Citations

Introduction: Age ≥ 70 is used to exclude patients from cardiac transplantation. Elderly patients may be offered left ventricular assist device (LVAD) therapy as an alternative. It remains poorly defined how they respond to LVAD support. Hypothesis: Elderly patients have LVAD outcomes that are non-inferior to younger patients. Methods: Data on 1,149 continuous-flow LVAD recipients from May 2004 to May 2015 was pooled from the Mechanical Circulatory Support Research Network (MCSRN). Groups were assigned based on Age ≥ 70 (n = 163) and < 70 (n = 986). Results: Patients age ≥ 70 were more likely to be male (91%), have an ischemic cardiomyopathy (71%), atrial fibrillation (41%), hypertension (66%), diabetes (38%) and prior sternotomy (45%). Older patients also had a lower BMI and higher creatinine, 26.7 ± 0.4 v. 29.9 ± 0.5 and 1.46 ± 0.04 v. 1.35 ± 0.02, p < 0.05. The hazard ratio for mortality was highest in elderly patients in the early post-operative period and stabilized over time with no long-term differences in survival, p = 0.18, Figure 1a. Elderly patients had equivalent rates of device thrombosis and stroke, p = 0.47 and 0.44, Figures 1b-c. Survival free of gastrointestinal bleeding (GIB) at 1-year was 58% in elderly patients compared to 69% in younger patients, Figure 1d, p < 0.01. Multivariate cox regression revealed that age ≥ 70 was not a significant predictor of mortality (HR 0.93, 95% CI 0.69 - 1.25, p = 0.62), but pre-operative creatinine (HR 1.54, 95% CI 1.28 - 1.86, p < 0.01) and bilirubin (HR 1.2, 95% CI 1.03 - 1.4, p = 0.02) were. When age was considered a continuous variable, the HR was 1.2 (95% CI 1.07 - 1.3 per 10y, p < 0.01). Conclusions: Elderly patients, age ≥ 70, have equivalent long-term survival after LVAD implantation with similar rates of device thrombosis and stroke. Rates of GIB were higher in the elderly and this finding warrants caution when choosing anti-coagulation protocols in the elderly. Overall age ≥ 70 does not portend a poorer survival after LVAD implant.

Introduction: In vitro, ST2 is a marker of myocyte stress and inflammation but in vivo, there is no trans-cardiac ST2 concentration step-up to support cardiac ST2 activation in human heart failure (HF) calling into question the source of ST2 in HF. While ST2 is predictive of adverse outcomes in HF, the relationship between ST2 and key pathophysiologic domains in HF with preserved ejection fraction (HFpEF) is not well characterized. Hypothesis: ST2 levels increase in proportion to the severity of left ventricular (LV) remodeling and dysfunction in HFpEF. Methods: At enrollment, patients (n=174) from the RELAX trial testing sildenafil in HFpEF had serum ST2 levels measured and underwent assessment of pathophysiologic domains including congestion, cardiac structure and function, exercise performance (peak oxygen consumption (VO2)) and biomarkers of neurohumoral activation (NT-proBNP, aldosterone, endothelin-1), renal dysfunction (cystatin-C), fibrosis (pro-collagen III N-terminal peptide [NTP], C-telopeptide for type I collagen [CITP]), inflammation (high-sensitivity CRP [hsCRP]) and myocardial necrosis (high-sensitivity troponin-I [hsTnI]). Analysis adjusted for sex, a covariate associated with ST2 levels in normal persons. Results: See table. ST2 was associated with greater congestion, worse right ventricular (RV) pressure overload and dysfunction, lower peak VO2 and biomarkers of neurohumoral activation, renal dysfunction, fibrosis and myocardial necrosis and tended to be associated with systemic inflammation (hsCRP). ST2 was not associated with LV structure or LV systolic or diastolic function. Conclusions: In HFpEF, ST2 was associated with measures of right sided congestion, RV overload and dysfunction, exercise intolerance and other systemic markers of more advanced HF but not with LV structure or LV systolic or diastolic function. These data suggest that mechanisms distinct from LV stress stimulate ST2 activation in HFpEF.

