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Introduction Patients with elevated panel reactive antibodies (PRA) have longer waitlist times and worse outcomes post-transplant. PRAs are now better characterized with newer detection techniques and are classified as Class I and Class II antibodies. The prognostic role of Class I and Class II antibodies is currently unknown. Hypothesis Elevated Class I and Class II may not have the same prognostic implications. Methods Retrospective analysis of data reported to UNOS/OPTN registry for heart transplants between 2004 and 2015 was performed. All patients over the age of 18 were included in the study. Patients with missing PRA data and those with prior heart transplantation were excluded. Impact of Class I and Class II antibodies on treated rejection at one year and overall long-term survival was evaluated. Results Our cohort consisted of 17, 460 patients; of these 75.1% were male and 24.9% female. The mean age at transplant was 52.8 ±12.6 years. Class I PRA was ≤25% in 15,816 (90.6%) patients and ˃25% in 1600 (9.2%) patients. Class II PRA was ≤ 25% in 16,266 (93.2%) and ˃ 25% in 1121 (6.4%) patients. Multivariate analysis based on predictors identified in univariate analysis showed that recipient age, gender, year of transplantation, HLA mismatch and Class 2 antibodies ˃ 25% were predictive of treated rejection at one year. Similar analysis showed that recipient age, donor age, ischemic time, year of transplantation and Class I antibodies ˃ 25% were predictive of long-term survival ( Figure 1 ). Of these, elevated Class I antibodies was the strongest predictor of mortality with a hazard ratio of 25%. Conclusions Elevated Class I and Class II antibodies impact outcomes very differently. While higher Class II antibodies are associated with increased treated rejection at one year, higher Class I antibodies are associated with increased long-term mortality.

Background: Regular weight measurement is the standard of care among patients hospitalized for heart failure (HF) for monitoring response to diuretic therapy. While recent guidelines recommend routine daily weights in decompensated HF inpatients, the quality of weight measurement in clinical practice has not been well characterized. Methods: We conducted a retrospective single-center observational cohort study of consecutive adults with decompensated HF (N = 658) who were admitted from June 2012 through February 2013. We collected demographic, clinical, laboratory, imaging and weight measurement information during the hospitalization. Daily weights were defined as daily weights between day 2 of the hospitalization and the day prior to discharge. Discharge weights were defined as a weight on the day prior to or the day of discharge. We qualified whether weights were standing weights or not standing. We performed multivariable logistic regression analyses to assess association between documentation of weights and 30-day HF specific readmission. Results: The majority of patients were weighed on admission and discharge, though less than half of patients had daily weights and even fewer patients had admission, daily and discharge weights measured (Table). A small minority of patients had standing admission and discharge weights along with any daily weights (3.6%, 24 of 658). Although not meeting statistical significance, in multivariable logistic regression analyses patients who had admission, daily and discharge weights measured showed a tendency toward lower 30-day HF specific readmission (OR = 0.665, CI = 0.354-1.249, P = 0.20). Conclusion: In our single-center study, measurement of admission, discharge and daily weights among HF inpatients was inconsistent. A small minority of patients received daily weights and even fewer received ideal assessment - standing weights on admission and discharge with daily weights. Further study is needed to determine whether the quality of weight measurement seen in this study is generalizable to other institutions, to identify potential barriers to consistent inpatient weight measurement, and to perform a more robust assessment for the association of weight measurement with short-term clinical outcomes.

A complex case of inferior wall infarction with ventricular septal defect and severe tricuspid valve regurgitation due to acute papillary muscle rupture in a 65 year-old male is described. This constellation of pathological lesions and the surgical approach to the repair have not been previously described.

Left ventricular assist devices (LVADs) fill a critical need by providing circulatory support to patients with end-stage heart failure who are either ineligible for heart transplant or too ill to stably wait for an eventual donor organ. Furthermore, they are critical to the arsenal of the heart failure cardiologist, given the supply/demand mismatch for donor organs. Unfortunately, these devices present their own complications. Despite antiplatelet agents and systemic anticoagulation, a number of patients present with pump thrombosis, a life-threatening event requiring either pump exchange or treatment with systemic thrombolytics. In an effort to avoid these morbid therapies, glycogen IIb/IIIa inhibitors, which have both antiplatelet and thrombolytic properties, have been proposed to treat pump thrombosis. We report here the largest case series using these agents and document a previously unreported high failure rate with this therapy.

Mechanical circulatory support (MCS) is becoming the mainstay of therapy for patients with advanced heart failure, both for patients needing support as a bridge to transplantation and for those who require the device as a destination therapy. As more and more devices are implanted, there is a need to address effective discharge planning, arrange appropriate follow-up, anticipate and address complications, and develop strategies for long-term care. In this article, we will discuss issues surrounding discharge and challenges of managing patients with MCS in the outpatient setting.

Pulmonary venous hypertension is pulmonary hypertension resulting from elevated left sided filling pressures. This may result from chronic elevation of left atrial pressures from heart failure; either heart failure with reduced ejection fraction (HFrEF) or heart failure with preserved ejection fraction (HFpEF) or from valvular heart disease. This is classified as Group 2 pulmonary hypertension in the Dana point classification [1]. Pulmonary hypertension due to left heart disease is defined as mean pulmonary arterial pressure (mPAP) greater than or equal to 25 mm Hg, pulmonary capillary wedge pressure (PCWP) of greater than or equal to 15 mm Hg and pulmonary vascular resistance (PVR) greater than 3WU. Chronic elevation of left ventricular end diastolic pressures will result in increased left atrial pressures, initially causing passive congestion and rise in pulmonary venous pressures and resulting pulmonary arterial hypertension. This usually reverses readily with diuresis and lowering the left atrial pressures. Transpulmonary gradient (TPG = mPAP – PCWP) is normal at this stage. Continued elevation in PCWP may result in pulmonary vasoconstriction and reactive pulmonary hypertension where the TPG is greater than 12 mm HG and pulmonary vascular resistance (PVR) is greater than 3WU. This reactive pulmonary hypertension responds to diuresis and pulmonary vasodilation with agents such as nipride, nesiritide, inhaled nitric oxide or milrinone. Over time, the passive congestion and vasocontiction causes pulmonary vascular remodeling resulting in abnormalities of elastic fibres, smooth muscle proliferation and endothelial proliferation causing pulmonary arterial remodeling and resulting obliterative arteriopathy which is in part mediated by endothelin and is histologically indistinguishable from pulmonary arterial hypertension [2] Table 1. Epidemiology

