrome and its treatment options. See p 1620 In ambulatory heart failure patients, the presence of concomitant renal dysfunction consistently has been one of the strongest risk factors for mortality.2–4 This risk becomes evident even at serum creatinine clearance levels >1.3 mg/dL and estimated creatinine clearance values ≤60 to 70 mL/min. Furthermore, renal function is at least as powerful an adverse prognostic factor as most clinical variables, including ejection fraction and New York Heart Association function class. Although renal dysfunction predicts all-cause mortality, it is most predictive of death from progressive heart failure, which suggests that it is a manifestation of and/or exacerbating factor for left ventricular dysfunction.2 In the setting of hospitalization for decompensated heart failure, worsening renal function is even more important than baseline renal function for predicting adverse outcomes.5–8 Although any increase in creatinine is associated with poorer survival rates, longer hospitalization, and more frequent readmission, several studies have used a threshold of a …

The “Obesity Paradox”: Does It Persist Among Israeli Patients With Decompensated Heart Failure? A Subanalysis of the Heart Failure Survey in Israel (HFSIS)

THE AIM: to evaluate the morphological picture and its relationship with markers of acute kidney injury and other prognostic parameters in patients with severe fatal acute decompensation of heart failure (ADHF).PATIENTS AND METHODS: material obtained from 62 patients 47–82 years old (mean age 72.8±2.1 years) with severe acute decompensation of chronic heart failure resulting in death. The red cell distribution width, erythrocyte sedimentation rate haemoglobin, creatinine, total bilirubin, C-reactive protein content in blood at admission and shortly before death were determined. Autopsy with subsequent detailed examination of renal tissue was performed in all cases.RESULTS: The average duration of hospitalization of deceased patients with ADHF was 6,9±1,1 days. The main cause of death in 25 patients (40,3%) was pulmonary oedema due to pulmonary embolism, or against the background of heart failure, its acute decompensation developed – 37 patients (59,7%). On autopsy acute tubular injury was found in 36 patients (58.1%), with its direct strong correlation with the red cell distribution width, creatinine level, C-reactive protein; medium strength correlation with erythrocytes, total bilirubin; weak strength correlation – with transaminases was revealed.CONCLUSION: In fatal ADHF, AKI occurred with high frequency and was characterized mainly by acute tubular epithelial injury of varying severity. Acute kidney injury in fatal ADHF was strongly associated with elevated levels of CRP, RDW, and creatinine, increased heart weight, and the presence of hydrothorax. There was a correlation of medium strength with decreased red blood cell count and increased total bilirubin levels, and a weak correlation with elevated transaminase concentrations. Acute kidney injury is one of the components of thanatogenesis associated with the combined effect of inflammatory factors.

Funding Acknowledgements None. Aim To study N-terminal propeptide natriuretic hormone (NT-proBNP) values in patients with non-alcoholic fatty liver disease (NAFLD) with acute decompensated heart failure (ADHF) at admission and discharge to evaluate its impact on clinical outcomes. Material and methods Included were 566 patients hospitalized with ADHF, functional classes II–IV (NYHA) [49,3% men, mean age 72,4 ± 11.4 years, left ventricular ejection fraction (LVEF) - 45 (33; 55) %. Patients were divided into 2 groups: 1 – ADHF and NAFLD (n=168), 2 – ADHF without NAFLD (n=398). All patients had NT-proBNP levels determined upon admission and discharge. The degree of liver steatosis was determined using a sensor device using the CAP (Controlled Attenuation Parameter) ultrasound option. Threshold CAP values corresponded to the degree of hepatic steatosis - S0 (<294 dB/m), S1 (295-309 dB/m), S2 (310-330 dB/m), S3 (≥331 dB/m). Results NAFLD was diagnosed in 29.7% of all patients. The incidence of NAFLD was higher in patients with preserved LVEF - 43% vs 25% - reduced LVEF. Patients with severe steatosis (S3) had significantly lower NT-proBNP values than patients with moderate steatosis (S1,S2) and no steatosis (S0) at admission [926 (256;1870) pg/ml, 1246 (298; 2000) pg/ml, 1850 (798;3515) pg/ml, respectively, p<0.001] and at discharge [480 (107;1406) pg/ml, 1077 (250;1649) pg/ml, 1685 (628;2733) ) pg/ml, respectively, p<0.001]. In patients with NAFLD and ADHF, according to multivariate Cox regression analysis, NTproBNP level >1593 pg/ml at discharge (hazard ratio (HR) 3.14; 95% confidence interval (CI) 1.52– 6.43; p<0.001) and LVEF<40% (HR 2.90; 95% CI 1.46–5.76; p=0.002) were independently associated with a higher likelihood of all-cause death during the 3-year follow-up period. Conclusions NAFLD and ADHF group was characterized by lower NT-proBNP values, with an inverse correlation with the degree of steatosis, which may complicate timely diagnosis and prescription of adequate therapy. At the same time, assessment of NTproBNP and LVEF values in patients with ADHF and NAFLD at discharge had an important prognostic role for stratifying by risk of death from all causes during the observed period, despite lower NTproBNP threshold values.

