Methods and Results—We examined REMADHE trial and grouped patients according to etiology (Chagas vs non-Chagas) and beta-blocker therapy. Primary end-point was all-cause mortality/heart transplantation. Altogether 456 patients were studied; 27 (5.9%) were submitted to heart transplantation and 202 (44.3%) died. Chagas etiology was present in 68 (14.9%) patients; they had lower body mass index (BM)(24.1±4.1 vs 26.3±5.1, p=0.001), smaller end-diastolic left ventricle diameter (6.7±1.0mm vs 7.0±0.9mm, p=0.001), smaller proportion of beta-blocker therapy (35.8% vs 68%, p<0.001) and higher proportion of spironolactone therapy (74.6% vs 57.8%, p=0.003). Twenty-four (35.8%) Chagas patients were under beta-blocker therapy and had lower serum sodium (136.6±3.1 vs 138.4±3.1 mEqs, p=0.05) and lower BMI (22.5±3.3 vs 24.9±4.3, p=0.03) compared to those who received beta-blockers. Survival was lower in patients with Chagas heart disease as compared to other etiologies. When only patients under beta-blockers were considered, the survival of patients with Chagas was similar to that of other etiologies. The survival of patients with beta-blockers was higher than that of patients without beta-blockers. In Cox regression model left ventricle end-diastolic diameter (HR 1.78; CI 1.15-2.76; p=0.009) and beta-blockers (HR 0.37; CI 0.14-0.97; p=0.044) were associated with better survival.

Conclusions—Our study suggests that beta-blockers may have beneficial effects on survival of patients with heart failure and Chagas heart disease, and warrants further investigation in a prospective, randomized trial.

Methods and Results—Patients presenting to The Alfred and The Northern Hospital EDs with a chief complaint of dyspnoea were enrolled prospectively from August 2005 to April 2007. Patients were randomly allocated to have BNP levels tested or not. The diagnostic "gold" standard for HF was determined by one cardiologist and one emergency or respiratory physician who, blinded to the BNP result, independently reviewed all available information.

The ED diagnosis of HF in the non BNP group, showed a sensitivity, specificity and accuracy of 65%, 92% and 81% respectively. The BNP group had a similar sensitivity, specificity and accuracy of 66%, 90% and 78% respectively for the diagnosis of HF in the ED. There was no significant difference between the BNP and non BNP groups in any of the measures of diagnostic accuracy for HF.

Conclusion—In the clinical setting of emergency departments, availability of BNP levels did not significantly improve the accuracy of a diagnosis of HF.

Methods and Results—Thirty-one patients with CHF, defined as left ventricular ejection fraction (LVEF) <50% and New York Heart Association (NYHA) class ≥II, with coexisting OSA and CSR-CSA, were randomly assigned to either CPAP or flow-triggered ASV. The suppression of respiratory events, changes in cardiac function, and compliance with the devices during the 3-month study period were compared. Although both devices decreased respiratory events, ASV more effectively suppressed respiratory events (AHI: -35.4±19.5 with ASV, -23.2±12.0 with CPAP, P<0.05). Compliance was significantly greater with ASV than with CPAP (5.2±0.9 versus 4.4±1.1 h/night, P<0.05). The improvements in quality of life and LVEF were greater in the ASV group (LVEF: +9.1%±4.7% versus +1.9%±10.9%).

Conclusions—These results suggest that patients with coexisting OSA and CSR-CSA may receive greater benefit from treatment with ASV than with CPAP.

Methods and Results—Serum UA, urinary UA (uUA) excretion and renal clearance test for UA (Cl_UA) were measured in 82 CHF patients. Serum UA was significantly increased compared to controls of similar age (control 5.45±0.70 mg/dl, NYHA I 6.48±1.70 mg/dl, NYHA II 7.34±1.94 mg/dl, NYHA III 7.61±2.11 mg/dl, p<0.01). CHF Patients showed lower uUA excretion and Cl_UA. On multivariate analysis, insulin, brain natriuretic peptide (BNP; p<0.01) and creatinine levels (p=0.05) showed independent correlation with serum UA. The treatment effect of the uricosuric agent benzbromarone was tested in fourteen CHF patients with hyperuricemia in a double-blinded, placebo-controlled, randomized cross-over study design. Benzbromarone significantly decreased sUA (p<0.01). BNP, left ventricular ejection fraction and dimensions in echocardiographic assessment did not change after benzbromarone therapy. In contrast, fasting insulin (placebo: 18.8±8.9 µU/ml, benzbromarone: 11.0±6.2 µU/ml; p<0.05), HOMA insulin resistance index (placebo: 5.4±2.6, benzbromarone: 3.0±1.7; p<0.05) and TNF-; (placebo: 2.59±0.63 pg/ml, benzbromarone: 2.14±0.51 pg/ml, p<0.05) improved after benzbromarone, the changes in TNF-; levels were correlated with reduction of serum UA (p<0.05).

