Remote Monitoring of Patients With Heart Failure: A White Paper From the Heart Failure Society of America Scientific Statements Committee.

BACKGROUND: After several neutral telehealth trials, the positive findings and subsequent Food and Drug Administration approval of an implantable pulmonary arterial pressure monitor (PAPM) led to renewed interest in remote patient monitoring (RPM). Here we seek to provide contemporary guidance on the appropriate use of RPM technology. RESULTS: Although early trials of external RPM devices suggested benefit, subsequent multicenter trials failed to demonstrate improved outcomes. Monitoring features of cardiac implantable electronic devices (CIEDs) also did not deliver improved HF outcomes, newer, multisensor algorithms may be better. Earlier technologies using direct pressure measurement via implanted devices failed to show benefit owing to complications or failure. Recently, 1 PAPM showed benefit in a randomized controlled trial. Although not showing cost reduction, cost-benefit analysis of that device suggests that it may meet acceptable standards. Additional research is warranted and is in progress. Consumer-owned electronic devices are becoming more pervasive and hold hope for future benefit in HF management. Practical aspects around RPM technology include targeting of risk populations, having mechanisms to ensure patient adherence to monitoring, and health care team structures that act on the data. CONCLUSIONS: Based on available evidence, routine use of external RPM devices is not recommended. Implanted devices that monitor pulmonary arterial pressure and/or other parameters may be beneficial in selected patients or when used in structured programs, but the value of these devices in routine care requires further study. Future research is also warranted to better understand the cost-effectiveness of these devices.

Evidence for right ventricular lipotoxicity in heritable pulmonary arterial hypertension.

RATIONALE: Shorter survival in heritable pulmonary arterial hypertension (HPAH), often due to BMPR2 mutation, has been described in association with impaired right ventricle (RV) compensation. HPAH animal models are insulin resistant, and cells with BMPR2 mutation have impaired fatty acid oxidation, but whether these findings affect the RV in HPAH is unknown. OBJECTIVES: To test the hypothesis that BMPR2 mutation impairs RV hypertrophic responses in association with lipid deposition. METHODS: RV hypertrophy was assessed in two models of mutant Bmpr2 expression, smooth muscle-specific (Sm22(R899X)) and universal expression (Rosa26(R899X)). Littermate control mice underwent the same stress using pulmonary artery banding (Low-PAB). Lipid content was assessed in rodent and human HPAH RVs and in Rosa26(R899X) mice after metformin administration. RV microarrays were performed using human HPAH and control subjects. RESULTS: RV/(left ventricle + septum) did not rise directly in proportion to RV systolic pressure in Rosa26(R899X) but did in Sm22(R899X) (P < 0.05). Rosa26(R899X) RVs demonstrated intracardiomyocyte triglyceride deposition not present in Low-PAB (P < 0.05). RV lipid deposition was identified in human HPAH RVs but not in controls. Microarray analysis demonstrated defects in fatty acid oxidation in human HPAH RVs. Metformin in Rosa26(R899X) mice resulted in reduced RV lipid deposition. CONCLUSIONS: These data demonstrate that Bmpr2 mutation affects RV stress responses in a transgenic rodent model. Impaired RV hypertrophy and triglyceride and ceramide deposition are present as a function of RV mutant Bmpr2 in mice; fatty acid oxidation impairment in human HPAH RVs may underlie this finding. Further study of how BMPR2 mediates RV lipotoxicity is warranted.

Are peripherally inserted central catheters associated with increased risk of adverse events in status 1B patients awaiting transplantation on continuous intravenous milrinone?

