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Introduction Acute decompensated heart failure (ADHF) readmission rates are high and act as a burden to both the patient and the healthcare system. Non-invasive measures of hemodynamic status are limited in accuracy, leading to patients being discharged with residual congestion and a higher likelihood of subsequent readmission for ADHF. Peripheral venous pressure (PVP) measurement involves transducing a peripheral intravenous (PIV) catheter and may serve as a minimally invasive method of determining hemodynamic status in patients with ADHF. PVP measurements have been shown to correlate with CVP measurements in heart failure patients, but the clinical relevance of this has not yet been established. We sought to examine if PVP measurements may predict heart failure readmission. Methods A prospective feasibility study was conducted from July to December 2018. Patients admitted with ADHF were enrolled on day-of-discharge. Using a standard pressure transducer leveled to the phlebostatic access, measurement of PVP was performed at the bedside using a previously-inserted PIV. The electronic medical record was reviewed for subsequent readmissions. The primary end-point was readmission at 30 days post-discharge. Results 29 patients were enrolled. The mean age of participants was 65.6 +/- 10.8 years. 66% of patients were male and 55% of patients were black. 72% of patients had a reduced ejection fraction (EF) and 28% had a preserved EF. At the time of discharge, the mean PVP was 11.6 +/- 4.9 mmHg. 5 patients (17%) were readmitted within 30 days. Mean PVP for those readmitted was 12.0 +/- 2.1 mmHg vs 11.5 +/- 5.3 mmHg for those without readmission (difference of the means 0.5 mmHg, p= 0.86). PVP was not significantly impacted by whether a 22-gauge or 20-gauge PIV was used (difference of means 2.3 mmHg, p= 0.51). Waveform analysis on a subset of patients showed lower PVP in those with a sinusoidal waveform as opposed to a flatline or static waveform (12.8 vs. 17.4 mmHg, p=0.32). Conclusion In this small feasibility study, few patients were readmitted for heart failure in 30 days. PVP was similar among the 5 patients readmitted with ADHF. PVP measurement was readily obtainable and PVP was not significantly impacted by PIV gauge. Further study of this clinical application to PVP measurement is warranted.

Introduction The vasoactive inotropic score (VIS) is an emerging method to estimate total inotropic and vasopressor support after cardiothoracic surgery. Whether the post-operative VIS score can predict mortality in patients following LVAD implantation is unknown. Methods We performed a single-center retrospective study of 268 patients who received a continuous-flow durable LVAD between Jan 1, 2006 and Dec 31, 2017. The VIS score was calculated as: dobutamine (mcg/kg/min) + 10 x milrinone (mcg/kg/min) + dopamine (mcg/kg/min) + 100 x epinephrine (mcg/kg/min) + 100 x norepinephrine (mcg/kg/min) + 10,000 x vasopressin (units/kg/min). The VIS score at 6, 24, and 48 hours postoperatively were abstracted and then the maximum VIS score within 48 hours after implantation for each patient was used to stratify the cohort into quartiles. Kaplan-Meier method was used to estimate 90-day survival and Cox Hazard model was performed to evaluate for predictors of 90-day mortality. Results The VIS quartiles groups were 0-9, 10-16, 17-23, and 24-87. Patients in quartile 4 were older and had a higher preoperative right atrial pressure (Table 1). VIS quartiles demonstrate a stepwise increase in adjusted hazard ratio compared to the 1st quartile in our multivariable model (which included age, total bilirubin over 2.5, gender, and VIS) with VIS quartile 2 HR 2.45 (95% CI 0.65 - 9.24, p = 0.18), VIS quartile 3 HR 3.39 (95% CI 0.90 - 12.79, p = 0.07), VIS quartile 4 HR 4.53 (95% CI 1.28 - 16.05, p = 0.02). Figure 1 demonstrates worsened survival by VIS quartiles up to 90-days post LVAD implantation (logrank test p=0.048). Conclusion Elevated VIS score within the first 48 hours after LVAD implantation correlates with an increased risk of mortality at 90 days. Further work is needed to confirm this relationship.