Conclusions—These results show that UA lowering without XO inhibition may not have an effect on hemodynamic impairment in CHF pathophysiology. To the extent that these data are correct, this finding suggests that up-regulated XO activity rather than UA itself is actively involved in hemodynamic impairment in CHF.

Methods and Results—We performed echocardiography in 196 HIV-infected adults and 52 controls. Left ventricular ejection fraction (LVEF), left ventricular mass indexed to the body surface area (LVMI), and diastolic function were assessed according to American Society of Echocardiography standards. LVMI was higher in HIV-infected patients (77.2g/m² in HIV patients vs. 66.5g/m² in controls, p<0.0001). LVEF was similar in both groups. Eight (4%) of the HIV patients had evidence of LV systolic dysfunction (defined as an EF<50%) versus none of the controls; 97 (50%) had mild diastolic dysfunction compared to 29% of the HIV-uninfected subjects (p=0.008). After adjustment for hypertension and race, HIV-infected participants had a mean 8g/m² larger LVMI compared to controls (p=0.001). Higher LVMI was independently associated with lower nadir CD4 T cell count, suggesting that immunodeficiency may play a role in this process. After adjustment for age and traditional risk factors, HIV patients had a 2.4 greater odds of having diastolic dysfunction as compared to controls (p=0.019).

Conclusions—HIV-infected patients had a higher prevalence of diastolic dysfunction and higher LVMI compared to controls. These differences were not readily explained by differences in traditional risk factors and were independently associated with HIV infection. These results suggest that contemporary asymptomatic HIV patients manifest mild functional and morphological cardiac abnormalities which are independently associated with HIV infection.

Methods and Results—We studied 41 HfpEF patients, 41 healthy controls and 16 hypertensive controls. None were taking HR-limiting medications. All study participants had clinical examination, 12-lead electrocardiogram, pulmonary function test, echocardiogram and metabolic exercise test with HR monitoring throughout exercise. Chronotropic response was measured by the percentage of the HR reserve used during maximal exercise (%HHR) and the peak exercise HR as a percentage of predicted maximal HR (%Max-PPHR).

HfpEF Patients were generally females (70%), overweight, aged 69±8 years old. Controls were of similar gender (63%) and age (67±6 years old). Patients with HfpEF had significantly reduced peak VO₂ compared to controls (20±4 ml/Kg/min vs. 31±6 ml/Kg/min, p<0.001) and greater minute ventilation–carbon dioxide production relationship (VE/VCO₂ slope) (33±6 vs. 29±4, p<0.001). Chronotropic incompetence was significantly more common in patients with HfpEF compared to matched-healthy controls as measured by %HHR (63% vs. 2%, <0.001) and %Max-PPHR (34% vs. 2%, <0.001). In addition, abnormal HR recovery 1-minute post exercise (defined as the reduction in the HR from peak exercise one minute post-exercise) was also significantly more common in patients with HfpEF compared to controls (23% vs. 2%, p=0.01). Hypertensive controls showed similar chronotropic response to peak exercise and HR recovery following exercise as healthy controls

Conclusions—Patients with HfpEF have impaired chronotropic incompetence during maximal exercise and abnormal heart rate recovery post exercise.

Methods and Results—1513 patients with AMI (417 diabetic) underwent echocardiographic examination during the index hospitalization. Severe diastolic dysfunction was defined as a restrictive filling pattern (RFP) based on E/A ratio >1.5 or deceleration time <130 msec. The primary endpoints of the study were readmission for HF and all-cause mortality.

The frequency of RFP was higher in patients with diabetes (20 vs. 14%; P=0.005). During a median follow up of 17 months (range, 8 to 39 months), 52 (12.5%) and 62 (5.7%) HF events occurred in patients with and without diabetes, respectively (P<0.001). There was a significant interaction between diabetes and RFP (P=0.04), such that HF events among diabetic patients occurred mainly in those with RFP. The adjusted hazard ratio for HF was 2.77 [95% CI 1.41-5.46] in diabetic patients with RFP and 1.21 [95% CI 0.75-1.55] in diabetic patients without RFP. A borderline interaction (P=0.059) was present with regard to mortality (adjusted hazard ratio 3.39 [95% CI 1.57-7.34] vs. 1.61 [95% CI 1.04-2.51] in diabetic patients with and without RFP, respectively).