For normal cardiac performance, the left ventricle (LV) must be able to eject an adequate stroke volume at arterial pressure (systolic function) and fill without requiring an elevated left atrial (LA) pressure (diastolic function). These systolic and diastolic functions must be adequate to meet the needs of the body both at rest and during stress. Response by Tschope and Paulus on p 809 Systolic function is conveniently (although not always accurately) measured as the ejection fraction (EF), calculated as stroke volume divided by end-diastolic volume.1 The LV EF is easily interpreted. The lower limit of normal is ≈50%. The lower the EF is, the greater the reduction in systolic function. Diastolic function has been more difficult to evaluate.2 Traditionally, invasive measures of LV diastolic pressure-volume relations and the rate of LV pressure fall during isovolumetric relaxation have been used. However, these methods are not practical for routine clinical use and do not adequately evaluate all aspects of diastolic filling.3 Comprehensive echocardiographic evaluation of the dynamics of LV filling using blood pool and tissue Doppler has now progressed so that it provides clinically important information that can be used to direct patient care. We present data that support the use of echocardiographic evaluation of diastolic function to recognize cardiac dysfunction in patients with heart failure, especially those with preserved EF; to guide the management of patients by identifying those with and without elevated left filling pressures regardless of underlying EF; and to determine prognosis in a wide variety of patient populations. Although the LV end-diastolic pressure-volume relation describes the passive properties of the LV, LV filling is not a passive or slow process.3 In fact, the peak flow rate across the mitral valve is equal to or greater than the peak flow rate across the aortic valve. …

To study the possibilities of previously diagnosing acute renal damage in patients with acute decompensation of chronic heart failure with reduced systolic function using biomarkers of acute renal injury. The study included 60 patients (62.0±11.1 years) with HADS (BNP >500 pg/ml) and a reduced left ventricular ejection fraction (LV 27.05% [23.25; 32.75], c FC III-IV NYHA). The level of creatinine, urea, uric acid, albumin in serum was determined in all patients, as well as a number of biomarkers: lipocalin associated with neutrophil gelatinase (NGAL) and cystatin C (CysC) in serum; kidney damage molecule-1 (KIM-1) and angiotensinogen (AGT) in the urine. AKI is determined based on changes in serum creatinine concentration or diuresis value. The results obtained indicate a high specificity and sensitivity of the use of biomarkers for the diagnosis of AKI in patients with ADHF. NGAL AUC - 0.833 (p<0.001), Se - 82.8%, Sp - 4.2%. CysC AUC - 0.823 (p<0.001), Se - 79.3%, Sp - 74.2%. KIM-1 AUC - 0.782 (p<0.001), Se - 75.9%, Sp - 74.2%. AGT AUC - 0.829 (p<0.001), Se - 82.8%, Sp - 77.4%. In a multifactorial regression analysis, it was found that with NGAL greater than 157.35 ng/ml, the risk of AKI increases 13.1 times (95% CI 1.365-126.431), with an increase in KIM-1, the risk of the development of AKI increases 20.6 times (95% CI 1.802-235.524), and with an increase in AGT more than 14.31 leng/ml, the risk of AKI increases 32.8 times (95% CI 2.752-390.110). Acute kidney injury develops in 48.3% of patients hospitalized with acute decompensation of chronic heart failure. Patients with acute decompensation of chronic heart failure and AKI have significantly higher serum NGAL and CysC, KIM-1 and AGT values in the urine compared with patients without impairing renal function. These biomarkers can serve both for the early diagnosis of acute kidney damage and the prediction of AKI in patients with acute decompensation of chronic heart failure.

In patients with acute decompensated heart failure (ADHF), sex differences considering clinical and pathophysiologic features are not fully understood. We investigated sex differences in left ventricular (LV) ejection fraction (LVEF), plasma B-type natriuretic peptide (BNP) levels, and prognostic factors in patients with ADHF in Japan. We studied 748 consecutive ADHF patients of 821 patients registered in the ADHF registry between January 2007 and December 2014. Patients were divided into four groups based on sex and LVEF [reduced (ejection fraction, or EF, <50%, heart failure with reduced EF, or HFrEF) or preserved (EF ≥50%, heart failure with preserved LVEF, or HFpEF)]. The primary endpoint was the combination of cardiovascular death and heart failure (HF) admission. The present study consisted of 311 female patients (50% HFrEF, 50% HFpEF) and 437 male patients (63% HFrEF, 37% HFpEF). There was significant difference between sexes in the LVEF distribution profile. The ratio of HFpEF patients was significantly higher in female patients than in male patients (P= 0.0004). Although there were no significant sex differences in median plasma BNP levels, the prognostic value of BNP levels was different between sexes. Kaplan-Meier analysis revealed that the high BNP group had worse prognosis than the low BNP group in male but not in female patients. In multivariate analysis, log transformed BNP at discharge predicted cardiovascular events in male but not in female HF patients (female, hazard ratio: 1.169; 95% confidence interval: 0.981-1.399;P= 0.0806; male, hazard ratio: 1.289; 95% confidence interval: 1.120-1.481;P= 0.0004). In patients with ADHF, the distribution of LV function and the prognostic significance of plasma BNP levels for long-term outcome were different between the sexes.