BACKGROUND: Peripherally inserted central catheters (PICCs) are used to deliver continuous intravenous (IV) milrinone in stage D heart failure (HF) patients awaiting heart transplantation (HT). METHODS: We retrospectively analyzed PICC adverse events (AEs) and associated cost in 129 status 1B patients from 2005 to 2012. End points were HT, left ventricular assist device (LVAD), and death. Regression analysis was used to identify AE risk factors. RESULTS: Fifty-three PICC AEs occurred in 35 patients (27%), consisting of 48 infections, 4 thromboses, and 1 bleeding event. Median duration of PICC support was 63 (interquartile range [IQR] 34-131) days, and median time to first PICC infection was 44 (IQR 14-76) days. Among PICC infections, 9% required defibrillator removal and 30% were inactivated on the HT list for a mean of 23 ± 17 days. Rate of HT, LVAD, or death was similar between groups (P > .05). Regression analysis found that a double lumen PICC was associated with a shorter time to first PICC infection (hazard ratio 7.59, 95% CI 1.97-29.23; P = .003). Median cost per PICC infection was $10,704 (IQR $7,401-$26,083). CONCLUSIONS: PICC infections were the most frequent AEs. PICCs with >1 lumen were associated with increased risk of infection. PICC AEs accounted for increased intensive care unit admissions, HT list inactivations, and overall cost.

Familial evaluation for diagnosis of arrhythmogenic right ventricular dysplasia.

Most sudden cardiac deaths in young athletes are caused by previously undetected inherited cardiac diseases. Here, we report a case of a young male athlete in whom a presumptive diagnosis of hypertrophic cardiomyopathy (HCM) was made following a near sudden cardiac death. Although his imaging studies initially suggested HCM, a detailed clinical and genetic evaluation of the patient and his asymptomatic father led to the diagnosis of arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVD) in both. DNA sequencing revealed that each individual was heterozygous for two rare variants in the PKP2 and DSC2 genes, both of which were previously shown to be associated with ARVD and to encode desmosomal proteins, i.e. the previously reported splicing variant c2489 + 1A > G in the PKP2 gene and the novel p.I109M variant in the DSC2 gene. Imaging and electrophysiologic studies further supported a diagnosis of ARVD in the father. This case highlights the importance of detailed clinical evaluation and genetic testing of family members when dealing with sudden cardiac death or unexplained cardiomyopathies in the young.

Effects of Percutaneous LVAD Support on Right Ventricular Load and Adaptation.

Both operative and hemodynamic mechanisms have been implicated in right heart failure (RHF) following surgical left ventricular assist device (LVAD) implantation. We investigated the effects of percutaneous LVAD (pLVAD; Impella®, Abiomed) support on right ventricular (RV) load and adaptation. We reviewed all patients receiving a pLVAD for cardiogenic shock at our institution between July 2014 and April 2017, including only those with pre- and post-pLVAD invasive hemodynamic measurements. Hemodynamic data was recorded immediately prior to pLVAD implantation and up to 96 h post-implantation. Twenty-five patients were included. Cardiac output increased progressively during pLVAD support. PAWP improved early post-pLVAD but did not further improve during continued support. Markers of RV adaptation (right ventricular stroke work index, right atrial pressure (RAP), and RAP to pulmonary artery wedge pressure ratio (RAP:PAWP)) were unchanged acutely implant but progressively improved during continued pLVAD support. Total RV load (pulmonary effective arterial elastance; EA) and resistive RV load (pulmonary vascular resistance; PVR) both declined progressively. The relationship between RV load and RV adaptation (EA/RAP and EA/RAP:PAWP) was constant throughout. Median vasoactive-inotrope score declined after pLVAD placement and continued to decline throughout support. Percutaneous LVAD support in patients with cardiogenic shock did not acutely worsen RV adaptation, in contrast to previously described hemodynamic effects of surgically implanted durable LVADs. Further, RV load progressively declined during support, and the noted RV adaptation improvement was load-dependent as depicted by constant EA/RA and EA/RAP:PAWP relationships. These findings further implicate the operative changes associated with surgical LVAD implantation in early RHF following durable LVAD.

High mortality without ESCAPE: the registry of heart failure patients receiving pulmonary artery catheters without randomization.