Conclusion—Severe diastolic dysfunction is more common among diabetic patients after AMI and portends adverse outcome. HF and mortality in diabetic patients occur predominantly in those with concomitant RFP.

Methods and Results—We used 2004-2006 Medicare administrative data to identify all fee-for-service beneficiaries admitted to a U.S. acute care hospital for heart failure and discharged alive. We estimated mean annual RSRRs, a National Quality Forum-endorsed metric for quality, using two-level hierarchical models that accounted for age, sex, and multiple co-morbidities; variation in quality was estimated by the standard deviation of the RSRRs. There were 570,996 distinct hospitalizations for heart failure in which the patient was discharged alive in 4728 hospitals in 2004; 544,550 in 4694 hospitals in 2005; and 501,234 in 4674 hospitals in 2006. Unadjusted 30-day all-cause readmission rates were virtually identical over this period: 23.0% in 2004, 23.3% in 2005, and 22.9% in 2006. The mean and standard deviation (SD) of RSRRs were also similar: mean [SD] of 23.7% [1.3] in 2004, 23.9% [1.4] in 2005, and 23.8% [1.4] in 2006, suggesting similar hospital variation throughout the study period.

Conclusions—National mean and RSRR distributions among Medicare beneficiaries discharged after heart failure hospitalization have not changed in recent years, indicating that there was neither improvement in hospital readmission rates nor in hospital variations in rates over this time period.

Methods and Results—We used non-invasive, high-fidelity tonometry of the radial artery and a mathematical transfer function to generate the AoPW in 25 treated patients with LVSD (mean LV ejection fraction, 24±8.8%; range, 11-40%; 21 patients <30%). Pulse wave analysis (PWA) of the AoPW was used to characterize ventricular/vascular coupling and compared to PWA performed in 25 normal subjects matched for age, gender, height, BMI and heart rate. Measurements obtained using PWA in LVSD patients indicated features of poor LV stroke performance and also reduced indices of arterial stiffness: increased travel time of the pressure wave (147±10 vs 132±21 msec; P<0.001); decreased systolic duration of reflected wave (134±24 vs 167±26 msec; P<0.001), ejection duration (277±22 vs 299±25 msec; P<0.008), percent systolic duration (32±5.3 vs 35±4.0%; P<0.02), aortic systolic pressure (100±16 vs 121±16 mmHg; P<0.001), unaugmented pressure (24±6.3 vs 32±6.4 mmHg; P<0.001), augmented pressure (4.8±3.1 vs 9.6±4.5 mmHg; P<0.001), pulse pressure (28±7.4 vs 42±9.5 mmHg; P<0.001), augmentation index (12±6.6 vs 23±7.6%; P<0.006), wasted LV effort (5.3±2.8 x 10² vs 17±10 x 10² dyne-sec/cm²; P<0.001), systolic pressure time index (17±4.1 x 10² vs 23±4.2 x 10² mmHg-sec/min; P<0.001) and pressure systolic area (383±121 vs 666±150 mmHg-sec/min; P<0.001).

Conclusions—Severe LVSD causes measurable changes in the AoPW. Standardization of AoPW findings in LVSD patients may allow for the clinical use of radial artery PWA to non-invasively determine the severity of dysfunction and aid in logical therapy.

Methods and Results— Mice with cardiac-restricted overexpression of low levels of TNF (MHCsTNF₃) and TRAF2 (MHC-TRAF2_LC), and mice lacking TNFR1, TNFR2 and TNFR1/TNFR2 were subjected to ischemia (30 min) reperfusion (30 min) injury (I/R) ex vivo, using a Langendorff apparatus. MHC-sTNF₃ mice were protected against I/R injury as shown by a significant ~ 30 % greater LV developed pressure, and ~ 80% lower creatine kinase (CK) release and Evans blue dye uptake compared to littermates (LM). The extent of I/R induced injury was similar in wild-type, TNFR1 and TNFR2 deficient mice; however, mice lacking TNFR1/TNFR2 had a significant ~ 40% lower LV developed pressure, a ~ 65 % greater CK release and ~ 40% greater Evans blue dye uptake compared to LM. Interestingly, MHC-TRAF2_LC mice had a significant ~ 50 % lower LV developed pressure, a ~ 70% lower CK release and ~ 80% lower Evans blue dye uptake compared to LM controls following I/R injury. Biochemical analysis of the MHC-TRAF2_LC hearts showed that there was activation of NF-B but not JNK activation.

