Ternus, Bradley

Introduction: Baseline hemodynamic parameters have been shown to predict postoperative outcomes such as right ventricular failure (RVF) in LVAD patients. The pressure adjusted heart rate (PaHR) is a hemodynamic parameter that has not been reported in LVAD recipients. Hypothesis: Patients with an elevated PaHR at baseline will have an increased risk of adverse outcomes following LVAD implantation. Methods: Historical cohort study of 273 patients with preoperative invasive hemodynamic assessment before durable LVAD implantation from January 1 st , 2007 to April 10 th 2017. Baseline patient characteristics and hemodynamic parameters were assessed. The primary endpoint was a composite of 30 day mortality, stage 3 acute kidney injury (AKI), and postoperative RVF. Univariate analysis was used to identify predictors of the composite endpoint, which were entered into stepwise backwards multivariate logistic regression to determine independent predictors of the composite outcome. Results: The mean age was 59 and 79% of the patients were male. The median INTERMACS profile was 4 and 166 (60%) of LVADs placed were as destination therapy. The primary composite endpoint was reached by 74 (27%) patient, including 30-day mortality in 13 (5%), severe AKI in 48 (18%) and RVF in 53 (19%). Univariate predictors of the composite endpoint (p <0.05) included atrial fibrillation, INTERMACS profile, home inotropes, preoperative IABP, admission creatinine, baseline Vasoactive-Inotropic Score, mean right atrial pressure (mRAP), mRAP/wedge, mean arterial pressure/mRAP, mean pulmonary artery pressure/mRAP, right ventricular stroke work index (RVSWi), pulmonary artery pulsatility index, and the PaHR. Logistic regression identified PaHR (OR 0.96, 95% CI 0.93-0.99, p=.026), RVSWi (OR 1.002, 95% CI 1.001-1.004, p=.002), home inotropes (OR 0.46, 95% CI 0.22-0.94, p=.034), atrial fibrillation (OR 0.48, 95% CI 0.26-0.88, p=.019) and admission creatinine (OR 0.51, 95% CI 0.34-0.77, p=0.002) as predictors of the composite endpoint. Conclusions: The PaHR is a readily available, novel hemodynamic parameter, that when elevated on baseline hemodynamic assessment can predict those patients at increased risk of postoperative adverse outcomes after durable LVAD implantation.

Introduction: Patients at increased risk of complications following LVAD placement are admitted to the hospital for hemodynamic optimization prior to LVAD implantation, which can include adjustment of medical therapy and/or placement of an IABP. Hypothesis: Prior to LVAD placement patients treated with an IABP during hemodynamic optimization will have similar outcomes despite worse baseline characteristics compared with patients treated medically. Methods: This single-center study included 199 non-inotrope dependent patients who underwent durable LVAD implantation between January 1 st , 2007 and April 10 th 2017. Hemodynamic data was collected retrospectively. Patients who received an IABP were compared to those who did not. Stage 2 or 3 acute kidney injury, right ventricular failure, and 30 day mortality was compared between patients with and without and IABP. Results: The mean age was 62.7 and 82.9% were male; 72 (36.2%) received an IABP. Baseline characteristics between groups were similar. Patients treated with an IABP had worse INTERMACS profiles and worse baseline hemodynamic parameters. The incidence of the primary composite endpoint was similar between patients who had an IABP and those who did not (23.6% vs 19.7%; p=0.517), as were each of the individual endpoints: stage 2 or 3 acute kidney injury (18.1% vs 14.2%; p=0.472), right ventricular failure (13.9% vs 13.4%; p=0.796), and 30 day mortality (6.9 % vs 3.2%; p=0.226). Patients treated with an IABP had greater relative reductions in mean right atrial pressure (-24.1% vs -5.9%; p=0.044), pulmonary artery systolic (-11.7% vs +3.3%; p=<0.001), diastolic (-17.0% vs +12.0%; p=0.015), and mean pressures (-15.2% vs 0.5%; p=<0.001). Conclusions: Despite worse hemodynamic parameters and INTERMACS profile at baseline, ambulatory heart failure patients who received an IABP prior to LVAD implantation did not have an increased incident of stage 2 or 3 acute kidney injury, right ventricular failure, or 30 day mortality, and had more favorable reductions in right atrial and pulmonary artery pressures. These results suggest that the use of the IABP prior to LVAD implantation in non-inotrope dependent patients with poor baseline hemodynamics may mitigate the risk of postoperative complications.