BACKGROUND: In the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE), there was no difference in days alive and out of the hospital for patients with decompensated heart failure randomly assigned to therapy guided by pulmonary artery catheter (PAC) plus clinical assessment versus clinical assessment alone. The external validity of these findings is debated. METHODS AND RESULTS: ESCAPE sites enrolled 439 patients receiving PAC without randomization in a prospective registry. Baseline characteristics, pertinent trial exclusion criteria, reasons for PAC use, hemodynamics, and complications were collected. Survival was determined from the National Death Index and the Alberta Registry. On average, registry patients had lower blood pressure, worse renal function, less neurohormonal antagonist therapy, and higher use of intravenous inotropes compared with trial patients. Although clinical assessment anticipated less volume overload and greater hypoperfusion among the registry population, measured filling pressures were similarly elevated in the registry and trial patients, whereas measured perfusion was slightly higher among registry patients. Registry patients had longer hospitalization (13 vs 6 days, P < .001) and higher 6-month mortality (34% vs 20%, P < .001) than trial patients. CONCLUSIONS: The decision to use PAC without randomization identified a population with higher disease severity and risk of mortality. This prospective registry highlights the complex context of patient selection for randomized trials.

Characterization and prognostic value of persistent hyponatremia in patients with severe heart failure in the ESCAPE Trial.

BACKGROUND: Mild hyponatremia is relatively common in patients hospitalized with heart failure (HF). To our knowledge, the association of hyponatremia with outcomes has not been evaluated in the context of in-hospital clinical course including central hemodynamics and changes in serum sodium level. METHODS: The ESCAPE trial (Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness) was a randomized, controlled study designed to evaluate the utility of a pulmonary artery catheter plus clinical assessment vs clinical assessment alone in guiding therapy in patients hospitalized with New York Heart Association class IV HF due to systolic dysfunction (left ventricular ejection fraction <30%). A Cox proportional hazards model with baseline serum sodium level as a continuous variable was used to examine the association of serum sodium level with 6-month postdischarge mortality, HF rehospitalization, and death or rehospitalization. A categorical analysis was also performed comparing persistent and corrected hyponatremia. RESULTS: A total of 433 hospitalized patients with HF were enrolled in ESCAPE. Hyponatremia (serum sodium level < or = 134 mEq/L) was present in 103 patients (23.8%). (To convert serum sodium to millimoles per liter, multiply by 1.0.) Of these, 71 had persistent hyponatremia (68.9%). Hyponatremia was associated with higher 6-month mortality after covariate adjustment (hazard ratio [HR] for each 3-mEq/L decrease in sodium level, 1.23; 95% confidence interval [CI], 1.05-1.43) (P = .01). After controlling for baseline variables and clinical response, we found that patients with persistent hyponatremia had an increased risk of all-cause mortality (31% vs 16%; HR, 1.82) (P = .04), HF rehospitalization (62% vs 43%; HR, 1.52) (P = .03), and death or rehospitalization (73% vs 50%; HR, 1.54) (P = .01) compared with normonatremic patients. CONCLUSION: Persistent hyponatremia was an independent predictor of mortality, HF hospitalization, and death or rehospitalization despite clinical and hemodynamic improvements that were similar to those in patients without hyponatremia.

Survival in biopsy-proven myocarditis: a long-term retrospective analysis of the histopathologic, clinical, and hemodynamic predictors.