Purpose The pre-operative pulmonary artery pulsatility index (PAPi) is associated with severe right ventricular failure (RVF) after LVAD implantation. We set out to assess how the PAPi trends pre- to post-operatively in patients with and without severe RVF. Methods A single-center retrospective study of 230 patients who received a continuous-flow durable LVAD between 1/2006 and 9/2016. PAPi was defined as: [(PA systolic - PA diastolic) ÷ RA pressure]. Severe RVF was defined as meeting criteria for clinical RVF and having inotropes > 14 days after implant, inotropes re-started after 14 days of implant, RVAD placement during implant admission, and death from RVF during implant admission. The hemodynamics pre-implant and post-operatively at 6, 24, and 72 hours were examined. Results In our 230-patient cohort, 62 patients (27%) were found to have severe RVF. Patients with severe RVF had a lower pre-operative (p-value = 0.04), 6-hour post-LVAD (p-value Conclusion The PAPi declines significantly post-operatively in patients with severe RVF and without severe RVF at 6 and 24 hours. For patients with severe RVF, the PAPi significantly improves from 6 to 72 hours post-operatively.

Purpose Although intravenous anticoagulation is the mainstay medical therapy employed during CF LVAD thrombosis, the comparative impact of indirect thrombin inhibition with unfractionated heparin (UH) and direct thrombin inhibition with bivalirudin (BV) is unknown. Methods We conducted a single center review of all patients with a Heart Mate(HM) II who were admitted for suspected device thrombosis (SDT) from September 2011 to September 2018. Device thrombosis was suspected due to elevated outpatient lactate dehydrogenase (LDH), evidence of systemic emboli, or device alarms. After admission, patients were categorized into those receiving UH or BV. Crossovers were excluded. Freedom from device exchange was calculated with Kaplan Meier analysis. Results Twenty-three patients were admitted for SDT, of whom 13 received UH and 10 received BV. There were no differences in age (UH: 49.2 vs. BV: 46.9 years, p=0.60) and time from implant to SDT (UH: 10.3 vs. BV: 10.4 months, p=0.98). LDH remained elevated after UH (879, IQR: 755-1049 to 1028, IQR: 550-1438 U/L, p=0.34) but dropped with BV (839, IQR: 733-914 to 453, IQR: 352-465 U/L, p=0.002). During the follow up period, there was a lower likelihood of a device exchange in patients treated with BV (HR: 0.28, 95% CI: 0.09-0.89, p=0.04, figure 1). Conclusion In this sample of HM II patients, intravenous direct thrombin inhibition was more effective in treating device thrombosis.

Purpose Neutrophil to lymphocyte ratio (NLR), calculated from a CBC, is a marker of systemic inflammation and long-term risk in chronic illness, including heart failure (HF). Vasoplegia syndrome is a severe vasodilatory shock state after cardiac surgery. Patients undergoing heart transplantation (HTx) may be at an increased risk of vasoplegia due to inflammatory cytokine release secondary to HF. The role of NLR as a predictive marker for vasoplegia in patients undergoing HTx has not been studied. Methods Retrospective review of consecutive patients who underwent HTx from 7/2016 to 7/2018. Patients with conditions or treatments known to affect WBC count were excluded. Pre-HTx NLR was calculated from day of HTx and stratified by tertile. Vasoplegia was defined as vasopressor administration for > 24 hours to maintain mean arterial pressure > 65 mmHg for hypotension not attributed to other etiologies within 48 hours of HTx. The primary outcome was rates of vasoplegia between tertiles. Results 78 patients underwent HTx of which 70 met inclusion criteria. 18 patients had vasoplegia. Vasoplegia occurred in 8.7% (n=2) in the 1st tertile, 25% (n=6) in the 2nd tertile and 43.4% (n= 10) in the 3rd tertile (comparison 1st vs 3rd tertile, p=0.04) (Figure). In a multivariate analysis, adjusted for prior LVAD, patients in the 3rd tertile had higher rates of vasoplegia (adjusted OR 2.47, 95% CI 1.87-4.55) compared to the 1st. Mean NLR in patients without vasoplegia was 3.68±0.48 compared to 6.72±1.7 in patients with vasoplegia (p=0.019). There was no demographic or medical comorbidity difference other than hypothyroidism (p=0.04) between groups. Conclusion Vasoplegia is associated with elevated pre-HTx NLR compared to patients without vasoplegia. Chronic inflammation due to HF may play a role in the development of post-HTx vasoplegia. NLR is an inexpensive tool which clinicians may use pre-HTx to stratify which patients are at an increased risk of development of vasoplegia post-HTx.