Background Shock and preshock are defined on the basis of the presence of hypotension, hypoperfusion, or both. We sought to determine the hemodynamic underpinnings of shock and preshock noninvasively using transthoracic echocardiography (TTE). Methods and Results We included Mayo Clinic cardiac intensive care unit patients from 2007 to 2015 with TTE within 1 day of admission. Hypotension and hypoperfusion at the time of cardiac intensive care unit admission were used to define 4 groups. TTE findings were evaluated across these groups, and in‐hospital mortality was evaluated according to TTE findings in each group. We included 5375 patients with a median age of 69.2 years (36.8% women). The median left ventricular ejection fraction was 50%. Groups based on hypotension and hypoperfusion were assigned as follows: no hypotension or hypoperfusion, 59.7%; isolated hypotension, 15.3%; isolated hypoperfusion, 16.4%; and both hypotension and hypoperfusion, 8.7%. Most TTE variables of interest varied across these groups, with worse biventricular function, lower forward flow, and higher filling pressures as the degree of hemodynamic compromise increased. In‐hospital mortality occurred in 8.2%, and inpatient deaths had more TTE parameter abnormalities. In‐hospital mortality increased with the degree of hemodynamic compromise, and a marked gradient in in‐hospital mortality was observed when the clinical classification of shock and preshock was combined with TTE findings reflecting worse biventricular function, lower forward flow, or higher filling pressures. Conclusions Substantial differences in cardiac function are observed between cardiac intensive care unit patients with preshock and shock using TTE, and the combination of the clinical and TTE hemodynamic assessment provides robust mortality risk stratification.

AbstractAimsThe aims of the Critical Care Cardiology Trials Network (CCCTN) are to develop a registry to investigate the epidemiology of cardiac critical illness and to establish a multicentre research network to conduct randomised clinical trials (RCTs) in patients with cardiac critical illness.Methods and resultsThe CCCTN was founded in 2017 with 16 centres and has grown to a research network of over 40 academic and clinical centres in the United States and Canada. Each centre enters data for consecutive cardiac intensive care unit (CICU) admissions for at least 2 months of each calendar year. More than 20 000 unique CICU admissions are now included in the CCCTN Registry. To date, scientific observations from the CCCTN Registry include description of variations in care, the epidemiology and outcomes of all CICU patients, as well as subsets of patients with specific disease states, such as shock, heart failure, renal dysfunction, and respiratory failure. The CCCTN has also characterised utilization patterns, including use of mechanical circulatory support in response to changes in the heart transplantation allocation system, and the use and impact of multidisciplinary shock teams. Over years of multicentre collaboration, the CCCTN has established a robust research network to facilitate multicentre registry-based randomised trials in patients with cardiac critical illness.ConclusionThe CCCTN is a large, prospective registry dedicated to describing processes-of-care and expanding clinical knowledge in cardiac critical illness. The CCCTN will serve as an investigational platform from which to conduct randomised controlled trials in this important patient population.

Introduction: Renal dysfunction, as defined by elevated serum creatinine, is associated with decreased survival among patients resuscitated after out-of-hospital cardiac arrest (OHCA). Less is known about other measures of renal function and outcomes after OHCA. Hypothesis: BUN and urine output will predict mortality after OHCA. Methods: Retrospective single-center cohort study of 276 adult OHCA patients treated with targeted temperature management after OHCA between December 2005 and September 2016. Fluid balance and urine output were recorded for the first 6, 12 and 24 hours. Initial laboratory values were determined from electronic records. Hospital survivors and non-survivors were compared using the Wilcoxon test, and multivariate analysis was performed to determine predictors of hospital death. Results: Mean age was 63±12 years, and 204 (73%) were male; shockable rhythm occurred in 241 (87%). Inpatient death occurred in 111 (40%). Hospital survivors had lower initial BUN (13 vs. 20 mg/dL) and creatinine (1.1 vs. 1.5 mg/dL); all p <.001. Hospital survivors had higher (p <.001) urine output during the first 6 hours (1,091 vs. 559 ml), 12 hours (1,583 vs. 843 ml), and 24 hours (2,215 vs. 1,294 ml). Higher initial BUN (OR 1.12, 95% CI 1.07-1.18) and creatinine (OR 3.036, 95% CI 1.65-5.59) predicted hospital mortality; all p <.001. Urine output during the first 24 hours was associated with hospital mortality (OR 0.57 per each 1 L, 95% CI 0.45-0.72, p <.001; AUROC 0.73, optimal cut-off 1 L). Patients with 24-hour urine output <1 L were at increased risk of hospital death (66.3% vs. 26.0%, unadjusted OR 5.61, 95% CI 3.27-9.63, p <.001). Initial BUN (adjusted OR 1.09, 95% CI 1.01-1.16, p=.02) and urine output during the first 24 hours (adjusted OR 0.71 per each 1 L; 95% CI 0.52-0.97, p=.03) remained predictive of hospital mortality after adjustment for patient characteristics and illness severity. Conclusions: Lower 24-hour urine output and higher initial BUN were associated with higher hospital mortality among patients resuscitated from OHCA, even after adjustment for illness severity. Serum creatinine was not a significant predictor of mortality. This emphasizes the importance of low urine output as a prognostic marker and therapeutic target after OHCA.