OBJECTIVE: We hypothesized that histopathology predicts survival without cardiac transplantation in patients with biopsy-proven myocarditis. BACKGROUND: The role of endomyocardial biopsy in diagnosing myocarditis remains controversial. Histopathology has been integrated with clinical and hemodynamic features to predict prognosis. However, the influence of histopathology on survival > 5 years has not been explored. METHODS: We retrospectively identified 112 consecutive patients with histopathologic confirmation of myocarditis. We examined these patients' clinical presentation, hemodynamic assessment, hospital course, and treatment. We selected 14 variables that might influence survival without cardiac transplantation. RESULTS: A total of 62 (55%) of 112 patients had lymphocytic myocarditis; 88 (79%) and 63 (56%) were alive without cardiac transplantation at 1 and 5 years, respectively. Median follow-up was a mean 95.5 months and median 74.5 months. Among the 55 with complete data of the 14 candidate predictor variables, age, sex, and clinical presentation with congestive heart failure and ventricular (ventricular tachycardia or fibrillation) or atrial arrhythmias (atrial fibrillation or flutter) did not predict the study end point of death or need for transplantation. In univariate analysis, pulmonary capillary wedge pressure > or = 15 mm Hg significantly predicted the study end point. In multivariate analysis, pulmonary capillary wedge pressure > or = 15 mm Hg and histopathology of lymphocytic, granulomatous, or giant cell myocarditis each significantly predicted mortality or transplant (P = .047, P = .013, and P = .054, respectively) on cumulative survival without cardiac transplantation. CONCLUSIONS: Histopathology predicts long-term survival in patients with myocarditis. Clinical presentation, including presentation with congestive heart failure, ventricular tachycardia/ventricular fibrillation, or atrial fibrillation/atrial flutter, does not predict survival without transplantation. Endomyocardial biopsy can play a role in predicting transplant-free survival in patients with myocarditis.

Mechanical circulatory support and simultaneous heart-kidney transplantation: An outcome analysis.

BACKGROUND: Single-donor simultaneous heart-kidney transplantation (SHKT) can significantly improve the survival of those with advanced heart failure and advanced renal insufficiency. Data on pre-transplant use of mechanical circulatory support (MCS) devices and outcomes after SHKT are limited and conflicting. METHODS: Using the United Network for Organ Sharing registry data, we evaluated 749 adults undergoing SHKT after January 1, 2000. Patients were categorized into the following groups according to their type of pre-transplant MCS device: none (n = 568), pulsatile-flow left (n = 28), continuous-flow left (n = 68), temporary (n = 12), biventricular (n = 19), total artificial heart (n = 20), and unknown (n = 34). Regression analyses were performed to assess the association between types of MCS and post-transplant outcomes. RESULTS: Pre-transplant MCS was not associated with in-hospital mortality (univariate odds ratio [OR], 1.57; 95% confidence interval [CI], 0.82-2.97; p = 0.170) or post-discharge mortality (univariate hazard ratio, 0.92; 95% CI, 0.58-1.47; p = 0.733). Patients supported with pre-transplant temporary MCS devices were more likely to suffer from serious complications (composite of cardiac or non-cardiac surgeries, stroke, any drug-treated infection, and permanent pacemaker; multivariable adjusted OR, 10.0; 95% CI, 2.77-36.0; p < 0.001) after SHKT. Pre-transplant MCS did not increase risk of post-transplant dialysis (multivariable adjusted OR, 1.19; 95% CI, 0.81-1.75; p = 0.375) or cardiac rejection (univariate OR, 0.71; 95% CI, 0.34-1.51; p = 0.382), and did not prolong the length of hospital stay (≥ 4 weeks; multivariable adjusted OR, 1.05; 95% CI, 0.69-1.59; p = 0.832). Post-transplant dialysis status was a major determinant of adverse in-hospital (multivariable adjusted OR, 6.17; 95% CI, 3.14-12.1; p < 0.001) and post-discharge (multivariable adjusted hazard ratio, 1.56; 95% CI, 1.02-2.39; p = 0.041) mortality after SHKT. CONCLUSIONS: In the current transplant era, survival after SHKT in patients with pre-transplant MCS was equivalent to that of conventional SHKT. Pre-transplant dialysis, and not MCS status, determined the need for post-SHKT dialysis, which in-turn was a major risk factor for in-hospital and long-term mortality.

Health outcomes in decompensated congestive heart failure: a comparison of tertiary hospitals in Brazil and United States.