Background: As the United States medical system transitions to value-based reimbursement, interested parties will increase scrutiny in testing that may not alter management or outcomes. We investigated whether transesophageal echocardiography (TEE) provokes treatment alteration across age strata in hospitalized patients undergoing a TIA/stroke work-up. Methods: Consecutive patients admitted to the Mayo Clinic Arizona healthcare system between 1/1/2010 and 2/9/2015 were evaluated. A total of 832 patients were identified of which 314 were excluded primarily due to the fact that the TEE was performed as an outpatient. Therefore, 518 subjects (mean age = 68.2 +/- 14.1 y, 42.5% female) were included. A change in treatment was defined a priori as: anticoagulation (AC) initiated for atrial fibrillation found on TEE only (i.e. not identified on telemetry), complex proximal aortic arch plaque, left atrial or left atrial appendage thrombus, intracardiac mass, intracardiac shunt (atrial septal defect (ASD)/ patent foramen ovale (PFO)) ; PFO closure; cardiac mass removal; valve replacement for endocarditis; antibiotics for endocarditis. Results: See Tables A & B Conclusion: TEE in the evaluation of hospitalized patients with TIA/stroke resulted in a change in treatment in approximately 7% of patients regardless of age. Many of the decisions to change treatment were judgment-based and therefore adoption of the routine use of TEE in all patients with TIA/stroke is dependent on institutional practice standards.

Introduction: Exercise parameters such as peak heart rate (HR) are generally adjusted for age, whereas HR recovery is generally given as an absolute value: < 13 bpm at 1 minute post-peak exercise being abnormal. Hypothesis: We analyzed a large cohort of patients to determine the impact of age on HR recovery (HRRec) and if the prognostic performance of HRRec is improved by adjustment for age. Methods: Non-imaging exercise tests performed on patients aged 30-79 years from 1993 to 2010 were included. Patients with known cardiovascular diseases were excluded. Patients were assigned to 5 groups according to age: 30-39, 40-49, 50-59, 60-69, and 70-79. Mortality was reported according to HRRec during the first minute of active recovery using Cox regression analysis. Mortality was determined from Minnesota and National Death Indices. Results: 22,643 patients (64 % male) were included. The median HRRec in the age groups with IQR were as follows: 30-39: 20 [15-26]; 40-49: 19 [14-25]; 50-59: 18 [13-23]; 60-69: 15 [10-20]; and 70-79: 11 [6-16]. There were 1566 deaths (6.9%) over a mean follow-up of 11.8 ± 5.0 years. HRRec of 13 would fall at the 17 th percentile for patients 30-39 years old, but this increased to the 20 th , 27 th , 40 th , and 60 th percentiles with increasing age group. The mortality in age groups according to HRRec is shown in the Figure. For age groups 30-39 and 40-49, the hazard ratio for mortality at a HRRec of 11-12 bpm (i.e. just below the standard of 13) versus patients with a HRRec of ≥ 20 bpm was > 2.0. For age 50-59 and 60-69, however, a HRRec of < 11 bpm is necessary to obtain a doubling of risk, and for age 70-79 a HRRec of < 9 bpm is necessary. Conclusions: HRRec decreases significantly with age. The performance of abnormal HRRec defined as < 13 bpm is inconsistent across age groups. To standardize the ability of HRRec to identify at least a 2.0-fold increased risk, lowering the cup-point to < 11 bpm for ages 50-59 and 60-69 and < 9 bpm for age 70-79 is required.

Background: The mosquito-borne Chikungunya virus infection is one of the most important emerging virus diseases globally. Local transmission has been found in the United States. There are very few published reports concerning the cardiac complications in general and less of arrhythmias in particular. Chikungunya can be fatal: there have been sudden deaths reports . Objective: To investigate arrhythmic complications of Chikungunya myocarditis. Methods: Prospective multicenter observational study of 280 patients with a Chikunguya infection from a Venezuelan Outbreak. Clinical evaluation, ECG, laboratory including virological evaluation and cardiac biomarkers, Echocardiogram, Holter and cardiac MRI procedures were carried out. Results: Of the 280 patients examined, 113 patients were male, with a mean age of 59 ± 9; 270 patients presented with fever and polyarthralgia and 85 developed palpitations. Arrhythmias occured in 45% of cases; they included bradyarrhythmias (33%), atrial and ventricular ectopic beats and tachyarrhythmias in which atrial fibrillation was observed in 19 cases. There were also ectopic atrial tachycardia and non sustained ventricular tachycardia, conduction disturbances and 3 cases of sudden death. Conclusion: Physicians should know that almost half of the Chikungunya patients will develop arrhythmias and manifest or silent myocarditis. In the proper epidemiological context, the triad of fever, polyarthralgia and new arrhythmia including bradiarrhythmias suggest Chikungunya Myocarditis.