Introduction: Lactate is a known prognostic marker in critically ill patients, including patients with shock and cardiac arrest (CA). We sought to describe the association between admission lactate and hospital mortality in cardiac intensive care unit (CICU) patients, particularly those with CA. Methods: We retrospectively evaluated adult patients admitted to a tertiary care CICU from January 1, 2007, to April 30, 2018, with measured lactate on admission. We examined hospital mortality as a function of admission lactate level in patients with and without CA. Multivariable logistic regression was used to determine predictors of hospital mortality in the overall cohort, after adjustment for clinical characteristics, therapies, and illness severity. Results: We included 3,042 patients with a median age of 70 years (IQR 60-80), including 40.5% (n=1,233) females. There were 789 patients (26.1%) with a diagnosis of CA. The median APACHE-4 predicted mortality was 24.2% (IQR 10.9-50.7), and 50.8% (n=1546) were treated with vasoactive infusions. The median lactate on admission was 1.8 mmol/L (IQR 1.1-3.0). CICU mortality occurred in 478 (15.7%) patients) and hospital mortality occurred in 706 (23.2%) patients. Hospital mortality rose progressively as a function of admission lactate ( Figure ). On univariable analysis, lactate was associated with increased hospital mortality among the overall cohort (OR 1.36, CI 1.31-1.42, P < .001; AUROC 0.71), patients with CA (OR 1.33 (95% CI 1.25-1.41, P < .01; AUROC 0.73), and patients without CA (OR 1.27, CI 1.21-1.34, P < .01; AUROC 0.64). On multivariable analysis, lactate was one of the most significant predictors of hospital mortality (adjusted OR 1.13 per mmol/L, 95% CI 1.08-1.18, P < .001). Conclusions: Admission lactate levels are strongly associated with increased hospital mortality among CICU patients, especially those with CA. The prognostic value of lactate levels may help inform clinicians caring for CICU patients.

Introduction: A low cardiac power output (CPO), measured invasively, identifies critically ill patients at increased risk of mortality. CPO can also be measured non-invasively with transthoracic echocardiography (TTE), although prognostic data in critically ill patients is not available. Hypothesis: Reduced CPO measured by TTE is associated with increased hospital mortality in cardiac intensive care unit (CICU) patients. Methods: Using a database of CICU patients admitted between 2007 and 2018, we identified patients with TTE within one day (before or after) of CICU admission who had data necessary for calculation of CPO. Multivariable logistic regression determined the relationship between CPO and adjusted hospital mortality. Results: We included 5,585 patients with a mean age of 68.3±14.8 years, including 36.7% females. Admission diagnoses included acute coronary syndrome (ACS) in 57%, heart failure (HF) in 50%, cardiac arrest (CA) in 12%, and cardiogenic shock (CS) in 13%. The mean left ventricular ejection fraction (LVEF) was 47±16%, and the mean CPO was 1.0±0.4 W. CPO was inversely associated with the risk of hospital mortality (Figure A), including among patients with ACS, HF, and CS (Figure B). On multivariable analysis, lower CPO was associated with higher hospital mortality (OR 0.96 per 0.1 W, 95% CI 0.0.93-0.99, p=0.03). Hospital mortality was highest in patients with low CPO coupled with reduced LVEF, increased vasopressor requirements, or higher admission lactate. Hospital mortality was higher among patients with a CPO <0.6 W (adjusted OR 1.57, 95% CI 1.13-2.19, p = 0.007), particularly in the presence of admission lactate level >4 mmol/L (50.9%). Conclusions: Echocardiographic CPO was inversely associated with hospital mortality in CICU patients, particularly among patients with increased lactate and vasopressor requirements. Routine measurement of CPO provides important information beyond LVEF and should be considered in CICU patients.

ABSTRACT Background: Recent data suggests improved outcomes among cardiac intensive care unit (CICU) patients treated with norepinephrine, especially patients with severe shock. We aimed to describe the association between norepinephrine and mortality in CICU patients with severe shock, defined as those requiring high-dose vasopressors (HDV). Materials and Results: We retrospectively evaluated Mayo Clinic CICU patients treated with vasopressors from 2007 to 2015. HDV was defined as a peak Cumulative Vasopressor Index of four for any vasopressor. Peak norepinephrine equivalent (NEE) dose was used to compare vasopressor doses. Multivariable logistic regression was used to determine predictors of hospital mortality. Results: We included 2,090 patients with a median age of 69 years (IQR 59–78), including 35% females; 44% of patients received HDV. Hospital mortality was higher among patients receiving HDV (42% vs. 16%, unadjusted OR 3.87, 95% CI 3.16–4.75, P < 0.01). On multivariable analysis in HDV patients, hospital mortality increased with rising peak NEE (adjusted OR 1.02 per 0.01 mcg/kg/min, 95% CI 1.01–1.02, P < 0.01) and the use of NE was associated with lower hospital mortality (adjusted OR 0.46, 95% CI 0.31–0.72, P < 0.01). After adjustment for illness severity, peak NEE and norepinephrine use were not associated with mortality among patients who did not require HDV. Conclusions: Mortality is high among CICU patients requiring HDV, and rises with increasing vasopressor requirements. Use of NE was associated with lower mortality among patients requiring HDV, but not among those without HDV, implying that patients with more severe shock may benefit from preferential use of NE.