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Patients who had cardiac arrest without ST-segment elevation were assigned to undergo either immediate coronary angiography or delayed coronary angiography (after neurologic recovery). All patients underwent PCI if indicated. There was no significant between-group difference in overall survival at 90 days.

Ischemic heart disease is a major cause of out-of-hospital cardiac arrest. The role of immediate coronary angiography (CAG) and percutaneous coronary intervention (PCI) after restoration of spontaneous circulation following cardiac arrest in the absence of ST-segment elevation myocardial infarction (STEMI) remains debated. We hypothesize that immediate CAG and PCI, if indicated, will improve 90-day survival in post–cardiac arrest patients without signs of STEMI. In a prospective, multicenter, randomized controlled clinical trial, 552 post–cardiac arrest patients with restoration of spontaneous circulation and without signs of STEMI will be randomized in a 1:1 fashion to immediate CAG and PCI (within 2 hours) versus initial deferral with CAG and PCI after neurological recovery. The primary end point of the study is 90-day survival. The secondary end points will include 90-day survival with good cerebral performance or minor/moderate disability, myocardial injury, duration of inotropic support, occurrence of acute kidney injury, need for renal replacement therapy, time to targeted temperature control, neurological status at intensive care unit discharge, markers of shock, recurrence of ventricular tachycardia, duration of mechanical ventilation, and reasons for discontinuation of treatment. The COACT trial is a multicenter, randomized, controlled clinical study that will evaluate the effect of an immediate invasive coronary strategy in post–cardiac arrest patients without STEMI on 90-day survival.

To investigate the effects of inotropic agents on parameters of tissue perfusion in patients with cardiogenic shock. Thirty patients with cardiogenic shock were included. Patients received dobutamine, enoximone, or norepinephrine. We performed hemodynamic measurements at baseline and after titration of the inotropic agent until cardiac index (CI) ≥ 2.5 L.min-1.m(-2) or mixed-venous oxygen saturation (SvO2) ≥ 70% (dobutamine or enoximone), and mean arterial pressure (MAP) ≥ 70 mmHg (norepinephrine). As parameters of tissue perfusion, we measured central-peripheral temperature gradient (delta-T) and sublingual perfused capillary density (PCD). All patients reached predefined therapeutic targets. The inotropes did not significantly change delta-T. Dobutamine did not change PCD. Enoximone increased PCD (9.1 [8.9-10.2] vs. 11.4 [8.4-13.9] mm.mm(-2); p<0.05), and norepinephrine tended to decrease PCD (9.8 [8.5-11.9] vs. 8.8 [8.2-9.6] mm.mm-2, p = 0.08). Fifteen patients (50%) died within 30 days after admission. Patients who had low final PCD (≤ 10.3 mm.mm-2; 64%) were more likely to die than patients who had preserved PCD (>10.3 mm.mm(-2); mortality 72% vs. 17%, p = 0.003). This study demonstrates the effects of commonly used inotropic agents on parameters of tissue perfusion in patients with cardiogenic shock. Despite hemodynamic optimization, tissue perfusion was not sufficiently restored in most patients. In these patients, mortality was high. Interventions directed at improving microcirculation may eventually help bridging the gap between improved hemodynamics and dismal patient outcome in cardiogenic shock.