Conclusion—Taken together these results suggest that TNF confers cytoprotection in the heart through TRAF2 mediated activation of NF-B.

Methods and Results—In the Beta-Blocker Evaluation of Survival Trial ("BEST"), adrenergic activation was estimated by systemic venous norepinephrine measured at baseline, 3 months and 12 months post-treatment in patients treated with placebo or bucindolol. In the BEST Adrenergic Receptor Polymorphisms Substudy, DNA was collected from 1040 of the 2708 randomized patients, and _2C-AR gene polymorphisms (_2C Del322-325 or the wild type counterpart) were measured by PCR and gel electrophoresis. Patients who were _2C Del carriers (heterozygotes or homozygotes) exhibited a much greater sympatholytic response to bucindolol (decrease in NE at 3 months of 153±57 (SEM) pg/ml, p = 0.012 compared to placebo vs. decrease of 50±13 pg/ml in _2C wild type, p = 0.0005 vs. placebo; p = 0.010 by interaction test). _2C Del carriers had no evidence of a favorable survival benefit from bucindolol (mortality compared to placebo hazard ratio = 1.09; 95% confidence intervals (CIs) 0.57, 2.08; p = 0.80), whereas bucindolol-treated subjects who were wild type for the _2C-AR had a 30% reduction in mortality (HR = 0.70; 95% CIs 0.51, 0.96; p = 0.025).

Conclusions—In the BEST Adrenergic Receptor Polymorphism Substudy, the NE-lowering and clinical therapeutic responses to bucindolol were strongly influenced by _2C receptor genotype.

Methods and Results—We used data from patients recruited to the 3CPO trial (a pragmatic multicentre trial comparing continuous positive airway pressure , noninvasive positive pressure ventialition and standard oxygen therapy in Emergency Department patients with ACPE) to investigate the association between baseline characterisitics and 7-day mortality. Factors associated with mortality (P<0.1) were entered into a multivariable model. Independent predictors of mortality from the multivariable model (P<0.05) were assigned integer weights based on their coefficients and incorporated into a risk score. The discriminant ability of the score was tested by receiver-operator-characteristic (ROC) analysis. Data from 1069 patients (78±10 years; 43% male; 7-day mortality 9.6%) were analysed. Multivariable analysis identified age (P=0.003), systolic blood pressure (P<0.001) and Glasgow Coma Scale (GCS) motor component dichotomised and simplified to the ability to obey commands or not (P=0.02) as the only independent predictors of 7-day mortality. These were weighted and used to develop a risk score ranging from zero (7-day mortality 1.9%, 95% CI 0.8 to 4.5%) to seven (7-day mortality 100%, 95% CI 34.2 to 100%). ROC analysis demonstrated good risk prediction with a c-statistic of 0.794 (95% CI 0.745 to 0.843). A simplified 3-point score with no weighting had a c-statistic of 0.754 (95% CI 0.701 to 0.807).

Conclusion—A simple clinical score based on age, systolic blood pressure and the ability to obey commands predicts early mortality in patients with ACPE.

Methods and Results—Of the 2689 patients with advanced chronic systolic HF in the Beta-Blocker Evaluation of Survival Trial, 441 had a history of PAD. Propensity scores for a history of PAD, calculated for each patient using a multivariable logistic regression model, were used to assemble a matched cohort of 299 and 1015 patients respectively with and without PAD who were well-balanced on 65 measured baseline characteristics. Cox regression models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for associations between PAD and outcomes during 4.1 years of follow-up. Patients had a mean age of 63 (±11) years, 19% were women and 19% were African Americans. All-cause mortality occurred in 43% and 33% of patients with and without a history of PAD, respectively (HR when PAD was compared with no-PAD, 1.40; 95% CI, 1.14–1.72; p=0.001). All-cause hospitalization occurred in 78% and 63% of patients with and without PAD, respectively (HR when PAD was compared with no-PAD, 1.36; 95% CI, 1.16–1.58; p<0.0001). PAD-associated HRs for cardiovascular mortality, HF mortality and HF hospitalization were respectively 1.31 (95% CI, 1.04–1.63; p=0.019), 1.40 (95% CI, 0.97–2.02; p=0.076) and 1.05 (95% CI, 0.86–1.29; p=0.635).

