Clinical Impact of Ventricular Tachycardia and/or Fibrillation During the Acute Phase of Acute Myocardial Infarction on In-Hospital and 5-Year Mortality Rates in the Percutaneous Coronary Intervention Era.

Background: The aim of this study was to investigate the prognostic impact of acute-phase ventricular tachycardia and fibrillation (VT/VF) on ST-segment elevation myocardial infarction (STEMI) patients in the percutaneous coronary intervention (PCI) era.

Methods and results: Using the database of the Osaka Acute Coronary Insufficiency Study (OACIS), we studied 4,283 consecutive patients with STEMI who were hospitalized within 12 h of STEMI onset and underwent emergency PCI. Acute-phase VT/VF, defined as ≥3 consecutive ventricular premature complexes and/or VF within the 1st week of hospitalization, occurred in 997 (23.

Reduced risk of recurrent myocardial infarction in homozygous carriers of the chromosome 9p21 rs1333049 C risk allele in the contemporary percutaneous coronary intervention era: a prospective observational study.

Objectives: Chromosome 9p21 single nucleotide polymorphism (SNP) is a susceptibility variant for acute myocardial infarction (AMI) in the primary prevention setting. However, it is controversial whether this SNP is also associated with recurrent myocardial infarction (ReMI) in the secondary prevention setting. The purpose of this study is to evaluate the impact of chromosome 9p21 SNP on ReMI in patients receiving secondary prevention programmes after AMI.

Association of lifestyle-related factors with circadian onset patterns of acute myocardial infarction: a prospective observational study in Japan.

Objective: The onset of acute myocardial infarction (AMI) shows characteristic circadian variations involving a definite morning peak and a less-defined night-time peak. However, the factors influencing the circadian patterns of AMI onset and their influence on morning and night-time peaks have not been fully elucidated.

Design, Setting And Participants: An analysis of patients registered between 1998 and 2008 in the Osaka Acute Coronary Insufficiency Study, which is a prospective, multicentre observational study of patients with AMI in the Osaka region of Japan.

Comparison of 5-year survival after acute myocardial infarction using angiotensin-converting enzyme inhibitor versus angiotensin II receptor blocker.

Few studies have investigated whether angiotensin II receptor blocker (ARB) is a practical alternative to angiotensin-converting enzyme inhibitor (ACEI) for long-term use after acute myocardial infarction (AMI) in real-world practice in the percutaneous coronary intervention era. We compared 5-year survival benefits of ACEI and ARB in patients with AMI registered in the Osaka Acute Coronary Insufficiency Study. Study subjects were divided into 3 groups: ACEI (n = 4,425), ARB (n = 2,158), or patients without either drug (n = 2,442).

Renin-angiotensin-aldosterone system polymorphisms and 5-year mortality in survivors of acute myocardial infarction: a report from the Osaka Acute Coronary Insufficiency Study.

This study sought to evaluate whether genetic variants in the renin-angiotensin-aldosterone system (RAAS) have an impact on long-term mortality after acute myocardial infarction (AMI) in the percutaneous coronary intervention (PCI) era. We investigated the impacts of individual and combinations of 4 major RAAS genetic variants, angiotensinogen (AGT) T1311C, angiotensin-converting enzyme (ACE) insertion/deletion (I/D), angiotensin 2 type 1 receptor A1166C, and aldosterone synthase T4660C on 5-year mortality in 3149 post-AMI patients using multivariate Cox regression analysis. The predictive accuracy of all possible RAAS genetic combinations was evaluated using Cox regression analysis, and the best combination that affected prognosis was determined based on the minimal Akaike Information Criterion.

Clinical impact of acute hyperglycemia on development of diabetes mellitus in non-diabetic patients with acute myocardial infarction.

Background: Acute hyperglycemia (AH) after the onset of acute myocardial infarction (AMI) is a manifestation of transient abnormal glucose metabolism that may reflect AMI severity, and thus be a predictor of poor prognosis. However, it remains unknown whether AH may predict development of de novo diabetes mellitus (dn-DM) in non-diabetic AMI patients.

Methods And Results: Among AMI patients registered in the Osaka Acute Coronary Insufficiency Study between 1998 and 2007, we investigated hospital records of 1493 patients who had an admission glycated hemoglobin A1c (HbA1c) level of ≤6.

Living alone and risk of cardiovascular events following discharge after acute myocardial infarction in Japan.

Background: Little is known about the long-term risk of cardiovascular events after discharge among acute myocardial infarction (AMI) survivors living alone in Japan.