BACKGROUND: Few international studies prospectively compared evidence-based practices and health outcomes among congestive heart failure (CHF) cohorts from countries with different cultural and economic backgrounds. METHODS: Patients consecutively admitted with congestive heart failure to tertiary care teaching hospitals in Brazil and in the United States (U.S.) were systematically evaluated using a structured data form. Follow-up data 3 months after discharge were obtained using chart review and telephone interviews. RESULTS: U.S. patients were older (p < 0.01), had higher prevalence of ischemic etiology (p < 0.01) and less previous hospitalizations for congestive heart failure (p = 0.03) than Brazilian patients, but similar Charlson comorbidity scores (p = 0.54) and left ventricular (LV) function (p = 0.45). Prescription of angiotensin-converting enzyme inhibitors at discharge was lower at the U.S. hospital (57% vs. 68%; p = 0.03), but beta-blockers prescription was higher (37% vs. 10%; p < 0.01). Length-of-stay was significantly shorter (5 [interquartile range, 3-9] vs. 11 [6-19] days; p < 0.001) and in-hospital mortality was lower (2.4% vs. 13%; p < 0.001) in the U.S. cohort, but fewer clinical events within 3 months after discharge were observed in Brazilian patients (42% vs. 54%; p = 0.02). Combined clinical outcomes within 3 months, including overall mortality and hospital readmission, were similar between cohorts (57% vs. 55%; p = 0.80). In multivariate analysis, hospital site remained significantly associated with health outcomes. CONCLUSIONS: Medical practice and health-related outcomes were different between U.S. and Brazilian congestive heart failure patients. In order to improve management worldwide, potential factors (structural, cultural or disease-related) that might be associated with these differences need to be evaluated in future studies.

Epigenetic regulation in heart failure: part II DNA and chromatin.

Epigenetic regulatory mechanisms play key roles in cardiac development, differentiation, homeostasis, response to stress and injury, and disease. Human heart failure (HF) epigenetic regulatory mechanisms have not been deciphered to date. This 2-part review distills the rapidly evolving research focused on human HF epigenetic regulatory mechanisms. Part I, which was published in the September/October issue, focused on epigenetic regulatory mechanisms involving RNA, specifically the role of short, intermediate, and long noncoding RNAs (lncRNAs) and endogenous competing RNA regulatory networks. Part II, now in the November/December issue, focuses on the epigenetic regulatory mechanisms involving DNA, including DNA methylation, histone modifications, and chromatin conformational changes. Part II concludes with 2 examples of well-studied integrated epigenetic regulatory mechanisms: the structural and functional roles of the Mediator complex in regulating transcription and the epigenetic networked "cross-talk" regulating atrial natriuretic peptide and brain natriuretic peptide promoter activation.

Effects of treatment recommendations and specialist intervention on care provided by primary care physicians to patients with myocardial infarction or heart failure.

PURPOSE: To assess the effects of an intervention involving dissemination of treatment recommendations to primary care physicians treating outpatients with acute myocardial infarction or heart failure. METHODS: The study comprised 509 patients with myocardial infarction and 323 patients with heart failure who were discharged from hospital. The primary care physicians caring for these patients were assigned randomly to either the intervention or control group; the intervention group was mailed practice guidelines immediately after patient discharge, and patients were cited by name. During a 6-month assessment period, the records of primary care physicians (and cardiologists, if any) were reviewed to assess mean conformance with the guidelines, using seven measures of care for myocardial infarction and eight measures of care for heart failure. RESULTS: After adjusting for demographic and clinical characteristics of patients, and the number of eligible measures per patient, we observed no effect of the intervention on care of patients with myocardial infarction (odds ratio [OR] = 0.98; 95% confidence interval [CI]: 0.81 to 1.17) or heart failure (OR = 1.25; 95% CI: 0.96 to 1.59). However, there was a higher likelihood of conformance with measures for patients with infarction (OR = 1.56; 95% CI: 1.29 to 1.87) or heart failure (OR = 1.71; 95% CI: 1.29 to 2.23) who had also been seen by a cardiologist during the 6-month assessment period. CONCLUSION: Mailing treatment recommendations did not improve the quality of care of recently discharged patients with myocardial infarction or heart failure. However, efforts to include cardiologists in the care of these patients might be worthwhile.