Conclusion—In a well-balanced propensity-matched population of chronic systolic HF patients, a history of PAD was independently associated with increased mortality and hospitalization.

Methods and Results—A total of 2131 patients enrolled in 76 sites participating in the GISSI-Heart Failure trial provided a first morning spot sample of urine at any of the clinical visits scheduled in the trial to calculate the urinary albumin-to-creatinine ratio (UACR). The relation between log-transformed UACR and all-cause mortality (428 deaths, time from urine collection to event or censoring) was evaluated with Cox multivariable models adjusted for all significant risk factors at the time of urine collection, in the study population and in patients without diabetes or hypertension. Almost 75% of the patients had normal urinary albumin excretion but 19.9% had microalbuminuria [30-299 mg/g creatinine] and 5.4% overt albuminuria [≥300 mg/g]. There was a progressive, significant increase in the adjusted rate of mortality in the study population (HR [95%CI] = 1.12 [1.05-1.18] per 1 unit increase of log(UACR), p=0.0002) and in the subgroup of patients without diabetes or hypertension. Randomized treatments (n-3 polyunsaturated fatty acids or rosuvastatin) had no major impact on albumin excretion.

Conclusions—Independently of diabetes, hypertension or renal function, elevated albumin excretion is a powerful prognostic marker in patients with chronic HF.

Methods and Results—In this prospective study with a one-month follow-up, 376 patients aged 65 and older with a diagnosis of HF were enrolled. A standardized CGA that included information on functional (Activities of Daily Living, ADL and Instrumental-ADL), cognitive (Short Portable Mental Status Questionnaire) and nutritional status (Mini Nutritional Assessment), as well as on risk of pressure sore (Exton-Smith Scale), comorbidities (CIRS Index), medications and social support network was used to calculate the MPI for mortality using a previously validated algorithm. The New York Hearth Association (NYHA), the Enhanced Feedback for Effective Cardiac Treatment (EFFECT) and the Acute Decompensated Heart Failure National Registry (ADHERE) regression model scores were also calculated. Higher MPI values were significantly associated with higher 30-day mortality both in men (MPI-1=2.8%, MPI-2=15.3%; MPI-3=47.4%; p=0.000) and women (MPI-1=0%, MPI-2=6.5%; MPI-3=14.6%; p=0.011). The discrimination of the MPI was also good, with areas under the ROC curves (men= 0.83 95%CI 0.75-0.90, women=0.80 95%CI 0.71-0.89) greater than ROC areas of NYHA (men=0.63, 95%CI 0.57-0.69, p=0.015; women=0.65, 95%CI 0.55-0.75, p=0.064), EFFECT (men=0.69, 95%CI 0.58-0.79,p=0.045; women=0.71, 95%CI 0.55-0.87, p=0.443) and ADHERE scores (men=0.65, 95%CI 0.52-0.78,p=0.023; women=0.67, 95%CI 0.49-0.83,p=0.171).

Conclusions—The MPI, calculated from information collected in a standardized CGA, is useful to estimate the risk of 1 month mortality in older patients with HF.

Methods and Results—424 HCM patients [age = 55 ± 16 years (range 2–90), 41% females], without prior history of septal ablation/myectomy, underwent CE-MRI (GE 1.5T). We evaluated the relation between LGE and HCM genes status, severity of symptoms, and the degree of ventricular ectopy on Holter ECG. Subsequent SCD and appropriate defibrillator (ICD) therapies were recorded during a mean follow-up of 43 ± 14 months (range 16–94). 239 patients (56%) had LGE on CE-MRI, ranging from 0.4–65% of the left ventricle. Gene-positive patients were more likely to have LGE (p<0.001). The frequencies of NYHA class ≥3 dyspnea and angina class ≥3 were similar in patients with and without LGE [125/239 (52%) vs 94/185 (51%) and 24/239 (10%) vs 18/185 (10%), respectively, p=NS]. LGE-positive patients were more likely to have episodes of non-sustained ventricular tachycardia (NSVT) [34/126 (27%) vs 8/94 (8.5%), p <0.001], had more episodes of NSVT per patient (4.5 ± 12 vs 1.1 ± 0.3, p=0.04), and higher frequency of ventricular extrasystoles/24 hours (700 ± 2080 vs 103 ± 460, p =0.003). During follow-up, SCD occurred in 4 patients, and additional 4 patients received appropriate ICD discharges. All 8 patients were LGE-positive (event rate of 0.94%/year, p=0.01 vs LGE negative). Two additional heart failure related deaths were recorded among LGE-positive patients. Univariate associates of SCD or appropriate ICD discharge were positive LGE (p=0.002) and presence of NSVT (p=0.04). The association of LGE with events remained significant after controlling for other risk factors.