Background: Bystander cardiopulmonary resuscitation (BCPR) significantly improves survival from out-of-hospital cardiac arrest (OHCA). Telecommunicator CPR (TCPR) has been shown to increase BCPR rates, yet TCPR performance varies widely. We assess whether a bundled TCPR protocol, training, and continuous quality improvement (CQI) intervention improves TCPR performance. Methods: The intervention was implemented at a regional 9-1-1 dispatch center and had three main components: (1) the installation of the AHA-recommended 2-question TCPR protocol, (2) training to enhance telecommunicator OHCA recognition and (3) CQI with system and case-level feedback. Training included a two-hour lecture, 30 minutes of video training, and one hour of simulation training. Audio recordings of suspected OHCAs from pre (P1, 10/5/10 - 11/6/11) and post-intervention (P2, 11/7/11 - 11/4/13) periods were collected by searching center archives for calls originally processed as cardiac arrests. Recordings were analyzed according to six key TCPR metrics. Times to telecommunicator recognition of cardiac arrest, start of TCPR instructions, and initiation of chest compressions were measured using a standardized timestamp format. Results: Rates of OHCA recognition (80% to 95%, p<0.0001), TCPR instructions started (32% to 72%, p<0.0001), and bystander chest compressions initiated (18% to 70%, p<0.001) all increased significantly. Reductions in the time from call receipt to the start of TCPR instructions (176s to 133s, p<0.0001) and to the start of compressions (265s to 162s, p<0.0001) were also observed. Conclusion: This bundled protocol, training and CQI intervention was associated with a significant increase in TCPR rates and a reduction in the time to first chest compression.

Background: Circulating cardiac troponin T concentrations are higher in men than in women, but the biological causes and clinical implications of this observation are poorly understood. Methods and Results: We measured cardiac troponin T with a high-sensitivity assay (hsTnT) in 684 women and 1601 men with type 2 diabetes (T2D) and stable ischemic heart disease (SIHD) who were enrolled in the BARI 2D trial. Median (IQR) hsTnT was higher in men [12.4 ng/L (8.7-20.8)] than in women [9.1 ng/L (6.4-15.6); P<0.0001] and a higher proportion of men (43.6%) than women (29.1%) were above the current established upper reference limit of 14 ng/L (P<0.0001). Sex remained a significant predictor of natural log normalized hsTnT after adjusting for a wide array of covariables, including age, race, insulin use, renal function, ejection fraction, and HbA1c. Within quintiles of hsTnT measured at baseline, the 5-year incidence of the composite cardiovascular outcome of myocardial infarction, stroke, heart failure, or death was consistently higher in women than in men (Figure 1). In sex-stratified Cox models adjusting for possible confounders, the increase in the relative risk of the composite endpoint across quintiles of hsTnT appeared similar in men and women (Figure 2). Conclusions: In the BARI 2D trial, women have lower baseline hsTnT concentrations, but higher absolute risk of myocardial infarction, stroke, heart failure, or death for a given concentration of hsTnT. These data raise the question of whether sex-specific cutoffs for cardiac troponin T should be considered.

Background: Concerns exist regarding orthotropic heart transplantation (OHT) in hepatitis C (HCV) seropositive recipients. The UNOS national registry was accessed to evaluate HCV recipient sero-positivity and outcomes. Method: Retrospective analysis of the UNOS registry (2000-2014) to evaluate recipient profile and clinical outcome of HCV sero-positive (HCV+ve) and sero-negative (HCV -ve) pts. Early and late adjusted survival and adverse events at follow-up were compared. Results: From 23,507 patients (mean age 52 yrs; 75% male), 481 (2%) were HCV +ve (mean age 52 yrs; 77% male). Annual proportion of HCV +ve recipients was comparable over the study period (range 1.3-2.7%; p=0.2). The HCV +ve cohort had more African American (22% vs 17%; p=0.01), pts with a prior LVAD (21 vs 14%; p<0.01 and more hepatitis B core Ag+ve recipients (17% vs 5%; p<0.01). However, ECMO (p=0.7), inotropic (p=0.2), and intra-aortic balloon pump (p=0.7) support, serum creatinine (p=0.7) and serum bilirubin (p=0.7) were similar. Proportion of Status 1A pts was similar (24% HCV+ vs 21% HCV -); however wait-time for HCV + recipients was longer (mean 23 vs 19 days; p<0.01). Among donor variables, age (p=0.8), hepatitis B status (p=0.4) and CDC high risk status (p=0.9) were comparable. At a median follow up of 4 years, 67.1% patients were alive, 28.4% died and 1.1% were re-transplanted (3.4% missing). Overall survival was worse in the HCV+ cohort (64.3 vs 72.9 % and 43.2 vs 55% at five and ten years; p<0.01). Late renal [OR 1.2(1-1.6); p = 0.02] and liver dysfunction [OR 4.5 (1.2-15.7); p=0.01] occur in HCV +ve recipients. On adjusted analysis, HCV sero-positivity is associated with poorer survival [HR0.6 (0.5-0.8); p<0.01]. Conclusion: A small proportion of patients receiving a heart transplant in the United States have hepatitis C. In spite of comparable pre-operative hepatic function, hepatitis C sero-positive recipients develop late liver dysfunction and have poorer long-term survival.