Hospital outcomes in major teaching, minor teaching, and nonteaching hospitals in New York state.

PURPOSE: The possible benefit that hospital teaching status may confer in the care of patients with cardiovascular disease is unknown. Our purpose was to determine the effect of hospital teaching status on in-hospital mortality, use of invasive procedures, length of stay, and charges in patients with myocardial infarction, heart failure, or stroke. SUBJECTS AND METHODS: We analyzed a New York State hospital administrative database containing information on 388 964 consecutive patients who had been admitted with heart failure (n = 173 799), myocardial infarction (n = 121 209), or stroke (n = 93 956) from 1993 to 1995. We classified the 248 participating acute care hospitals by teaching status (major, minor, nonteaching). The primary outcomes were standardized in-hospital mortality ratios, defined as the ratio of observed to predicted mortality. RESULTS: Standardized in-hospital mortality ratios were significantly lower in major teaching hospitals (0.976 for heart failure, 0.945 for myocardial infarction, 0.958 for stroke) than in nonteaching hospitals (1.01 for heart failure, 1.01 for myocardial infarction, 0.995 for stroke). Standardized in-hospital mortality ratios were significantly higher for patients with stroke (1.06) but not heart failure (1.0) or myocardial infarction (1.06) in minor teaching hospitals than in nonteaching hospitals. Compared with nonteaching hospitals, use of invasive cardiac procedures and adjusted hospital charges were significantly greater in major and minor teaching hospitals for all three conditions. The adjusted length of stay was also shorter for myocardial infarction in major teaching hospitals and longer for stroke in minor teaching hospitals. CONCLUSION: Major teaching hospital status was an important determinant of outcomes in patients hospitalized with myocardial infarction, heart failure, or stroke in New York State.

Tricuspid Regurgitation and Right Heart Dimensions at Early and Late Follow-Up After Orthotopic Cardiac Transplantation.

Tricuspid regurgitation is common immediately after cardiac transplantation, but its course over long-term follow-up is not known. This study was performed to determine the prevalence of valvular regurgitation and to evaluate if pulmonary hypertension or right ventricular enlargement were associated with the severity of tricuspid regurgitation at early and late follow-up after cardiac transplantation. Fifty-five patients had hemodynamic and echocardiographic studies performed at 1 week and 2.4 +/- 1.3 years after cardiac transplantation. Right ventricular dimensions were measured and related to the severity of tricuspid regurgitation as assessed by Doppler color flow. There was a fall in right heart filling pressures with decreases in the systolic pulmonary artery pressure (31 mmHg +/- 7 mmHg vs 27 mmHg +/- 7 mmHg, P = 0.0001) and right atrial pressure (8 +/- 5 mmHg vs 6 +/- 4 mmHg, P < 0.01). Sixty-three percent of patients had mild or higher grade tricuspid regurgitation initially and 71% at follow-up (P = NS). The major determinant of tricuspid regurgitation severity at late follow-up was the presence of flail tricuspid leaflets (P < 0.0001). There was an association between the change in grade of tricuspid regurgitation and the change in right ventricular diastolic area (P = 0.002) and the change in tricuspid annulus diameter (P < 0.0001). The prevalence of tricuspid regurgitation remains high at late follow-up after cardiac transplantation and neither pulmonary hypertension nor right ventricular dilatation are prerequisites for tricuspid regurgitation, which can persist in their absence. Flail tricuspid leaflets are the most important predictors of the severity of tricuspid regurgitation following cardiac transplantation.

Institutional volume of heart transplantation with left ventricular assist device explantation influences graft survival.