Introduction Microcirculatory abnormalities are frequently observed in patients with severe heart failure and correlate to worse outcomes. We tested the hypothesis that nitroglycerin dose-dependently improves perfusion in severe heart failure and that this could be monitored by measuring central-peripheral temperature gradient and with Sidestream Dark Field imaging of the sublingual mucosa. Methods A dose-response study was performed in 17 patients with cardiogenic shock ( n  = 9) or end-stage chronic heart failure ( n  = 8) admitted to Erasmus University Medical Center. We did hemodynamic measurements at baseline and during increasing infusion rates of nitroglycerin (up to a maximum dose of 133 μg min −1 ). As parameters of tissue perfusion, we measured central-peripheral temperature gradient (delta-T) and sublingual perfused capillary density (PCD). Results Nitroglycerin dose-dependently decreased mean arterial pressure ( p  < 0.001) and cardiac filling pressures (both central venous pressure (CVP) and pulmonary capillary wedge pressure: p  < 0.001). It increased cardiac index ( p  = 0.01). Nitroglycerin decreased delta-T ( p  < 0.001) and increased sublingual PCD ( p  < 0.001). Significant changes in delta-T and PCD occurred earlier, i.e., at a lower doses of NTG, than changes in global hemodynamics. Macrohemodynamic and microcirculatory responses to nitroglycerin infusion were consistent in patients with either cardiogenic shock or end-stage chronic heart failure. Changes in microcirculatory parameters occurred independently of changes in cardiac index. Conclusions Nitroglycerin dose-dependently increases tissue perfusion in patients with severe heart failure, as observed by a decrease in central-peripheral temperature gradient and an increase in sublingual perfused capillary density.

Purpose: we evaluated the effects of the shift of a targeted temperature management (TTM) strategy from 33 °C to 36 °C in comatose out-of-hospital cardiac arrest (OHCA) patients admitted to the Intensive Care Unit (ICU). Methods: we performed a retrospective study of all comatose (GCS < 8) OHCA patients treated with TTM from 2010 to 2018 (n = 798) from a single-center academic hospital. We analyzed 90-day mortality, and neurological outcome (CPC score) at ICU discharge and ICU length of stay, as primary and secondary outcomes, respectively. Results: we included 798 OHCA patients (583 in the TTM33 group and 215 in the TTM36 group). We found no association between the TTM strategy (TTM33 and TTM36) and 90-day mortality (hazard ratio (HR)] 0.877, 95% CI 0.677–1.135, with TTM36 as reference). Also, no association was found between TTM strategy and favorable neurological outcome at ICU discharge (odds ratio (OR) 1.330, 95% CI 0.941–1.879). Patients in the TTM33 group had on average a longer ICU LOS (beta 1.180, 95% CI 0.222–2.138). Conclusion: no differences in clinical outcomes—both 90-day mortality and favorable neurological outcome at ICU discharge—were found between targeted temperature at 33 °C and 36 °C. These results may help to corroborate previous trial findings and assist in implementation of TTM.

Objectives: It was the aim of this study to evaluate the effects of intra-aortic balloon pump (IABP) counterpulsation on sublingual microcirculation as a model for tissue perfusion. Methods: In 13 patients with cardiogenic shock treated with IABP, the IABP assist ratio was reduced from 1:1 to 1:8 for 15 min. Using sidestream dark field imaging, 117 movie files of the sublingual microcirculation were obtained and quantified at different IABP assist ratios at 3 time points: 1:1 (T0), 1:8 (T1) and 1:1 (T2), respectively. Data are presented as the median and interquartile range. Results: The median age of the patients was 59 years (range 56–73), and 62% were males. Discontinuation of IABP decreased the mean arterial pressure [75 mm Hg (71–84) at T0 vs. 69 mm Hg (64–79) at T1; p < 0.001], cardiac index [2.9 l/min/m 2 (1.6–3.3) at T0 vs. 2.4 l/min/m 2 (1.5–2.8) at T1; p = 0.005] and cardiac power index [0.46 W/m 2 (0.29–0.59) at T0 vs. 0.36 W/m 2 (0.24–0.50) at T1; p = 0.006]. However, these modest changes in macrohemodynamics did not significantly influence sublingual perfused capillary density and capillary red blood cell velocity (p = 0.28 and 0.73, respectively). Conclusion: A temporary, modest decrease in microcirculatory driving force, induced by lowering the IABP assist ratio, does not impair sublingual microcirculatory perfusion as measured by a novel 2-dimensional imaging technique.