BackgroundThe amount of epicardial adipose tissue (EAT) has been demonstrated to correlate with the severity of coronary artery disease (CAD) and the CAD activity.The aim of this study is to assess the impact of EAT on long term clinical outcomes in patients with ST elevation myocardial infarction (STEMI) after percutaneous coronary intervention (PCI).MethodsWe analyzed the data and clinical outcomes of 761 patients (614 males, 57 ± 12 year-old) with STEMI who underwent successful primary PCI from 2003 to 2009. All patients were divided into two groups: thick EAT group, EAT ≥ 3.5 mm and thin EAT group, EAT < 3.5 mm. The primary end points were all-cause death, recurrent MI, target vessel revascularization (TVR) and major cardiac adverse events (MACEs), composite of all-cause death, recurrent MI and TVR, within 5 years.ResultsMedian and mean EAT of 761 patients were 3.3 mm and 3.6 ± 1.7 mm, respectively. Mean follow up period was 46 ± 18 months. MACE-free survival rate in the thick EAT group was significantly lower than in the thin EAT group (log-rank P = 0.001). The event-free survival rate of all-cause death of the thick EAT group was significantly lower than that of the thin EAT group (log-rank P = 0.005). The TVR-free survival rate in the thick EAT group was significantly lower than in the thin EAT group (log-rank P = 0.007). The event-free survival rate of recurrent MI were not significantly different between the groups (log-rank P = 0.206). In the Cox’s proportional hazard model, the adjusted hazard ratio of thick EAT thickness for TVR was 1.868 (95% confidence interval 1.181–2.953, P = 0.008).ConclusionThis study demonstrates that the EAT thickness is related with long term clinical outcome in patients with STEMI. The EAT thickness might provide additional information for future clinical outcome, especially TVR.

Objectives: With the present therapeutic advances in the era of primary percutaneous coronary intervention (PCI), the role of β-blockers in ST elevation acute myocardial infarction (STEMI) has remained contentious. Methods: We analyzed the data and clinical outcomes of 901 STEMI patients who had undergone primary PCI. We classified the patients into β-blocker (n = 598) and non-β-blocker groups (n = 303). Results: The cumulative incidence of all-cause death was 10.0% in the β-blocker group and 25.4% in the non-β-blocker group (p < 0.001). The incidence of major adverse cardiac events (MACE) was 22.1% in the β-blocker group and 34.3% in the non-β-blocker group (p < 0.001). The relative hazard ratio (HR) of β-blockers for all-cause death and MACE with low left ventricle ejection fraction (LVEF; <50%) was 0.55 [95% confidence interval (CI) 0.35-0.86, p = 0.009] and 0.75 (95% CI 0.51-1.09, p = 0.125), respectively. In patients with normal LVEF (≥50%), the relative HR of β-blockers for death and MACE were 0.50 (95% CI 0.29-0.88, p = 0.016) and 0.75 (95% CI 0.51-1.12, p = 0.162), respectively. After propensity score matching of the difference of the baseline characteristics, the Kaplan-Meier survival curve demonstrated lower mortality in the β-blocker group than in the non-β-blocker group with both low LVEF and normal LVEF (p = 0.02 and p = 0.001, respectively). Conclusions: β-Blockers have beneficial clinical outcomes in the era of primary PCI for STEMI, regardless of the LVEF.

LVH was associated with increased rate of adverse clinical outcomes in 30-day survivors after STEMI, who underwent successful coronary intervention.

Prognostic significance between progression of left ventricular hypertrophy (LVH) and clinical outcomes in patients with ST-elevation myocardial infarction (STEMI) is uncertain. The objective of this study was to investigate prognostic impact of progression of LV mass index (LVMI) in patients with STEMI.We analyzed the data and clinical outcomes of patients with STEMI who received successful coronary intervention. A total of 200 patients who had echocardiographic follow-up between 12 and 36 months were finally enrolled. According to change in LVMI compared to baseline LVMI, patients were classified into progression group and nonprogression group. Progression of LVMI was defined when increment of LMVI was greater than 10% compared to baseline LVMI. End points were major adverse cardiac events within 5 years, including death, recurrent MI, target vessel revascularization, and hospitalization due to heart failure.Progression of LVMI occurred in 55 patients. In the progression group, rate of recurrent MI was higher (13 vs 2%, P = .026) and the event-free survival of recurrent MI was significantly worse (log-rank P < .001) than that in the nonprogression group. Adjusted hazard ratio of progression of LVMI for recurrent MI was 10.253 (95% confidence intervals 2.019–52.061, P = .005).Increased LVMI was an independent predictor for adverse events, especially for recurrent MI, in patients with STEMI.

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