Kjærgaard, Jesper

Abstract Background/Introduction Optimal mean arterial pressure (MAP) in patients with acute myocardial infarction related out-of-hospital cardiac arrest (AMI-OHCA) and cardiogenic shock (AMI-CS) remains unclear. Randomized controlled trials (RCTs) comparing MAP targets have been performed in OHCA patients with presumed cardiac cause, but did not provide answers to the important question what MAP target would be optimal for the AMI-OHCA population. To our knowledge, no RCTs comparing MAP targets in AMI-CS patients have been performed. Purpose This comprehensive systematic review and meta-analysis aimed to evaluate the effect of low- and high-MAP levels on short-term mortality in AMI-OHCA and AMI-CS patients. Methods We conducted a systematic search of MEDLINE (OVID), EMBASE (OVID), CINAHL (Ebsco) and Cochrane CENTRAL databases. Eligible studies reported outcomes for AMI-OHCA or AMI-CS patients for at least two groups of different average MAP levels. Both RCTs and observational studies were eligible to ensure comprehensive data collection. Authors were proactively contacted for supplementary AMI data. Random-effects models were used to pool data. Results Of 7,728 screened studies, 57 were assessed for eligibility, and 11 were included in the final analysis (4 RCTs and 7 observational studies), encompassing 3,846 patients. The primary analysis included 1,251 AMI-OHCA patients. In the AMI-OHCA patients, no significant difference in short-term mortality was observed between low- and high-MAP groups in RCT (34.9% vs. 39.4%, RR 0.88, 95%-CI 0.70-1.10), observational-, and combined data. As only one of the 11 included studies reported on separate AMI-CS data, no meta-analyses of solely AMI-CS patients could be performed. Conclusions Our meta-analysis showed no significant difference in short-term mortality between low- and high-MAP levels in AMI-OHCA patients. Only one study in selected AMI-CS patients without OHCA patients was available. This highlights the importance of identifying tailored MAP strategies in both AMI-OHCA and AMI-CS patients.Flow chart of the selection of studies Short term mortality – AMI-OHCA patients

BACKGROUND: Cardiac troponin (cTn) is key in diagnosing myocardial infarction (MI). After MI, the clinically observed half-life of cTn has been reported to be 7 to 20 hours, but this estimate reflects the combined elimination and simultaneous release of cTn from cardiomyocytes. More precise timing of myocardial injuries necessitates separation of these 2 components. We used a novel method for determination of isolated cTn elimination kinetics in humans. METHODS: Patients with MI were included within 24 hours after revascularization and underwent plasmapheresis to obtain plasma with a high cTn concentration. After at least 3 weeks, patients returned for an autologous plasma retransfusion followed by blood sampling for 8 hours. cTn was measured with 5 different high-sensitivity cTn assays. RESULTS: Of 25 included patients, 20 participants (mean age, 64.5 years; SD, 8.2 years; 4 women [20%]) received a retransfusion after a median of 5.8 weeks (interquartile range, 5.0–6.9 weeks) after MI. After retransfusion of a median of 620 mL (range, 180–679 mL) autologous plasma, the concentration of cTn in participants’ blood increased 4 to 445 times above the upper reference level of the 5 high-sensitivity cTn assays. The median elimination half-life ranged from 134.1 minutes (95% CI, 117.8–168.0) for the Elecsys high-sensitivity cTnT assay to 239.7 minutes (95% CI, 153.7–295.1) for the Vitros high-sensitivity cTnI assay. The median clearance of cTnI ranged from 40.3 mL/min (95% CI, 32.0–44.9) to 52.7 mL/min (95% CI, 42.2–57.8). The clearance of cTnT was 77.0 mL/min (95% CI, 45.2–95.0). CONCLUSIONS: This novel method showed that the elimination half-life of cTnI and cTnT was 5 to 16 hours shorter than previously reported. This indicates a considerably longer duration of cardiomyocyte cTn release after MI than previously thought. Improved knowledge of timing of myocardial injury may call for changes in the management of MI and other disorders with myocardial injury.

Background— Left ventricular diastolic dysfunction (DD) is common after myocardial infarction (MI) despite preservation of left ventricular ejection fraction, yet it remains unclear how or whether DD affects cardiac hemodynamics with stress. Methods and Results— Invasive hemodynamic exercise testing was performed in 46 patients with a recent MI and left ventricular ejection fraction >45% and in 10 healthy volunteers. MI patients were enrolled prospectively and divided into those with DD (MI+DD; left atrial volume index >34 mL/m 2 and diastolic E/e′ ratio>8; n=35) and those without DD (MI–DD; left atrial volume index <34 mL/m 2 and E/e′ ratio<8; n=11). All underwent a supine cycle ergometer test with simultaneous right heart catheterization and echocardiography. At rest, 10 patients in MI+DD (29%) had pulmonary capillary wedge pressure >15 (14±4 mm Hg), whereas none of the MI−DD (10±2 mm Hg) or controls (9±2 mm Hg) displayed pulmonary capillary wedge pressure elevation ( P =0.03). During exercise, an abnormal rise in pulmonary capillary wedge pressure (>25 mm Hg) was observed in 94% of MI+DD (36±6 mm Hg) compared with 36% of MI−DD (24±6 mm Hg) and none of the controls (16±6 mm Hg; P <0.0001). Exercise right atrial pressure was the highest in MI+DD followed by MI−DD and control (15±5 versus 9±4 versus 7±5 mm Hg; P <0.001), whereas no difference in cardiac index was found between groups. Conclusions— In post-MI patients with preserved ejection fraction and left ventricular DD, cardiac output with exercise is maintained at the expense of substantially increased filling pressure. DD and loss of diastolic reserve may promote progression from stage B to stage C heart failure after MI. (Circ Heart Fail. 2012;5:-451.)