BACKGROUND: There are increasing numbers of patients undergoing orthotopic heart transplantation (OHT) with left ventricular assist device (LVAD) explantation (LVAD explant-OHT). We hypothesized that LVAD explant-OHT is a more challenging surgical procedure compared to OHT without LVAD explantation and that institutional LVAD explant-OHT procedural volume would be associated with post-transplant graft survival. We sought to assess the impact of institutional volume of LVAD explant-OHT on post-transplant graft survival. METHODS: This is a retrospective analysis of the Scientific Registry of Transplant Recipients for adult OHTs with long-term LVAD explantation. LVAD explant-OHT volume was characterized on the basis of the center's year-specific total OHT volume (OHTvol) and year-specific LVAD explant-OHT volume quartile (LVADvolQ). The effect of LVADvolQ on graft survival (death or re-transplantation) was analyzed. RESULTS: From 2004 to 2011, 2,681 patients underwent OHT with LVAD explantation (740 with HeartMate XVE, 1,877 with HeartMate II and 64 with HeartWare devices). LVAD explant-OHT at centers falling in the lowest LVADvolQ was associated with reduced post-transplant graft survival (p = 0.022). After adjusting for annualized OHTvol (HR = 0.998, 95% CI 0.993 to 1.003, p = 0.515 and pulsatile XVE (HR = 0.842, 95% CI 0.688 to 1.032, p = 0.098), multivariate analysis confirmed a significantly (approximately 37%) increased risk of post-transplant graft failure among explant-OHT procedures occurring at centers in the lowest volume quartile (HR = 1.371, 95% CI 1.030 to 1.825, p = 0.030). CONCLUSION: Graft survival is decreased when performed at centers falling in the lowest quartile of LVAD explant-OHT for a given year. This volume-survival relationship should be considered in the context of limited donor organ availability and the rapidly growing number of LVAD centers.

Does renal dysfunction and method of bridging support influence heart transplant graft survival?

BACKGROUND: Renal insufficiency is common in status 1B patients supported with inotropes or a continuous flow left ventricular device (CF-LVAD) as a bridge to heart transplantation. We evaluated the association of renal function and inotrope versus CF-LVAD support on posttransplant graft survival in status 1B patients. METHODS: The Scientific Registry for Transplant Recipients database was analyzed for posttransplant survival in status 1B patients bridged with inotropes or CF-LVAD who underwent transplantation between 2003 and 2012. Pretransplant renal function was measured by estimating glomerular filtration rate (GFR) and was stratified as less than 45 mL · min(-1) · 1.73 m(-2), 45 to 59, and 60 or greater. Univariate Kaplan-Meier and multivariate Cox regression models were used to evaluate the main effects of GFR strata and inotropes versus CF-LVAD, and the interaction effect of GFR strata by CF-LVAD, on graft survival. RESULTS: This study included 4,158 status 1B patients (74% male, aged 53 ± 12 years). Of those, 659 patients had a CF-LVAD (HeartMate-II [Thoratec, Pleasanton, CA], n = 638; HVAD [HeartWare, Framingham, MA], n = 21), and 3,530 were receiving inotropes (31 CF-LVAD patients were also receiving inotropes). Kaplan-Meier analyses demonstrated reduced graft survival (p = 0.022) in patients with pretransplant GFR less than 45 versus GFR 45 to 59 (p = 0.062) and versus GFR 60 or greater (p = 0.007), and no effect of inotrope versus CF-LVAD support on graft survival (p = 0.402). Multivariate analysis demonstrated that, after adjusting for the main effects of GFR stratum, CF-LVAD, and inotropes, status 1B patients bridged with a CF-LVAD and GFR in the lowest stratum had reduced graft survival (interaction effect p = 0.040). CONCLUSIONS: Pretransplant renal insufficiency was associated with reduced posttransplant graft survival in status 1B patients. This risk is increased for patients bridged with a CF-LVAD (versus inotropes) who have GFR in the lowest stratum.