Purpose The American Society of Transplantation has recently called for better risk stratification of donor hearts based on hepatitis C virus (HCV) antibody (Ab)/NAT status, advised to consider NAT negative (non-viremic) hearts noninfectious, and underscored the need for more research before HCV NAT+ (viremic) hearts can be used routinely. We examined early trends in utilization rates and outcomes of HCV donor hearts based on Ab and NAT status. Methods Between 8/2015 and 6/2018, we identified 29,225 donors with HCV Ab/NAT status and organ disposition in UNOS (for utilization trends). After excluding multi-organ and re-transplants, 7260 adult heart transplantation (HT) recipients were used to analyze baseline donor/recipient characteristics and outcomes in different donor HCV Ab/NAT categories. Results During the study period, the acceptance rates for HCV Ab+/NAT- donor hearts increased from 1.4% to 23.4%, Ab+/NAT+ from 0.6% to 26.0% and Ab-/NAT+ from 0% to 9.1% (p Conclusion Even though infectious risk starkly differs and long-term outcomes are unclear in the era of DAAs, we found a significant and near identical increase in utilization of both HCV viremic (NAT+) and non-viremic (Ab+/NAT-) donor hearts. Early survival was similar to recipients of HCV Ab-/NAT- donor hearts.

Purpose Early identification of right ventricular failure (RVF) after LVAD implantation is critical to reducing morbidity and mortality. The pre-operative pulmonary artery pulsatility index (PAPi) is associated with severe right ventricular failure (RVF) after LVAD implantation. We set out to assess if the PAPi in the immediate post-operative period is also predictive of severe RVF. Methods A single-center retrospective study of 230 patients who received a continuous-flow durable LVAD between 1/2006 and 9/2016. PAPi was defined as: [(PA systolic - PA diastolic) ÷ RA pressure]. Severe RVF was defined as meeting criteria for clinical RVF and having inotropes > 14 days after implant, inotropes re-started after 14 days of implant, RVAD placement during implant admission, or death from RVF during implant admission. The hemodynamics pre-implant and post-operatively were documented. A multivariate analysis for predictors of severe RVF was performed, and ROC curves were created. Results In our 230-patient cohort, 62 patients (27%) were found to have severe RVF. Patients in the severe RVF group had higher INTERMACS profile, were more likely to receive pre-operative vasopressors, have lower total bilirubin and lower PAPi. The multivariable model (which included age, INTERMACS level, creatinine over 1.5 mg/dL, total bilirubin over 2.5 mg/dL, and gender) found that a PAPi 16 at 6 hours post-op (OR 3.1 [1.1, 8.6], p = 0.03, n = 208) were significant predictors of severe RVF. The pulmonary artery (PA) pressure at 6 hours and the CVP, PAPi, and PA pressure at 24 hours were not predictive of severe RVF in our model. A PAPi 16 (ROC c-statistic 0.71) at 6 hours post-op. Conclusion The PAPi at 6 hours is a significant predictor of severe RVF and adds value to standard hemodynamic measurements.

Purpose CAV has an immunological component and continues to limit long term outcomes in heart transplantation (HT). Smaller single center studies have suggested that induction with r-ATG may reduce development of CAV. We evaluated the association of induction with r-ATG, Basiliximab (BxB), or ‘no induction’ and CAV in HT recipients, traditionally considered not highly sensitized [pre-transplant panel reactive antibody (PRA) class 1 and class 2 ≤ 10%]. Methods Between 6/2004 and 03/2015, we identified 4,654 adult HT recipients in UNOS who either had induction with r-ATG, BxB or ‘no induction’ at the time of HT, and had information on pre-HT PRA levels and CAV. Donor age above 55 years or structural abnormalities, multi-organ or repeat transplants were excluded. The 3 groups: r-ATG (n=644), BxB (n=991), no induction (n=3019) were compared for baseline donor/recipient characteristics and CAV. Results Overall, pre-transplant PRA 1 and 2 levels were 0.5±1.7% and 0.3±1.3% respectively. Compared to no induction or BxB, HT recipients in r-ATG group were slightly younger (53 vs 55 vs 56 yrs), more black race (23% vs 16% vs 22%), less Status 1A (49% vs 59 vs 62%). BxB group had more recipients with creatinine >1.5 (24% vs 23% in r-ARG vs 17% no-induction) (all p Conclusion Although rates of CAV were higher in our specific cohort than previously reported for the overall HT population, r-ATG was associated with lower CAV in HT recipients who are traditionally considered to be not highly sensitized.

