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Introduction. Platelet-derived microparticles (PDMPs) measurement adds prognostic implication for ST-elevation acute myocardial infarction (STEMI). The long-term implication of PDMPs in STEMI needs to be corroborated. Methods. The research design was a cohort study. Subjects were STEMI patients and were enrolled consecutively. The PDMPs were defined as microparticles bearing CD41(+) and CD62P(+) markers detected with flow cytometry. The PDMPs were measured on hospital admission and 30 days after discharge. The outcomes were major adverse cardiac events (MACE), i.e., a composite of cardiac death, heart failure, cardiogenic shock, reinfarction, and resuscitated ventricular arrhythmia, occurring from hospitalization until 1 year after discharge. Results. We enrolled 101 subjects with STEMI. During hospitalization, 17 subjects (16.8%) developed MACE. The PDMPs were not different between subjects with MACE and those without (median (IQR): 3305.0/μL (2370.0–14690.5/μL) vs. 4452.0/μL (2024.3–14396.8/μL), p=0.874). Forty-five subjects had increased PDMPs in 30 days after discharge as compared with on-admission measurement. Subjects with increased PDMPs had significantly higher 30-day MACE as compared to subjects with decreased PDMPs 17 (37.8%) vs. 6 (16.7%, p=0.036). There was a trend toward higher MACE in subjects with increased PDMPs as compared to those with decreased PDMPs in 90 days after discharge (48.9% vs. 30.6%, p=0.095) and 1 year after discharge (48.9% vs. 36.1%, p=0.249). Conclusion. The PDMPs level was increased from the day of admission to 30 days after discharge in patients with STEMI. The persistent increase in the PDMPs level in 30 days after the STEMI event was associated with the 30-day postdischarge MACE and trended toward increased MACE during the 90-day and 1-year follow-up.

In ST segment elevation acute myocardial infarction (STEMI), the endothelin (ET) system imbalance, reflected by circulating ET-1:ET-3 ratio has not been investigated. This study primary objective was to measure the circulating ET-1:ET-3 ratio and correlated it with the risk stratification for 1-year mortality of STEMI, based on TIMI score. On admission TIMI risk score and at discharge dynamic TIMI risk score were calculated in 68 consecutive subjects with STEMI. Subjects with high TIMI risk score associated with higher mean ET-1 level and ET-1:ET-3 ratio. The ET-1:ET-3 ratio more accurately predicted the high TIMI risk score than ET-1 level. Subjects with high dynamic TIMI risk score associated with higher mean ET-1 level and ET-1:ET-3 ratio. The ET-1:ET-3 ratio more accurately predicted the high dynamic TIMI risk score than ET-1 level. From multivariable analysis, the ET-1:ET-3 ratio did not independently associated with high on admission TIMI risk score but independently predicted high at discharge dynamic TIMI risk score (OR 9.186, p value 0.018). In conclusion, combining the ET-1 and ET-3 levels into the ET-1:ET-3 ratio provided a prognostic value by independently predicting the increased risk to 1-year mortality as indicated by at discharge dynamic TIMI risk score in patients with STEMI.

Key Clinical MessageUncorrected left‐to‐right shunt congenital heart defect is a predisposing factor for infective endocarditis (IE), especially right‐sided IE which has different clinical manifestations and complications from left‐sided IE. Prompt diagnosis by means of transthoracic echocardiography and timely antibiotics management for IE are encouraged to prevent multiorgan failure and fatal pulmonary embolism.

Dual antiplatelet therapy has been proven effective to reduce recurrent cardiovascular eventin patients with coronary artery disease and recommended as standard therapy for acute coronary syndrome and patients who underwent percutaneous coronary intervention. The adverse clinical occurrence in patients who taking aspirin and clopidogrel associates with antiplatelet non responsiveness, in addition to repetitive bleeding incident in such a way that platelet reactivity and genetic polymorphisms investigation rises intense interest. Resistance to antiplatelet or antiplatelet non responsiveness means a phenomenon in which antiplatelet drug fails to deliver pharmacological target and it is determined by platelet function measurement. Recent laboratorymethods have been developed to diagnose antiplatelet resistance, but none of them was considered as standard tool since its wide inter-individual variability and poor correlation between them. The mechanism of antiplatelet resistance is not fully understood, multifactorial, involving pharmaco dynamic and pharmacokinetic of the drugs. This review is aimed to comprehend theantiplatelet resistance mechanism and provide crucial information on managing patients who take dual antiplatelet treatment with adverse clinical events.