Conclusion—In patients with HCM, presence of LGE on CE-MRI was common, and more prevalent among gene-positive patients. LGE was not associated with severe symptoms. However, LGE was strongly associated with surrogates of arrhythmia and remained a significant associate of subsequent SCD and/or ICD discharge after controlling for other variables. If replicated, LGE may be considered an important risk factor for sudden death in patients with HCM.

Methods and Results—Markers of myocyte injury and ECM turnover were assessed in 80 patients prospectively divided into 3 groups: AHFS (n = 39); chronic stable systolic HF (n = 21); and control subjects without HF (n = 20). Myocyte injury was assessed by measuring plasma troponin I. ECM turnover was assessed by measuring plasma matrix metalloproteinases (MMPs), tissue inhibitors of MMPs (TIMPs), and pro-collagen N-terminal types I (PINP) and III (PIIINP). In the AHFS group, biomarkers were obtained a) at the time of hospital admission for an episode of HF decompensation, b) at the time of hospital discharge, and c) several weeks after discharge in patients who had returned to a chronic stable compensated state. In patients with stable HF (vs. non-HF controls), there was a small increase in troponin I, and little or no difference in any marker of ECM turnover. In patients with AHFS, troponin I and three markers of ECM turnover (MMP-2, TIMP-1 and PIIINP) were elevated (vs. chronic stable HF), and all fell toward chronic HF levels in patients who returned to a compensated state.

Conclusion—Episodes of AHFS are associated with transient increases in markers of myocyte injury and ECM turnover that may reflect an acceleration of pathologic myocardial remodeling during AHFS.

Methods and Results—Forty-one patients with HFNEF and 29 controls underwent dobutamine stress echocardiography (DSE) with colour tissue Doppler imaging (cTDI). Wall motion score index (WMSI) and regional myocardial systolic velocity (Sm) were measured at and peak stress. Systolic (Sa), early diastolic (Ea) and late diastolic (Aa) mitral annular velocities were averaged over the 6 peri-annular sites. Mitral annular long axis velocity was lower in the HFNEF than controls at rest. Global, regional and long axis systolic function did not worsen with stress in the HFNEF group. The Ea decreased and the E/Ea increased with stress in the HFNEF but not in controls. The 6 minute walk distance was shorter and negatively correlated to the E/Em ratio at rest and stress in the HFNEF group.

Conclusion—Impaired diastolic reserve results in stress-induced increase in the left ventricular end-diastolic pressure (LVEDP) in patients with HFNEF giving rise to exercise intolerance.

Methods and Results—We identified 61 patients with advanced HF undergoing evaluation for ventricular assist device (VAD) or cardiac transplantation from 1995-2006, who had liver tissue obtained during the same time period. Electronic medical records were reviewed for clinical data. Biopsy specimens were scored for hepatic fibrosis. Forty-seven patients (79.7%) had hepatic fibrosis on liver biopsy. Of these, 47% had severe fibrosis (Grade 3 or 4). Relative to those without fibrosis, patients with hepatic fibrosis were more likely to have renal dysfunction, moderate or severe tricuspid regurgitation (TR) (odds ratio [OR] 5.0; 95% confidence interval [CI] 1.2, 21.7), and obstructive or mixed liver function (LFTs) abnormalities (OR 5.7; 95% CI 1.4, 22.3). As anticipated, patients with no or mild fibrosis (Grade 1 or 2) on transjugular liver biopsy were more likely to undergo VAD or heart transplant than patients with severe fibrosis (OR 7.8, 95% CI 1.4, 44.0). Accordingly, patients with severe fibrosis were less likely to be alive at the time of data collection (OR 0.07; 95% CI 0.01, 0.42).

Conclusion—Hepatic fibrosis is common in advanced HF patients. Renal dysfunction, significant TR and abnormal LFTs are associated with hepatic fibrosis, but the predictive value of other clinical features is limited. Liver biopsy should be considered in patients undergoing VAD or transplant evaluation.