Shashank Desai

BACKGROUND: Cardiogenic shock (CS) is a multifactorial, hemodynamically complex syndrome associated with high mortality. Despite advances in reperfusion and mechanical circulatory support, management remains highly variable and outcomes poor. OBJECTIVES: This study investigated whether a standardized team-based approach can improve outcomes in CS and whether a risk score can guide clinical decision making. METHODS: A total of 204 consecutive patients with CS were identified. CS etiology, patient demographic characteristics, right heart catheterization, mechanical circulatory support use, and survival were determined. Cardiac power output (CPO) and pulmonary arterial pulsatility index (PAPi) were measured at baseline and 24 h after the CS diagnosis. Thresholds at 24 h for lactate (<3.0 mg/dl), CPO (>0.6 W), and PAPi (>1.0) were determined. Using logistic regression analysis, a validated risk stratification score was developed. RESULTS: Compared with 30-day survival of 47% in 2016, 30-day survival in 2017 and 2018 increased to 57.9% and 76.6%, respectively (p < 0.01). Independent predictors of 30-day mortality were age ≥71 years, diabetes mellitus, dialysis, ≥36 h of vasopressor use at time of diagnosis, lactate levels ≥3.0 mg/dl, CPO <0.6 W, and PAPi <1.0 at 24 h after diagnosis and implementation of therapies. Either 1 or 2 points were assigned to each variable, and a 3-category risk score was determined: 0 to 1 (low), 2 to 4 (moderate), and ≥5 (high). CONCLUSIONS: This observational study suggests that a standardized team-based approach may improve CS outcomes. A score incorporating demographic, laboratory, and hemodynamic data may be used to quantify risk and guide clinical decision-making for all phenotypes of CS.

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CONTEXT: Although liberalization of donor criteria could expand the donor pool, the use of certain "marginal donors," such as those who are hepatitis C virus (HCV) positive, is controversial. Little is known about the effect of donor HCV positivity on survival in cardiac transplantation. OBJECTIVES: To examine the association between donor HCV positivity and survival among heart transplant recipients and to determine the effects of recipient age and recipient HCV status on this association. DESIGN, SETTING, AND PARTICIPANTS: A multicenter cohort study was performed using the US Scientific Registry of Transplant Recipients. Adult heart transplant patients who received their transplants between April 1, 1994, and July 31, 2003, were eligible for inclusion. MAIN OUTCOME MEASURE: All-cause mortality. RESULTS: Of 10 915 patients meeting entry criteria, 261 received an HCV-positive donor heart. Mortality was higher among recipients of HCV-positive donor hearts at 1 year (16.9% vs 8.2%; P<.001), 5 years (41.8% vs 18.5%; P<.001), and 10 years (50.6% vs 24.3%; P<.001). Using Kaplan-Meier methods, 1-, 5-, and 10-year survival rates were 83%, 53%, and 25%, and 92%, 77%, and 53% for recipients of HCV-positive and HCV-negative donor hearts, respectively (P<.001, log-rank test). Recipients of HCV-positive donor hearts were more likely to die of liver disease and coronary vasculopathy. After propensity matching, the overall hazard ratio (HR) associated with receipt of an HCV-positive donor heart was 2.10 (95% confidence interval [CI], 1.60-2.75). Stratified analyses showed that HRs did not vary by recipient HCV status or by recipient age (for recipients aged 18-39 years: HR, 1.75 [95% CI, 0.70-4.40]; for recipients aged 40-59 years: HR, 2.23 [95% CI, 1.42-3.52]; and for recipients aged 60 years and older: HR, 2.07 [95% CI, 1.32-3.27]; overall P value for interaction, >.10). CONCLUSIONS: Receipt of a heart from an HCV-positive donor is associated with decreased survival in heart transplant recipients. This association appears to be independent of recipient HCV status and age. Preferential allocation of HCV-positive donors to HCV-positive recipients and/or older recipients is not warranted.

BACKGROUND: Assessment of gene expression in peripheral blood may provide a noninvasive screening test for allograft rejection. We hypothesized that changes in peripheral blood expression profiles would correlate with biopsy-proven rejection and would resolve after treatment of rejection episodes. METHODS AND RESULTS: We performed a case-control study nested within a cohort of 189 cardiac transplant patients who had blood samples obtained during endomyocardial biopsy (EMB). Using Affymetrix HU133A microarrays, we analyzed whole-blood expression profiles from 3 groups: (1) control samples with negative EMB (n=7); (2) samples obtained during rejection (at least International Society for Heart and Lung Transplantation grade 3A; n=7); and (3) samples obtained after rejection, after treatment and normalization of the EMB (n=7). We identified 91 transcripts differentially expressed in rejection compared with control (false discovery rate <0.10). In postrejection samples, 98% of transcripts returned toward control levels, displaying an intermediate expression profile for patients with treated rejection (P<0.0001). Cluster analysis of the 40 transcripts with >25% change in expression levels during rejection demonstrated good discrimination between control and rejection samples and verified the intermediate expression profile of postrejection samples. Quantitative real-time polymerase chain reaction confirmed significant differential expression for the predictive markers CFLAR and SOD2 (UniGene ID No. 355724 and No. 384944). CONCLUSIONS: These data demonstrate that peripheral blood expression profiles correlate with biopsy-proven allograft rejection. Intermediate expression profiles of treated rejection suggest persistent immune activation despite normalization of the EMB. If validated in larger studies, expression profiling may prove to be a more sensitive screening test for allograft rejection than EMB.