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Objective Predictors of 30-day mortality may differ from predictors of mortality at 1 year among 30-day survivors of ST-elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI). We aimed to evaluate the predictors of 30-day and 1-year mortality in unselected patients with STEMI treated with PCI.Methods Individual patient data from 4732 patients with STEMI, who were treated with primary PCI during an 11-year study period, were recorded prospectively. Patient characteristics, 30-day, and 1-year outcome were evaluated.Results At 30-day follow-up, 219 patients (4.6%) died; and out of the 4513 30-day survivors, 109 patients (2.8%) died at 1 year. Patients who died were older, had a higher risk profile. Higher rates of Killip class greater than 2 on admission, multivessel disease, and, more often, lower left ventricular ejection fraction were observed in patients who died. Mortality rate was 7.6% at 30 days among the females when compared with 3.7 among the males, P value less than 0.001. Age and sex-adjusted multivariate analysis revealed that previous myocardial infarction, diabetes, Killip class greater than 2, post-PCI thrombolysis in myocardial infarction flow less than 3, and left ventricular ejection fraction less than 30% were strong predictors of both 30-day and 1-year mortality. However, multivessel disease, anterior myocardial infarct location and in-hospital reinfarction, ischemic time, and pre-PCI thrombolysis in myocardial infarction flow less than 3 were particularly strong predictors of 30-day mortality.Conclusion Despite the fact that most characteristics of 30-day and 1-year mortality among 30-day survivors are similar, we found that variables that affect mortality beyond the acute phase may not necessarily be the same as those that influence early mortality. Coron Artery Dis 20:415-421 (C) 2009 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.

N -Acetyl-Ser-Asp-Lys-Pro (AcSDKP) is a specific substrate for the N-terminal site of ACE and increases 5-fold during ACE inhibitor therapy. It is known to inhibit the proliferation of hematopoietic stem cells and has also recently been reported to inhibit the growth of cardiac fibroblasts. We investigated its mode of action in cardiac fibroblasts by assessing its influence on transforming growth factor β 1 (TGFβ1)–mediated Smad signaling. AcSDKP inhibited the proliferation of isolated cardiac fibroblasts ( P 0 /G 1 phase to S phase of the cell cycle. In cardiac fibroblasts transfected with a Smad-sensitive luciferase reporter construct, AcSDKP decreased luciferase activity by 55±9.7% ( P =0.01). Moreover, phosphorylation and nuclear translocation of Smad2 was decreased in cardiac fibroblasts treated with AcSDKP. To conclude, AcSDKP inhibits the growth of cardiac fibroblasts and also inhibits TGFβ1-stimulated phosphorylation of Smad2. Because AcSDKP increases substantially during ACE inhibitor therapy, this suggests a novel pathway independent of angiotensin II, by which ACE inhibitors can inhibit cardiac fibrosis.