The pathophysiology of heart failure is complex, and downstream effects cause decline in multiple systems. Medical therapies intended to slow or reverse disease progression have been shown to improve prognosis in prospective trials. Improvement in prognosis has also been observed in large cohorts across time strata. However, near-term mortality for those with advanced disease remains unacceptably high. Prognosis in advanced heart failure may be assessed with the appropriate use of clinical prediction tools. Optimal timing of evaluation for heart transplantation and/or mechanical circulatory support depends on an understanding of these issues.

Although continuous-flow left ventricular assist device (LVAD) support has become standard therapy, the complexities of device and patient management remain a challenge. In particular, percutaneous site infections (PSI) are a serious complication during the post-implant course. We sought to study the incidence, risk factors, and clinical effect of PSI.Data were obtained from the Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) Registry. All adult patients who received a primary intracorporeal continuous flow LVAD between June 2006 and September 2010 were included. Descriptive statistics, Kaplan-Meier depictions, and multivariable analysis in the parametric hazard domain were used for statistical analysis.A total of 239 PSIs were documented in 197 of 2,006 recipients (9.8%) of a continuous-flow LVAD. Mean follow-up was 8.1 months. Mean time to development of a PSI was 6.6 months. At 1 year after implant, nearly 19% of continuous-flow LVAD recipients developed a PSI. Multivariate analysis showed younger age (hazard ratio, 1.20; p0.0001) was the only factor predicting a PSI. Continuous-flow LVAD recipients who did not develop a PSI had improved survival (p = 0.004). Twenty-three patients died after development of a PSI. Sepsis was the most common cause of death (26.1%).PSIs occur in approximately 19% of continuous-flow LVAD recipients by 12 months after implant. Young age is the only predictor of PSI. Importantly, development of a PSI adversely affects survival. Efforts to enhance driveline integration and to develop future totally implantable systems are warranted.

Background Net fluid and weight loss are used ubiquitously to monitor diuretic response in acute decompensated heart failure research and patient care. However, the performance of these metrics has never been evaluated critically. The weight and volume of aqueous fluids such as urine should be correlated nearly perfectly and with very good agreement. As a result, significant discrepancy between fluid and weight loss during the treatment of acute decompensated heart failure would indicate measurement error in 1 or both of the parameters. Methods The correlation and agreement (Bland-Altman method) between diuretic-induced fluid and weight loss were examined in 3 acute decompensated heart failure trials and cohorts: (1) Diuretic Optimization Strategies Evaluation (DOSE) (n = 254); (2) Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE) (n = 348); and (3) Penn (n = 486). Results The correlation between fluid and weight loss was modest (DOSE r = 0.55; ESCAPE r = 0.48; Penn r = 0.51; P P ≤ .002). A consistent pattern of baseline characteristics or in-hospital treatment parameters that could identify patients at risk of discordant fluid and weight loss was not found. Conclusions Considerable discrepancy between fluid balance and weight loss is common in patients treated for acute decompensated heart failure. Awareness of the limitations inherent to these commonly used metrics and efforts to develop more reliable measures of diuresis are critical for both patient care and research in acute decompensated heart failure.

ObjectivesWe examined the impact of kidney transplantation on left ventricular ejection fraction (LVEF) in end-stage renal disease (ESRD) patients with congestive heart failure (CHF).BackgroundThe ESRD patients with decreased LVEF and a poor New York Heart Association (NYHA) functional class are not usually referred for transplant evaluations, as they are considered to be at increased risk of cardiac and surgical complications.MethodsBetween June 1998 and November 2002, 103 recipients with LVEF ≤40% and CHF underwent kidney transplantation. The LVEF was re-assessed by radionuclide ventriculography gated-blood pool (MUGA) scan at six and 12 months and at the last follow-up during the post-transplant period.ResultsMean pre-transplant LVEF% increased from 31.6 ± 6.7 (95% confidence interval [CI] 30.3 to 32.9) to 52.2 ± 12.0 (95% CI 49.9 to 54.6, p = 0.002) at 12 months after transplantation. There was no perioperative death. After transplantation, 69.9% of patients achieved LVEF ≥50% (normal LVEF). A longer duration of dialysis (in months) before transplantation decreased the likelihood of normalization of LVEF in the post-transplant period (odds ratio 0.82, 95% CI 0.74 to 0.91; p < 0.001). The NYHA functional class improved significantly in those with normalization of LVEF (p = 0.003). After transplantation, LVEF >50% was the only significant factor associated with a lower hazard for death or hospitalizations for CHF (relative risk 0.90, 95% CI 0.86 to 0.95; p < 0.0001).ConclusionsKidney transplantation in ESRD patients with advanced systolic heart failure results in an increase in LVEF, improves functional status of CHF, and increases survival. To abrogate the adverse effects of prolonged dialysis on myocardial function, ESRD patients should be counseled for kidney transplantation as soon as the diagnosis of systolic heart failure is established.