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Background: The clinical implications of applying the new criteria of acute myocardial infarction (AMI) with cardiac troponins in terms of their diagnostic and prognostic impact in patients with suspected acute coronary syndromes (ACS) have not been well evaluated., Methods and Results: The study group comprised 973 consecutive patients who were diagnosed as having ACS with or without ST elevation (STE). They were divided into 3 groups: unstable angina (UA) group (n=195) representing patients with no significant elevations of creatine kinase (CK) and troponin T (TnT); TnT-myocardial infarction (MI) group (n=170) with TnT elevation and no CK elevation (additionally detected AMI by the new criteria); CK-MI group (n=608) with significant elevation of CK (AMI by the old criteria). In the TnT-MI group, 140 (76%) patients had non-STE ACS. In-hospital mortality rates for STE ACS were 0%, 2.5% and 9.7% in the UA, TnT-MI and CK-MI groups, respectively. The corresponding values for non-STE ACS were 1.8%, 4.6%, and 16.5%, respectively (p<0.0001), suggesting a pivotal role of TnT. In multiple logistic regression analysis, significant CK elevation was selected as an independent predictor of in-hospital death in concurrence with age > or =75 years, prior MI, shock and low left ventricular ejection fraction in non-STE ACS., Conclusions: The new criteria result in a substantial increase in the diagnosis of AMI from non-STE ACS in particular. They assist greatly in detailed risk stratification of ACS patients, notably in cooperation with the old CK criteria.

Background: Acute massive or submassive pulmonary embolism (PE) has high mortality, but the clinical course according to the location of onset (ie, in-hospital or out-of-hospital) is unknown., Methods and Results: In the present study 56 consecutive patients with acute massive or submassive PE were studied retrospectively and a comparison made of the clinical characteristics, and outcomes between in-hospital onset (Group A) and out-of-hospital onset (Group B). Patients in Group A (n=28) had more frequent comorbidities with hemodynamic instability (54% vs 4%, p<0.0001) and temporary risk factors (93% vs 11%, p<0.0001), whereas patients in Group B (n=28) had a longer duration of symptoms (median: 5.5 days vs 0.5 day; p<0.0001), and had higher systolic pulmonary artery pressure (63+/-17 mmHg vs 46+/-12 mmHg, p=0.0006). Although in-hospital mortality did not differ between the 2 groups, the recurrence rate was higher in Group B (23% vs 0%, p=0.03)., Conclusions: Patients who had in-hospital onset of PE had mostly temporary risk factors, unstable hemodynamics and a lower recurrence rate compared with the cases of out-of-hospital onset. In cases of in-hospital onset, prompt diagnosis and suitable treatment is needed to prevent fatalities and cases of out-of-hospital onset should be followed carefully for recurrence.

Cilostazol, a novel cyclic adenosine monophosphate phosphodiesterase type III inhibitor, has been developed as an antiplatelet drug with a vasodilating action on peripheral arteries. The present study was designed to test, in humans, whether cilostazol can dilate the epicardial coronary arteries and what are its hemodynamic effects. Eight patients with chest pain syndrome were subjected to serial quantitative coronary arteriography immediately before and at 30, 60 and 150min after a single oral dose of cilostazol (200mg). Luminal cross-sectional areas (mm2) at the proximal and distal sites of major coronary arteries (6 segments at each sampling time) were significantly increased at 150 min after taking the drug. The percent increases relative to the baseline values were 25+/-7 (6.8+/-0.8-->8.3+/-1.0*) and 42+/-7% (2.1+/-0.3-->3.0+/-0.4*) in the right coronary artery, 24+/-5 (5.1+/-0.7-->6.1+/-0.8*) and 28+/-10% (1.6+/-0.31-->9+/-0.3*) in the left anterior descending artery, and 14+/-6 (5.9+/-0.9-->6.6+/-0.9*) and 24+/-10% (1.3+/-0.2-->1.5+/-0.2*) in the left circumflex artery, respectively (*p<0.05 vs baseline). This action, relative to that of nitroglycerine, was between 27% and 54%. Moreover, small but sustained decreases in systolic pulmonary pressure and stroke work index were observed. Thus, cilostazol has a mild coronary vasodilating action with minimal hemodynamic effects, thereby giving it a possible role in the treatment of coronary artery disease.