20 research outputs found

    Racial differences in long-term outcomes among older survivors of in-hospital cardiac arrest

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    Background: Black patients have worse in-hospital survival than white patients after in-hospital cardiac arrest (IHCA), but less is known about long-term outcomes. We sought to assess among IHCA survivors whether there are additional racial differences in survival after hospital discharge and to explore potential reasons for differences. Methods: This was a longitudinal study of patients ≥65 years of age who had an IHCA and survived until hospital discharge between 2000 and 2011 from the national Get With The Guidelines–Resuscitation registry whose data could be linked to Medicare claims data. Sequential hierarchical modified Poisson regression models evaluated the proportion of racial differences explained by patient, hospital, and unmeasured factors. Our exposure was black or white race. Our outcome was survival at 1, 3, and 5 years. Results: Among 8764 patients who survived to discharge, 7652 (87.3%) were white and 1112 (12.7%) were black. Black patients with IHCA were younger, more frequently female, sicker with more comorbidities, less likely to have a shockable initial cardiac arrest rhythm, and less likely to be evaluated with coronary angiography after initial resuscitation. At discharge, black patients were also more likely to have at least moderate neurological disability and less likely to be discharged home. Compared with white patients and after adjustment only for hospital site, black patients had lower 1-year (43.6% versus 60.2%; relative risk [RR], 0.72), 3-year (31.6% versus 45.3%; RR, 0.71), and 5-year (23.5% versus 35.4%; RR, 0.67; all P<0.001) survival. Adjustment for patient factors explained 29% of racial differences in 1-year survival (RR, 0.80; 95% confidence interval, 0.75–0.86), and further adjustment for hospital treatment factors explained an additional 17% of racial differences (RR, 0.85; 95% confidence interval, 0.80–0.92). Approximately half of the racial difference in 1-year survival remained unexplained, and the degree to which patient and hospital factors explained racial differences in 3-year and 5-year survival was similar. Conclusions: Black survivors of IHCA have lower long-term survival compared with white patients, and about half of this difference is not explained by patient factors or treatments after IHCA. Further investigation is warranted to better understand to what degree unmeasured but modifiable factors such as postdischarge care account for unexplained disparities.Lena M. Chen, Brahmajee K. Nallamothu, John A. Spertus, Yuanyuan Tang, Paul S. Chan, And the GWTG-R Investigator

    Association between a hospital's quality performance for in-hospital cardiac arrest and common medical conditions

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    Public reporting on hospital quality has been widely adopted for common medical conditions. Adding a measure of inpatient survival after cardiac arrest is being considered. It is unknown whether this measure would be redundant, given evidence that hospital organization and culture can have hospital-wide effects on quality. Therefore, we sought to evaluate the correlation between inpatient survival after cardiac arrest and 30-day risk-standardized mortality rates for common medical conditions.Using data between 2007 and 2010 from a national in-hospital cardiac arrest registry, we calculated risk-standardized in-hospital survival rates for cardiac arrest at each hospital. We obtained risk-standardized 30-day mortality rates for acute myocardial infarction, heart failure, and pneumonia from Hospital Compare for the same period. The relationship between a hospital's performance on cardiac arrest and these other medical conditions was assessed using weighted Pearson correlation coefficients. Among 26 270 patients with in-hospital cardiac arrest at 130 hospitals, survival rates varied across hospitals, with a median risk-standardized hospital survival rate of 22.1% and an interquartile range of 19.7% to 24.2%. There were no significant correlations between a hospital's outcomes for its cardiac arrest patients and its patients admitted for acute myocardial infarction (correlation, -0.12; P=0.16), heart failure (correlation, -0.05; P=0.57), or pneumonia (correlation, -0.15; P=0.10).Hospitals that performed better on publicly reported outcomes for 3 common medical conditions did not necessarily have better cardiac arrest survival rates. Public reporting on cardiac arrest outcomes could provide new information about hospital quality.Lena M. Chen, Brahmajee K. Nallamothu, Harlan M. Krumholz, John A. Spertus, Fengming Tang and Paul S. Chan and for the American Heart Association’s Get With The Guidelines-Resuscitation Investigator

    Baseline inflammation is not predictive of periprocedural troponin elevation after elective percutaneous coronary intervention.

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    High-sensitivity C-reactive protein predicts future cardiovascular events in both healthy individuals and patients with unstable and stable coronary syndromes. Few data are available about the incidence and the relation to inflammation of troponin elevation following percutaneous coronary intervention (PCI), a potential predictor of longterm outcome. We sought to confirm the impact of embolization on long-term outcome and evaluate the ability of baseline inflammation to predict troponin elevation induced by PCI. We prospectively analyzed 200 patients treated by PCI for stable or Braunwald IIA class unstable angina. The patients were recruited between January 1997 and May 1999, and the population was followed during a mean follow-up of 32 months. Major adverse cardiac events (MACEs) were defined as the occurrence of death, myocardial infarction or recurrent angina requiring repeat PCI, or coronary artery bypass grafting. During the follow-up period, 58 MACEs were observed. By multivariate analysis, independent predictors for the occurrence of MACEs were unstable angina and troponin I level after PCI (P < 0.0001 for both). No correlation was found between baseline inflammation and significant troponin I elevation post PCI and by multivariate analysis, no biological variable was a predictor of troponin I elevation post PCI. Baseline inflammation cannot predict onset of minor myonecrosis damage (expressed by troponin elevation) induced by PCI, a significant predictor of long-term outcome in this setting
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