Periprocedural bleeding was significantly associated with CI-AKI, with CI-AKI incidence correlating with bleeding severity.

No abstract

Background: Right ventricular myocardial infarction (RVMI) is the major cause of hypotension and/or shock (HpS) after acute inferior myocardial infarction (inferior AMI). It is, however, unclear how RVMI affects the acute hemodynamic course. Methods and Results:In the present study, 153 patients with inferior AMI caused by right coronary artery occlusion were examined. Associations between in-hospital outcome and HpS before admission (preER-HpS) or HpS after admission (postER-HpS) were assessed using multivariate logistic regression analysis. Multivariate analysis was also conducted to determine a predictor for postER-HpS, including clinical findings in the emergency room as independent variables. HpS developed in 48.4% of patients with inferior AMI. Patients with RVMI more frequently had HpS than their counterparts in the first 6 h after infarction onset. RVMI was, however, not associated with preER-HpS, but was independently with postER-HpS (odds ratio (OR): 10.1; 4.0-27.7), whereas left ventricular failure was associated with preER-HpS, but not with postER-HpS. Furthermore, RVMI (OR: 9.4; 3.6-27.1) identified at presentation predicted postER-HpS.Conclusions: Independent of concomitant left ventricular involvement, RVMI was significantly associated with postER-HpS, but not with preER-HpS. These findings highlight the importance of identifying RVMI immediately after admission in the setting of inferior AMI. (Circ J 2010; 74: 148 - 155)

Periprocedural myocardial infarction (pMI) is an important complication associated with percutaneous coronary intervention (PCI). However, data on the frequency of biomarker testing and the incidence of pMI remain unclear. Using the multicenter Japan Cardiovascular Database, we identified 2182 patients who underwent PCI without preprocedural cardiac biomarker elevation (silent ischemia, stable angina, or unstable angina without biomarker elevation) from September 2008 to August 2011. Of these, 550 patients (25.2 %) underwent cardiac biomarker testing within 6-24 h after PCI. The incidence of pMI was 2.7 % among all identified patients and 7.5 % among those who underwent cardiac marker testing. Of note, cardiac biomarker testing was performed more frequently than no testing in patients with a higher risk profile such as unstable angina (32.7 vs 24.7 %, P < 0.001), higher symptom scaling (28.2 vs 22.5 %, P = 0.008), urgent or emergent procedures (19.3 vs 15.0 %, P = 0.022 or 4.2 vs 1.0 %, P < 0.001, respectively), and type C lesion (31.3 vs 25.2 %, P = 0.006). Presentation with silent ischemia (odds ratio = 1.51, 95 % confidence interval (CI) 1.16-1.97) and nonemergent PCIs (odds ratio = 3.45, 95 % CI 1.79-6.67) were associated with no postprocedural cardiac biomarker testing. The real-world multicenter PCI registry in Japan revealed an incidence of 2.7 % for pMI; however, cardiac biomarkers were assessed in only 25.2 % of patients after PCI. The results suggest an underuse of postprocedural biomarker testing and room for procedural quality improvement, particularly in cases of silent ischemia and nonemergent cases.

We investigated the clinical characteristics of acute myocardial infarction (AMI) not preceded by angina in 256 patients with first AMIs. Complications, including sustained ventricular tachycardia or ventricular fibrillation, pump failure and cardiac rupture, were more frequent in patients with AMI not preceded by angina (group 1 n = 92) than those preceded by angina (group 2, n = 164). The in-hospital mortality rate was higher in group 1 than in group 2. Poor preexisting collateral channels or lack of ischemic preconditioning may be responsible for the poorer outcome in group 1 patients.