Purpose Pre-transplant amiodarone and left ventricular assist device (LVAD) has been shown to be independently associated with severe PGD; however, the interaction between both exposures has not been examined. We evaluated the relationship of pre-transplant amiodarone, left ventricular assist device and severe PGD. Methods Single center, retrospective cohort, adult (age > 18) OHT patients between 2006-2018. Severe PGD was defined as left or right or biventricular failure requiring mechanical circulatory support within 24 hours of OHT. Pre-transplant amiodarone use was within 3 months preceding OHT. Patients were grouped by presence (denoted +) or absence (denoted -) of LVAD and amiodarone. Results A total of 257 patients were transplanted during the study period, mean age 53.8 years, 73 (28.4%) females, 162 (63%) BTT and 90 (35%) patients had amiodarone use. There were 21 (8.2%) patients with severe PGD. The prevalence of severe PGD was highest in LVAD+/Amiodarone+ group (20.3%), followed by LVAD+/Amiodarone - (6.8%), LVAD-/Amiodarone+ (3.2%) and LVAD-/Amiodarone- (1.6%), p=0.0008 (Figure 1). Multivariate logistic regression analysis of pre-operative risk factors revealed LVAD (OR 5.95; 95% CI 1.23-28.52; p=0.03), amiodarone (OR 3.52; 95% CI 1.26-9.87; p=0.02), recipient diabetes (OR 3.36; 95% CI 1.11-10.21; p=0.03) and recipient hypertension (OR 0.22; 95% CI 0.08-0.61; p=0.04) were independently associated with severe PGD. Additive interaction analysis of amiodarone and LVAD was inconclusive due to the small sample size [relative excess risk due to interaction 8.13; 95% CI -10.37-26.2; p=0.39, attributable proportion 0.66; 95% CI 0.19-1.13; p=0.01 and synergy index 3.61; 95%CI 0.49-26.32; p=0.21]. Conclusion LVAD and amiodarone are associated with severe PGD, however the interaction of both exposures requires further analysis with a larger cohort.

Objectives This study sought to determine outcomes of adult recipients of early adolescent (EA) (10 to 14 years) donor hearts. Background Despite a shortage of donor organs, EA donor hearts (not used for pediatric patients) are seldom used for adults because of theoretical concerns for lack of hormonal activation and changes in left ventricular mass. Nonetheless, the outcomes of adult transplantation using EA donor hearts are not clearly established. Methods All adult (≥18 years of age) heart transplant recipients in the United Network for Organ Sharing database between April 1994 and September 2015 were eligible for this analysis. Recipients of EA donor hearts were compared with recipients of donor hearts from the usual adult age group (ages 18 to 55 years). Main outcomes were all-cause mortality and cardiac allograft vasculopathy up to 5 years, and primary graft failure up to 90 days post-transplant. Propensity score analysis was used to identify a cohort of recipients with similar baseline characteristics. Results Of the 35,054 eligible adult recipients, 1,123 received hearts from EA donors and 33,931 from usual-age adult donors. With the use of propensity score matching, 944 recipients of EA donor hearts were matched to 944 recipients of usual-age adult donor hearts. There was no difference in 30-day, 1-year, 3-year, and 5-year recipient survival or primary graft failure rates in the 2 groups using both Cox hazards ratio and Kaplan-Meier analysis. Of note, adult patients who received EA donor hearts had a trend toward less cardiac allograft vasculopathy (Cox hazard ratio, 0.80; 95% confidence interval: 0.62 to 1.01; p = 0.07). Conclusions In this largest analysis to date, we found strong evidence that EA donor hearts, not used for pediatric patients, can be safely transplanted in appropriate adult patients and have good outcomes. This finding should help increase the use of EA donor hearts.

Background Centre volume is an important determinant of outcomes in patients requiring complex medical treatments or surgical procedures. Heart failure hospitalisation (HFH) has become an increasingly complex and resource intensive clinical event. We evaluated the effect of centre volume on mortality and costs in patients with HFH. Methods This was a retrospective registry-based analysis of adult patients discharged with a primary diagnosis of HF from hospitals across New York (NY) State over a 5-year period, between January 2009 and December 2013, using the Statewide Planning and Research Cooperative System inpatient discharge files. The primary outcome of interest was in-hospital mortality. All patients were followed from the day of admission to either in-hospital death or discharge alive. Results 300 972 HFHs from 198 facilities across NY State were included. Five-year centre volume was associated with a decrease in in-hospital mortality in unadjusted (HR=0.872, 95% CI 0.863 to 0.881, p Conclusions Higher centre volume was associated with lower HFH mortality but increased HFH costs and increased cardiac procedures in a cohort of Medicare and non-Medicare beneficiaries.

