Target temperature management is recommended in post-resuscitation care. Additionally, hypothermia is a promising option in adjunctive therapy of acute myocardial infarction (MI). However, first in men data are contradicting. There are still many open questions to identify the optimal regimen and target temperature. In this study, we aimed to investigate the effect of very mild hypothermia on infarct size (IS) in mice. Mice underwent cardiac ischemia by temporary occlusion of the left anterior descending (LAD) artery under conditions of very mild hypothermia (34-36 ℃). Hypothermia was reached within the first 5 minutes of ischemia (temperature: 34.6±0.5 vs. 36.8±1.1 ℃, P=0.035). Very mild hypothermia reduced IS in mice undergoing 30 minutes ischemia [IS/area at risk (AAR): 45±12% vs. 22±4%, P=0.018] as well as mice undergoing 60 minutes ischemia [IS/AAR: 67±7% vs. 28±2%, P=0.0003]. Very mild hypothermia reduces IS. This new approach in adjunctive therapy of patients with acute MI should be investigated in clinical trials.
Aspirin is indispensable in secondary prevention of ischemic events in patients with coronary artery disease (CAD). However, insufficient platelet inhibition despite aspirin medication is frequent. This is referred to as high on-treatment platelet reactivity (HTPR). Nevertheless, if this is associated with clinical outcome instead of only laboratory phenomenon remains unclear so far. In this study, we test whether patients with ischemic events have higher platelet reactivity despite aspirin medication than patients without ischemic events. In this prospective study of 72 CAD patients, we determined pharmacodynamic response to aspirin by arachidonic acid induced aggregation via light-transmission aggregometry and expressed as maximum of aggregation (MoA). During a mean follow-up duration of 3.2 years, major adverse cardiac and cerebrovascular events (MACCE), mortality, non-ST-elevation myocardial infarction (NSTEMI), and stroke were assessed as endpoints via yearly telephone interviews with the treating physician of the patients. Patients who suffered from MACCE, death, and NSTEMI had a significantly higher MoA than those without (MACCE: 5.4 vs. 16.4%, <i>p</i> < 0.05; death: 5.6 vs. 16.8%, <i>p</i> < 0.05; NSTEMI: 1.8 vs. 21%, <i>p</i> < 0.001). MoA did not differ with regard to the occurrence of stroke (10.1 vs. 14.9%, <i>p</i> = 0.59). Patients with MACCE, death, and NSTEMI show enhanced platelet reactivity despite aspirin medication as compared to patients without ischemic events. Hence, insufficient response to aspirin medication should be regarded as risk factor for ischemic events in CAD patients. Further trials are needed to assess options to overcome HTPR to aspirin.
Various tests are available for measuring on-treatment platelet reactivity. The pharmacologically most specific assays are time-consuming and elaborate. A highly specific and convenient assay would be desirable for clinical routine. In this pilot study, we aimed to examine the ability of a novel bedside whole-blood assay—ROTEM platelet—to evaluate platelet inhibition compared with established assays. Platelet reactivity was investigated in 93 patients. Forty-Seven patients were on permanent aspirin therapy and 46 on dual antiplatelet therapy (DAPT) with aspirin and clopidogrel. We used ROTEM platelet impedance aggregometry (ROTEM-PTL), light transmission aggregometry (LTA), Multiplate electrode aggregometry (MEA) and vasodilator-stimulated phosphoprotein flow cytometry. Receiver operating characteristic (ROC) analyses showed ROTEM-PTL differentiates well between patients on medication and healthy individuals: aspirin: ROCAUC 0.99 (95% confidence interval, 0.97–1.01); P < 0.0001; DAPT treatment: ROCAUC 0.80 (95% confidence interval, 0.69–0.91); P < 0.001. Pearson regression analyses showed moderate correlations between assays. Aspirin: MEA versus ROTEM-PTL r2 = 0.435, P ≤ 0.001; LTA versus ROTEM-PTL r2 = 0.048, P = 0.180. DAPT: MEA versus ROTEM-PTL r2 = 0.398, P = 0.001; LTA versus ROTEM-PTL r2 = 0.409, P = 0.001; vasodilator-stimulated phosphoprotein versus ROTEM-PTL r2 = 0.164, P = 0.055. ROTEM platelet distinguished well between treated and healthy individuals but correlated moderately with other assays. Clinical trials are needed to investigate the ability of this new assay to identify patients at risk of adverse events.
Prasugrel and ticagrelor are recommended over clopidogrel in patients with ST-elevation myocardial infarction (STEMI). In this registry analysis, we compared efficacy and safety of ticagrelor and prasugrel P2Y12 inhibition in patients with STEMI. We included 318 patients in this single-center analysis. Twelve-month follow-up was conducted during ambulatory care at our department. Patients were on dual antiplatelet therapy with aspirin and ticagrelor or prasugrel during the follow-up period. Prescription of prasugrel or ticagrelor, respectively, was according to the preference of the treating physician. Major adverse cardiac and cerebrovascular events (MACCE) [death, myocardial infarction (MI), stroke, and unplanned reintervention] and thrombolysis in myocardial infarction (TIMI) bleeding (major/minor) were registered during hospitalization and follow-up. TIMI bleeding events were more frequent in ticagrelor-treated patients [17 vs. 5 patients, hazard ratio (HR) 2.85, 95% confidence interval (CI) 1.2-6.6; log-rank P value = 0.01]. Prasugrel-treated patients were significantly younger (ticagrelor 63 ± 12 years vs. prasugrel 57 ± 10; P < 0.0001). Besides that, patients' characteristics were similar in both groups. Multivariate analysis revealed that ticagrelor medication was independently associated with bleeding risk after adjustment for age, percutaneous coronary intervention approach (femoral vs. radial), diabetes mellitus, and kidney function (HR 3.01; 95% CI 1.0-7.4; P = 0.043). In patients treated with ticagrelor, 35 MACCE were detected. There was no difference as compared to prasugrel-treated patients (24 events, HR 1.24, 95% CI 0.79-2.09; log-rank P value = 0.41). TIMI bleeding events were more frequent in ticagrelor-treated patients with STEMI during 12-month follow-up. There were no differences in MACCE between groups in this registry analysis.
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