Background-Platelet activation is a hallmark of acute coronary syndromes. Numerous lines of evidence suggest a mechanistic link between von Willebrand factor or platelet hyperfunction and myocardial damage in patients with acute coronary syndromes. Thus, we assessed whether platelet function under high shear rates (collagen adenosine diphosphate closure times [CADP-CTs]) measured with the platelet function analyzer (PFA-100) may be enhanced in patients with myocardial infarction (MI) and whether it may predict the extent of myocardial damage as measured by creatine kinase (CK-MB) or troponin T (TnT) levels. Methods and Results-Patients with acute chest pain or symptoms suggestive of acute coronary syndromes (nϭ216) were prospectively examined at an emergency department. CADP-CT was significantly shorter in patients with MI, particularly in those with an ST-segment-elevation MI (STEMI) compared with the other patient groups (unstable angina, stable coronary artery disease, or controls). Furthermore, CADP-CT and collagen epinephrine-CT at presentation were independent predictors of myocardial damage as measured by CK-MB or TnT. Patients with MI whose CADP-CT values fell in the first quartile had 3-fold higher CK-MB and TnT levels than those in the fourth quartile. Conclusions-Patients with STEMI have significantly enhanced platelet function when measured under high shear rates.CADP-CT is an independent predictor of the severity of MI, as measured by markers of cardiac necrosis. Measurement of platelet function with the PFA-100 may help in the risk stratification of patients presenting with MI. (Circulation.

We investigated the relationship between lactate clearance and outcome in patients surviving the first 48 hours after cardiac arrest. We conducted the study in the emergency department of an urban tertiary care hospital. We analyzed the data for all 48-hour survivors after successful resuscitation from cardiac arrest during a 10-year period. Serial lactate measurements, demographic data, and key cardiac arrest data were correlated to survival and best neurologic outcome within 6 months after cardiac arrest. Parameters showing significant results in univariate analysis were tested for significance in a logistic regression model. Of 1502 screened patients, 394 were analyzed. Survivors (n = 194, 49%) had lower lactate levels on admission (median, 7.8 [interquartile range, 5.4-10.8] vs 9 [6.6-11.9] mmol/L), after 24 hours (1.4 [1-2.5] vs 1.7 [1.1-3] mmol/L), and after 48 hours (1.2 [0.9-1.6] vs 1.5 [1.1-2.3] mmol/L). Patients with favorable neurologic outcome (n = 186, 47%) showed lower levels on admission (7.6 [5.4-10.3] vs 9.2 [6.7-12.1] mmol/L) and after 48 hours (1.2 [0.9-1.6] vs 1.5 [1-2.2] mmol/L). In multivariate analysis, lactate levels at 48 hours were an independent predictor for mortality (odds ratio [OR]: 1.49 increase per mmol/L, 95% confidence interval [CI]: 1.17-1.89) and unfavorable neurologic outcome (OR: 1.28 increase per mmol/L, 95% CI: 1.08-1.51). Lactate levels higher than 2 mmol/L after 48 hours predicted mortality with a specificity of 86% and poor neurologic outcome with a specificity of 87%. Sensitivity for both end points was 31%. Lactate at 48 hours after cardiac arrest is an independent predictor of mortality and unfavorable neurologic outcome. Persisting hyperlactatemia over 48 hours predicts a poor prognosis.

We found no evidence of substantial differences in total mortality between several vasopressors. Dopamine increases the risk of arrhythmia compared with norepinephrine and might increase mortality. Otherwise, evidence of any other differences between any of the six vasopressors examined is insufficient. We identified low risk of bias and high-quality evidence for the comparison of norepinephrine versus dopamine and moderate to very low-quality evidence for all other comparisons, mainly because single comparisons occasionally were based on only a few participants. Increasing evidence indicates that the treatment goals most often employed are of limited clinical value. Our findings suggest that major changes in clinical practice are not needed, but that selection of vasopressors could be better individualised and could be based on clinical variables reflecting hypoperfusion.

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Background and Purpose-Recently 2 randomized trials in comatose survivors of cardiac arrest documented that therapeutic hypothermia improved neurological recovery. The narrow inclusion criteria resulted in an international recommendation to cool only a restricted group of primary cardiac arrest survivors. In this retrospective cohort study we investigated the efficacy and safety of endovascular cooling in unselected survivors of cardiac arrest. Methods-Consecutive comatose survivors of cardiac arrest, who were either cooled for 24 hours to 33°C with endovascular cooling or treated with standard postresuscitation therapy, were analyzed. Complication data were obtained by retrospective chart review. Results-Patients in the endovascular cooling group had 2-fold increased odds of survival (67/97 patients versus 466/941 patients; odds ratio 2.28, 95% CI, 1.45 to 3.57; PϽ0.001). After adjustment for baseline imbalances the odds ratio was 1.96 (95% CI, 1.19 to 3.23; Pϭ0.008). When discounting the observational data in a Bayesian analysis by using a sceptical prior the posterior odds ratio was 1.61 (95% credible interval, 1.06 to 2.44). In the endovascular cooling group, 51/97 patients (53%) survived with favorable neurology as compared with 320/941 (34%) in the control group (odds ratio 2.15, 95% CI, 1.38 to 3.35; Pϭ0.0003; adjusted odds ratio 2.56, 1.57 to 4.17). There was no difference in the rate of complications except for bradycardia. Conclusion-Endovascular cooling improved survival and short-term neurological recovery compared with standard treatment in comatose adult survivors of cardiac arrest. Temperature control was effective and safe with this device.