Background— Despite a limited supply of organs, only 1 in 3 potential donor hearts is accepted for transplantation. Elevated donor troponin levels have generally been considered a contraindication to heart transplantation; however, the data supporting this practice are limited. Methods and Results— We identified 10 943 adult (≥18 years) heart transplant recipients in the United Network of Organ Sharing (UNOS) database with preserved donor left ventricular ejection fraction (≥50%) and where peak donor troponin I values were available. When analyzed as a continuous variable, there was no association between peak donor troponin levels and recipient mortality up to 1 year follow-up in unadjusted (hazards ratio, 0.999; 95% confidence interval, 0.997–1.002; P =0.856) and adjusted Cox models (hazards ratio, 1.000; 95% confidence interval, 0.997–1.002; P =0.950). Next, we divided the entire cohort into 3 groups based on donor troponin I values: 10 ng/mL (n=361). Using unadjusted and adjusted Cox models and Kaplan–Meier analysis, there was no significant difference in recipient mortality at 30 days, 1 year, 3 years, or 5 years between the 3 groups. Similarly, cardiac allograft vasculopathy up to 5 years and primary graft failure up to 30 days of follow-up post transplant did not differ between the 3 donor troponin groups. The median length of hospital stay post transplant was also similar across groups. Conclusions— Elevated donor troponin I levels in the setting of preserved left ventricular ejection fraction were not associated with intermediate-term mortality, cardiac allograft vasculopathy, or primary graft failure rates in hearts accepted for transplantation. This finding could help expand the donor pool.

Objectives This study sought to determine whether the nasal mucosa can serve as a surrogate for evaluating arteriovenous malformations (AVMs) related gastrointestinal (GI) bleeding in patients supported by continuous-flow left ventricular assist devices (CF LVADs). Background Bleeding from the mucosal surfaces of GI tract, particularly AVMs, is the most common complication of CF LVAD support. The pathophysiology of AVM formation during CF LVAD support is of critical interest yet poorly understood; in large part because of the length and accessibility of the GI tract. Nasal endoscopy is a minimally invasive, bedside test giving access to a mucosal surface possibly representative of the GI tract. Methods Eighty subjects (35 with CF LVAD, 30 with heart failure reduced ejection fraction [HFrEF], and 15 controls without heart failure) underwent nasal endoscopy for systematic evaluation of the intranasal mucosa for the presence of hypervascularity (HV). Patient records were reviewed for episodes and etiology of GI bleeding. Results Nasal HV was present in 63%, 57%, and 20% of the LVAD, HFrEF, and control groups, respectively (p = 0.018). Although the prevalence was similar, the severity of nasal HV was significantly higher in the CF LVAD group compared with the HFrEF group. Of the baseline characteristics in the entire cohort, only a history of heart failure was associated with HV (odds ratio: 4.8; 95% confidence interval: 1.02 to 22.31; p = 0.040) in adjusted logistic regression modeling. HV was strongly associated with GI bleeding in the CF LVAD cohort: the incidence was 32% in subjects with HV compared with 0% in subjects with normal mucosa (p = 0.023). Conclusions In this pilot study, HV of the nasal mucosa was associated with GI bleeding in subjects with CF LVADs. Nasal endoscopy has significant potential to further investigation into mechanisms of bleeding and risk stratification during CF LVAD support.

Continuous flow left ventricular assist devices (LVADs) have revolutionized the treatment of advanced heart failure; however, as experience with these devices has grown, a number of unanticipated adverse events have emerged. In this study, we review the current literature associating a lack of pulsatility with these events.It is now evident that continuous flow LVAD physiology reflects a spectrum of 'low pulsatile' rather than a truly 'nonpulsatile' state. Thus, the detrimental consequences of nonpulsatile flow noted in early experimental setups may or may not occur in humans supported with continuous flow LVADs. Such studies have demonstrated not only alterations in vascular function and structure during continuous flow LVAD support, but also a clear association of the degree of alterations in vascular, baroreceptor, and sympathetic nervous system function with the degree of actual pulsatility. In addition, a number of clinical events have been linked to continuous flow LVAD physiology, including a decreased extent of ventricular unloading possibly impairing myocardial recovery, hemolysis and device thrombosis, development of aortic insufficiency, and mucosal bleeding.Many of the adverse effects of the current continuous flow LVADs are associated with low pulsatile flow. An evolved understanding of pulsatility as a continuous rather than a binary variable may allow us to incorporate appropriate degrees of pulsatility into the next generation pumps and mitigate these effects.