e0716 An 81-year-old Man with dizziness, fatigue and shortness of breath

Objective To investigate early nasogastric nutrition on patients with acute decompensated chronic heart failure, and observe its influence on patient's disease outcome. Methods From January 2012 to December 2013, 100 cases with acute decompensated chronic heart failure were used as the research subjects, were randomly divided into experimental and control groups with 50 cases each group. Patients of two groups adopt expansion of blood vessels, strong heart, diuresis, and routine anti-infection treatment; Based on this scheme, experimental group adopt early nasogastric nutrition. The cardiac function index, the change of nutritional status and clinical curative effect and the result of follow-up within 1 year after discharge of two groups were compared. Results Left ventricular end-diastolic dimension (LVEDD) and left ventricular end-systolic dimension (LVESD) in two groups after treatment were decreased, and the descender of experimental group was superior to that of the control group with statistically significant difference (P<0.05). After treatment, left ventricular ejection fractions (LVEF) of two groups were improved, and the rise of experimental group was superior to that of control group with statistically significant difference (P<0.05). In the two groups after treatment, the serum brain natriuretic peptide (BNP) levels were significantly decreased, and the descender of the experimental group was more than that of control group with statistically significant difference (P<0.05). After treatment, body mass index (BMI), the level of serum prealbumin (PA), transferrin (TRF), and the total number of lymphocytes of two groups were increased significantly (P<0.05); and BMI, the level of serum PA and TRF, and the total number of lymphocytes of the experimental group were significantly better than those of the control group (P<0.05). The total effective rate of the experimental group was significantly higher than that of the control group (P<0.05). The exacerbation rates, readmission and mortality rate of experimental group follow-up within 1 year after discharge were significantly lower than that of the control group (P<0.05). Conclusions The early nasogastric nutrition on the patients with acute decompensated chronic heart failure was better able to improve patients' nutrition state, more conducive to patients with cardiac function recovery, improve the clinical curative effect, and reduce the exacerbation rates, and readmission and mortality rate. Key words: Heart failure/TH; Intubation, gastrointestinal; Enteral nutrition

Background: Myocardial injury (INJ) expressed by elevated high-sensitivity troponin (hs-Tn) is common in heart failure (HF), due to cardiovascular and non-cardiac conditions. The mechanisms of INJ in acute decompensated HF (ADHF) versus chronic HF (CHF) are still debated. This study’s purpose was to evaluate the determinants of elevated hs-TnT in ADHF and CHF. Methods: We retrospectively analyzed consecutive HF patients with hs-TnT measured on admission, hospitalized in a tertiary-care hospital. Rehospitalizations, acute coronary syndromes, embolisms, infections, autoimmunity and malignancy were excluded. Cut-off point for hs-TnT was 14 ng/L. Results: Our study included 488 HF patients, 56.55% with ADHF. Mean age was 72.52±10.09 years. 53.89% were females. 67.75% ADHF and 45.75% CHF patients had elevated hs-TnT. Median hs-TnT was higher in ADHF versus CHF (21.05[IQR 12.74-33.81] vs 13.20[IQR 7.93-23.25], p&lt;0.0001). In multivariable analysis in ADHF and CHF, log10NT-proBNP (HR=5.30, 95%CI 2.71–10.38, p&lt;0.001, respectively HR=5.49, 95%CI 1.71–17.57, p=0.004) and eGFR (HR=0.72, 95%CI 0.62–0.85, p&lt;0.001, respectively HR=0.71, 95%CI 0.55–0.93, p=0.014) were independent predictors for increased hs-TnT. Independent factors associated with elevated hs-TnT in ADHF were male sex (HR=2.52, 95%CI 1.31-4.87, p=0.006) and chronic pulmonary obstructive disease (COPD) (HR=10.57, 95%CI 1.26-88.40, p=0.029), while in CHF were age (HR=2.68, 95%CI 1.42-5.07, p=0.002) and previous stroke (HR=5.35, 95%CI 0.98-29.20, p=0.053). Conclusion: HF severity, expressed by NT-proBNP levels, and kidney disease progression, expressed by eGFR, were independent predictors associated with increased hs-TnT in both ADHF and CHF. Specific independent predictors were also indentified in ADHF (male sex, COPD) and CHF (age, history of stroke).

Remote Wireless Telemonitoring Combined with Health Coaching (Tele-HC) to Lower Readmission Rates for Patients with Acute Decompensated Heart Failure