Perioperative blood product use: a comparison between HeartWare and HeartMate II devices.

BACKGROUND: The HeartWare (HW) (Framingham, MA) and the HeartMate II (HM II) (Thoratec Inc, Pleasanton, CA) continuous-flow left ventricular assist devices (CF-LVADs) are commonly used to bridge patients to transplantation. We hypothesized that there are differences in perioperative blood product (BP) use and chest tube (CT) output between CF-LVAD types. METHODS: We retrospectively evaluated BP use in 71 patients who were implanted with a CF-LVAD (HM II = 38; HW = 33) by median sternotomy for bridge to transplantation (BTT) indications from 2009 to 2013. Detailed BP use data were collected during the intraoperative and postoperative periods and included packed red blood cells, platelets, fresh frozen plasma, and cryoprecipitate. RESULTS: Preoperative characteristics (age, left ventricular ejection fraction, previous sternotomy, ischemic cause), and risk stratification scores (Interagency Registry for Mechanically Assisted Circulatory Support [INTERMACS]) profile, Leitz-Miller score, Kormos score) were comparable between groups (all p > 0.05). Total average intraoperative and postoperative BP use was different between device types: HW = 8.3 ± 13 versus HM II = 12.6 ± 14.0 units (p = 0.002) and HW = 6.1 ± 12.0 units compared with HM II = 13.5 ± 24.1 units (p = 0.022), respectively. Average postoperative CT output for HW (3,231 ± 3,648 mL) and HM II (3,463 ± 3,050) (p < 0.008) were different between device types. Multivariate analysis revealed that a higher preoperative Leitz-Miller score, implantation of an HM II CF-LVAD, previous sternotomy, and a longer duration of cardiopulmonary bypass (CPB) time were independently associated with increased need for BP use, whereas only use of the HM II device and a longer bypass time predicted a greater CT output. CONCLUSIONS: Compared with HM II, implantation of the HW CF-LVAD was associated with reduced intraoperative and postoperative BP use and decreased CT output. Increased awareness of device-related differences in bleeding and BP use may improve CF-LVAD patient outcomes.

Contemporary management of tricuspid regurgitation: an updated clinical review.

Tricuspid regurgitation (TR) is a complex and insidious valvular pathology that represents a complex decision and management algorithm for patients. TR is present in a significant proportion of the population and is especially prevalent in patients with advanced heart failure. Patients with TR have been demonstrated to have a decreased survival even with normal left heart function. TR can be a result of pathology that directly affects the valvular structure (i.e., Ebstein anomaly) or as a result of increased forward pressures (ie, pulmonary hypertension, left heart failure). Conservative management of patients with TR is primarily symptomatic relief. Definitive therapy involves surgical repair of the tricuspid valve. Furthermore, as more patients develop advanced heart failure, the management of TR in patients with left ventricular assist devices has become necessary because of the evidence of increased in-hospital morbidity and a trend toward decreased survival.

Stem cell therapy for chronic heart failure: an updated appraisal.

INTRODUCTION: Significant advances have been made to understand the mechanisms involved in cardiac cell-based therapies. The early translational application of basic science knowledge has led to several animal and human clinical trials. The initial promising beneficial effect of stem cells on cardiac function restoration has been eclipsed by the inability of animal studies to translate into sustained clinical improvements in human clinical trials. AREAS COVERED: In this review, the authors cover an updated overview of various stem cell populations used in chronic heart failure. A critical review of clinical trials conducted in advanced heart failure patients is proposed, and finally promising avenues for developments in the field of cardiac cell-based therapies are presented. EXPERT OPINION: Several questions remain unanswered, and this limits our ability to understand basic mechanisms involved in stem cell therapeutics. Human studies have revealed critical unresolved issues. Further elucidation of the proper timing, mode delivery and prosurvival factors is imperative, if the field is to advance. The limited benefits seen to date are simply not enough if the potential for substantial recovery of nonfunctioning myocardium is to be realized.