We thank Dr. Madias and Dr. El-Battrawy et al. for their thoughtful comments on our recently published study [(1)][1], which showed that donor hearts with left ventricular systolic dysfunction (LVSD) that are successfully resuscitated can be transplanted without increasing recipient mortality

Introduction The pulmonary artery pulsatility index (PAPi) is an emerging hemodynamic marker correlated with severe post-LVAD RVF in single-center cohort studies. We set out to examine if this is generalizable in a multi-institutional analysis. Hypothesis The preoperative PAPi correlates with RVF as defined by new INTERMACS criteria (INTERMACS-RVF), severe RVF, and death at 1-year. Methods We performed a dual-center retrospective study of 404 patients from Ohio and New York who received a continuous-flow durable LVAD and had a pre-operative PAPi measurement. The PAPi was defined as: [(PA systolic - PA diastolic) ÷ RA pressure]. Severe RVF was defined as meeting criteria for clinical RVF and having inotropes > 14 days after implant, inotropes re-started 14 days after implant, RVAD placement during implant admission, and death from RVF during implant admission. A multivariate analysis of predictors of post-LVAD severe RVF was conducted. A survival analysis was performed to examine pre-operative PAPi as a predictor of 1-year mortality. Results In our cohort of 404 patients, 84 (21%) had severe RVF. Multivariable logistic regression for severe RVF (controlling for age, INTERMACS level, creatinine, and gender) showed that creatinine > 1.5 (OR 2.24, p=0.002, 95% CI [1.43-4.42]) and total bilirubin > 2.5 (OR 2.87, p=0.004, 95% CI [1.39-5.93]) significantly increased the odds of severe RVF, and a PAPi Figure 1 ) and INTERMACS-RVF (c-statistic=0.63) were similar. With respect to survival, the final multivariable model (controlling for age, gender, and ethnicity) showed a PAPi Conclusion PAPi

Introduction Preoperative cardiac ascites has been shown to be a predictor of mortality in the latest INTERMACS report. However, it has not been shown to be an independent risk factor for the development of RVF after LVAD implantation. Hypothesis Pre-operative ascites on imaging during implant admission is associated with post-operative RVF. Methods We performed a single-center retrospective study of 153 patients who received a continuous-flow durable LVAD between 1/2006 and 12/2016 and who also had preoperative abdominal ultrasound or CT aduring implant admission. Severe RVF was defined as meeting criteria for clinical RVF and having inotropes > 14 days after implant, inotropes re-started 14 days after implant, RVAD implant, and death from RVF. The severity of ascites was extracted from the radiology reports and was graded as either none/trace, mild, moderate, or severe. A multivariate analysis of pre-operative ascites stratified by severity and post-implant RVF was performed. Results In our 153 patient cohort, 43 (28.1%) were found to have significant ascites, with 35 (22.9%) having mild ascites, 8 (5.6%) having moderate ascites, and 0 having severe ascites. Patients with ascites had higher preoperative total bilirubin, lower platelet count, higher mean RA pressure, higher mean PA pressure, lower pulmonary artery pulsatility index (PAPi), higher PCWP, and higher mortality rate, p Table 1 ). The multivariable model (which included age, INTERMACS level, creatinine, gender, and total bilirubin) found that preoperative ascites (OR 1.98, 95% CI [1.02 - 3.81], p = 0.04) and total bilirubin (OR 1.50, 95% CI [1.07 - 2.10], p = 0.018) were independent predictors of post-implant RVF. The ROC curve of ascites and post-operative RVF had a c-statistic of 0.72 ( Figure 1 ). Conclusion The preoperative presence of ascites correlates with post-operative RVF. Abdominal imaging could be useful in further risk stratifying patients for post-implant RVF.