Introduction: Current dietary guidelines no longer recommend against egg consumption despite the high cholesterol content. However, considerable controversy remains on the relationship between high egg consumption and cardiovascular disease (CVD) risk. The objective of this systematic review and meta-analysis was to explore the association between egg consumption and CVD events. Methods: We systematically searched PubMed, Scopus, and the Cochrane Database of Systematic Reviews from database inception through April 2015 for observational studies with hazard ratio (HRs) or relative risks (RRs) and 95% confidence intervals (95% CI) that reported the association between egg consumption and CVD events which included coronary heart disease (CHD) and stroke. Data were extracted by one reviewer followed by independent screening and extraction of study characteristics and outcome data by two other reviewers. Conflicts were resolved through consensus. Random-effects meta-analyses were used to pool the hazard ratios or relative risks from the included studies. Subgroup analyses were performed to explore the potential sources of heterogeneity. The quality of the included studies and publication bias were assessed. Results: We identified 5 cross-sectional and 6 prospective studies with median follow-up of 13.1 years. A total of 301,339 individuals and 10,262 total CVD events were included with 7,225 CHD and 3,037 stroke cases. Compared to consumption of less than 1 egg/day, higher egg consumption was associated with an increased risk of CVD events (pooled HR, 1.43; 95% CI, 1.01-2.03; p=0.012; I 2 = 65.7% and pooled RR, 1.09; 95% CI, 0.89-1.34; p=0.145; I 2 = 41.4%). Conclusions: Our analysis suggests that higher consumption of eggs (more than 1 egg/day) may be associated with increased risk of cardiovascular disease. Large and diverse prospective community-based cohorts will be necessary to establish optimal dietary recommendations for public health.

Introduction: The popularity of energy drinks among young adults is rising. Warnings have been issued regarding potential health risks including adverse cardiovascular complications. We and others have previously shown that energy drink consumption increases blood pressure. The mechanisms are not fully understood. Hypothesis: We hypothesized that increase in blood pressure after drinking a commercially available energy drink, compared to a placebo, is secondary to increased sympathetic activation. Methods: In a randomized, double-blind, placebo-controlled, cross-over study, we studied 25 healthy subjects, age 29±1 years, who were free of known disease, had no known cardiovascular risk factors, and were not on any medications. Each subject consumed a can, 16-fluid ounces, of Rockstar energy drink or a placebo drink in random order on two separate days. Blood pressure (n=25) and plasma norepinephrine levels (n=23) were measured before and 30-minutes after drink consumption. Results: Despite the increase in blood pressure after drinking Rockstar energy drink, which would be expected to elicit reflex reductions in central sympathetic outflow, plasma norepinephrine levels increased markedly after energy drink consumption vs placebo (73.6±9.7% vs 30.9±9.7%, respectively, P=0.003; Figure). Specifically, plasma norepinephrine levels increased from 149.8±11.7pg/ml to 249.8±17.3pg/ml after the energy drink consumption and from 139.9±11.7pg/ml to 178.6±17.3pg/ml after placebo (P=0.0007 for timeхtreatment comparison). Conclusions: Increased blood pressure after consumption of commercially available energy drink is associated with significantly increased catecholamine levels in young healthy adults. These acute hemodynamic and adrenergic changes may predispose to increased cardiovascular risk by triggering arrhythmias or ischemia, particularly in individuals with a vulnerable cardiovascular substrate.