Introduction Early RVF after LVAD implant has been studied using varying definitions. We set out to compare the new INTERMACS post-LVAD RVF criteria and traditional severe RVF definitions in our multi-institutional cohort. Hypothesis The INTERMACS RVF and severe RVF definition will both show increased mortality at 1-year. Methods We performed a dual-center retrospective study of 471 patients who received a continuous-flow durable LVAD and data available to assess RVF severity. The new INTERMACS RVF definition stratifies RVF into mild, moderate, severe, and acute-severe. Severe RVF was defined as meeting criteria for clinical RVF and having inotropes > 14 days after implant, inotropes re-started after 14 days of implant, RVAD placement during implant admission, and death from RVF during implant admission. A survival analysis of the INTERMACS RVF and severe RVF definitions was performed. A multivariate analysis using clinical markers associated with post-LVAD mortality was then completed to assess the independent effect of the RVF definitions. Results Of the 471 patients, 100 (21%) had severe RVF. Stratified by INTERMACS-RVF, 279 (59%) had no RVF, 37 (8%) had mild RVF, 53 (11%) had moderate RVF, 57 (12%) had severe RVF, and 47 (17%) had acute-severe RVF. Our multivariate model (adjusted for age, gender, and ethnicity) for predictors of 1-year mortality showed that PAPi Conclusion Our multi-institutional cohort shows that severe RVF and INTERMACS RVF severe and acute-severe predict mortality at 1-year, and notably shows that mild and moderate INTERMACS RVF do not predict mortality. The new INTERMACS classification of RVF provides more granularity in stratifying RVF and may be more clinically applicable.

The reproducibility of cardiopulmonary exercise testing (CPX) has previously been reported in patients with NYHA Class II-III heart failure but not in patients with LVAD support. These two patient populations are known to have differing hemodynamic and metabolic responses to exercise. Here, we

Hydralazine-isosorbide dinitrate (H-ISDN) carries an indication for treating systolic heart failure (HF). Hydralazine-isosorbide mononitrate (H-ISMN) does not carry this indication, but is used nonetheless as ISMN is once a day, while ISDN is three times a day. How effective H-ISMN is compared to H

We investigated the effect of ranolazine on endothelial-dependent vasodilatation (EDV), serum markers of endothelial dysfunction, and inflammation.Endothelial dysfunction has been shown to be independently associated with the occurrence of cardiovascular events. We sought to investigate whether ranolazine, a novel antianginal medication with no effect on heart rate or blood pressure, improves endothelial function in patients with stable coronary artery disease (CAD).Twenty-seven patients with stable CAD were randomly assigned to either 1000 mg twice daily of ranolazine or to matching placebo for 6 weeks and then crossed over for an additional 6 weeks in a double-blind design. EDV was assessed using reactive hyperemia peripheral arterial tonometry (RH-PAT) at baseline, 6, and 12 weeks. Markers of endothelial dysfunction and inflammation were also evaluated.After 6 weeks, treatment with ranolazine significantly increased the EDV RH-PAT index as compared with baseline (1.85+/-0.42 vs. 2.08+/-0.57, P = 0.037). EDV RH-PAT did not change while on placebo (1.69+/-0.35 vs. 1.78+/-0.41, P = 0.29). In addition, there was a significant drop in asymmetric dimethylarginine levels with ranolazine treatment (0.66+/-0.12 vs. 0.60+/-0.11 micromol/l, P = 0.02) and a near significant decrease in C-reactive protein levels (0.40+/-0.80 vs. 0.30+/-0.61 mg/dl, P = 0.05).Ranolazine improves endothelial function, asymmetric dimethylarginine, and C-reactive protein levels in a group of patients with stable CAD. Our results suggest a novel mechanism of action of ranolazine.

Background — Hematologic adverse events are common during continuous flow left ventricular assist device support; yet, their relation to antiplatelet therapy, including aspirin (ASA) dosing, is uncertain. Methods and Results— A single-center retrospective review of all patients supported by a continuous flow left ventricular assist device (Heart Mate II) from June 2006 to November 2014 was conducted. Patients were categorized into 3 groups: (1) ASA 81 mg+dipyridamole 75 mg daily (n=26) with a target international normalized ratio (INR) of 2 to 3 from June 2006 to August 2009; (2) ASA 81 mg daily (n=18) from September 2009 to August 2011 with a target INR of 1.5 to 2; and (3) ASA 325 mg daily from September 2011 to November 2014 with a target INR of 2 to 3 (n=70). Hemorrhagic and thrombotic outcomes were retrieved ≤365 days after implantation. Cumulative survival free from adverse events was calculated using Kaplan–Meier curves and Cox proportional hazard ratios were generated. Hemorrhagic events occurred in 6 patients on ASA 81 mg+dipyridamole (26%; 0.42 events per patient year; mean INR at event, 2.2), 4 patients on ASA 81 mg (22%; 0.38 events per patient year; mean INR at event, 2.0), and in 38 patients on ASA 325 mg (54%; 1.4 events per patient year; mean INR at event, 2.2); P =0.004. Patients on ASA 325 mg had a higher adjusted hazard ratio of 2.9 (95% confidence interval, 1.2–7.0 versus ASA 81 mg+dipyridamole; P =0.02) and 3.4 (95% confidence interval, 1.2–9.5 versus ASA 81 mg; P =0.02) for hemorrhagic events. Thrombotic events rates were not different between groups. Conclusions— High-dose ASA in Heart Mate II patients treated concomitantly with warfarin is associated with an increased hazard of bleeding but does not reduce thrombotic events.

Introduction: Heart transplantation is the treatment of choice for end stage heart failure, but is limited to approximately 4000 globally every year due to donor shortage. Despite this, only one-third of the potential donor hearts are recovered for transplantation. Although elevated donor troponin levels have generally been considered a contraindication, the data supporting this practice is limited. Hypothesis: Elevated donor troponins in the presence of normal left ventricular ejection fraction (LVEF) do not impact outcomes after transplantation. Methods: All adult heart transplant recipients in the UNOS database between 2007 and 2014, with LVEF≥50%, and reported donor troponin I levels were included. The overall cohort was divided into groups based on clinically meaningful troponin I levels: below 1, 1-10, 10.1-20 and above 20 and compared for recipient survival and coronary allograft vasculopathy (CAV). Results: 11,640 transplants met the study criteria. On comparison of baseline characteristics, higher troponin groups had younger donors and greater donor CPR. Importantly, the ischemic time and proportion of recipients in the ICU and on temporary circulatory support were similar. As shown, there was no difference in survival (figure 1) or CAV (figure 2) up to 5 years of follow up using Kaplan-Meir analysis and cox-hazards ratio. After adjusting for differences in baseline covariates and clinically relevant factors, the findings remained unchanged. Conclusions: In this largest analysis to date, elevated donor troponin levels in the setting of preserved LVEF did not impact recipient survival or CAV up to 5 years of follow up. This finding can help expand the donor pool.

Background— Management of hemolysis in the setting of suspected device thrombosis in continuous-flow left ventricular assist device patients varies widely, ranging from watchful waiting with intensified antithrombotic therapy to early surgical device exchange. The aim of this study was to compare the outcomes of hemolysis events treated with surgical interventions versus medical management alone. Methods and Results— A retrospective review of Heartmate II continuous-flow left ventricular assist device patients at 2 centers from January 2009 to September 2014 was completed. Patients were categorized as surgical management if hemolysis refractory to intensification of standard antithrombotic therapy was treated surgically. The primary end point was the first occurrence of cerebrovascular accident (CVA) or death. Sixty-four hemolysis events occurred in 49/367 patients implanted with Heartmate II continuous-flow left ventricular assist devices. Of 49 primary hemolysis events, 24 were treated with surgical interventions. After surgical treatment, 1 patient died and 2 experienced CVAs, as compared with 3 deaths and 9 CVAs in the 25 patients who remained on intensified antithrombotic therapy alone. The 1-year freedom from CVA or death was 87.5% and 49.5% in the surgical and medical cohorts, respectively ( P =0.027). Resolution of a primary hemolysis event without CVA or death occurred in 21/24 patients treated with surgical interventions and in 13/25 who remained on medical therapy alone. A similar association between treatment and outcome was noted in the 15 recurrent hemolysis events. Conclusions— Hemolysis refractory to intensification of antithrombotic therapy identifies continuous-flow left ventricular assist device patients at major risk for CVA and death. Early device exchange should be considered to minimize these risks.

Acute allograft rejection is a prominent cause of graft failure in heart transplant recipients. Graft infiltration with immune-mediated cells is associated with changes in electric conduction. ECG patterns in heart transplant rejection generally include changes in the electric activity of the atria. ST-segment elevation is an uncommon presentation in acute rejection. We describe a case of mixed cellular and humoral rejection in a 74-year-old man 5 years after orthotopic heart transplantation presenting with lateral ST-segment elevations on ECG and normal coronary arteries on coronary angiography. Endomyocardial biopsy revealed International Society for Heart and Lung Transplantation grade 3R severe acute cellular rejection with associated pAMR1 (I+) antibody–mediated rejection. A 74-year-old man with chronic heart failure caused by an ischemic cardiomyopathy who underwent heart transplantation 5 years previously presented with left-sided chest pain of 4 days duration. Associated symptoms included dyspnea on exertion, fatigue, orthopnea, paroxysmal nocturnal dyspnea, and nausea. The past medical history was notable for an episode of acute cellular rejection 4 years before admission. The patient’s medications included aspirin, rosuvastatin, clonidine, and a 2-drug immunosuppresion regimen consisting of …