Methods And Results: A large-scale prospective, observational study in the Osaka region involved consecutive patients with AMI from January 2002 through December 2010. We evaluated the association between living alone and longitudinal risk of cardiovascular events following discharge after AMI.

Circulating p53-responsive microRNAs are predictive indicators of heart failure after acute myocardial infarction.

Rationale: Despite a recent decline of in-hospital mortality attributable to acute myocardial infarction (AMI), the incidence of ischemic heart failure (HF) in post-AMI patients is increasing. Although various microRNAs have been proposed as diagnostic indicators for AMI, no microRNAs have been established as predictors of ischemic HF that develops after AMI.

Objective: We attempted to identify circulating microRNAs that can serve as reliable predictors of ischemic HF in post-AMI patients.

Decreased mortality associated with statin treatment in patients with acute myocardial infarction and lymphotoxin-alpha C804A polymorphism.

Aims: We previously reported the association of single nucleotide polymorphisms in the lymphotoxin alpha (LTα) gene with susceptibility to acute myocardial infarction (AMI) and increased mortality after discharge. In the present study, we investigated whether the adverse effect of LTα C804A polymorphism on mortality could be pharmacologically modified by statin treatment after AMI.

Methods And Results: We conducted a multicenter study that included 3486 post-AMI patients between 1998 and 2008.

Elevated serum heart-type fatty acid-binding protein in the convalescent stage predicts long-term outcome in patients surviving acute myocardial infarction.

Background: Little is known about the prognostic significance of elevated serum heart-type fatty acid-binding protein (H-FABP) in post-acute myocardial infarction (post-AMI) patients.

Methods And Results: A total of 1,283 post-AMI patients with available serum samples collected in the convalescent stage were studied. During a median follow-up period of 1,785 days, 176 patients (14%) had adverse events (all-cause mortality, n=81; non-fatal MI, n=44; readmission for heart failure [HF], n=51).

Impact of beta blockade therapy on long-term mortality after ST-segment elevation acute myocardial infarction in the percutaneous coronary intervention era.

Although clinical guidelines recommend long-term β-blocker (BB) therapy to decrease mortality after acute myocardial infarction, these recommendations are based predominantly on evidence from before the reperfusion and thrombolytic eras. To investigate the effects of BB therapy for patients with acute myocardial infarctions on mortality in the percutaneous coronary intervention era, a total of 5,628 consecutive patients who were admitted <24 hours after the onset of ST-segment elevation myocardial infarction, treated with emergent percutaneous coronary intervention, and discharged alive were studied. During a median follow-up period of 1,430 days, mortality rates did not differ between patients with and without BB therapy (5.

Incidence, predictors, and subsequent mortality risk of recurrent myocardial infarction in patients following discharge for acute myocardial infarction.

Background: In the percutaneous coronary intervention (PCI) era, little evidence exists regarding the incidence, predictors and long-term mortality of recurrent myocardial infarction (Re-MI) following discharge for acute myocardial infarction (AMI).

Methods And Results: A total of 7,870 patients who survived AMI were studied with a median follow-up period of 3.9 years: 353 patients (4.

Low levels of serum n-3 polyunsaturated fatty acids are associated with worse heart failure-free survival in patients after acute myocardial infarction.

Background: Intake of long-chain n-3 polyunsaturated fatty acids (n-3 PUFA), including docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), is associated with a lower risk of atherosclerotic cardiovascular events, particularly acute myocardial infarction (AMI). However, limited data are available regarding the association between serum n-3 PUFA levels and heart failure (HF) events in survivors of AMI.

Methods And Results: We evaluated whether serum DHA and EPA levels were associated with HF-free survival and HF hospitalization rates after AMI.

A subset of circulating microRNAs are predictive for cardiac death after discharge for acute myocardial infarction.

To investigate the prognostic impact of circulating microRNAs (miRs) in patients who survived acute myocardial infarction (AMI), we compared the circulating miR signature at the time of survival discharge among samples in the serum bank of the Osaka Acute Coronary Insufficiency Study. Using a high-throughput array consisting of 667 miRs, 11 miRs were found to be differentially expressed in the serum among patients at high-risk for cardiac death. Real-time RT-PCR confirmed that the serum levels of miR-155 and miR-380* were approximately 4- and 3-fold higher, respectively, in patients who experienced cardiac death within 1 year after discharge.

Oral treatment with nicorandil at discharge is associated with reduced mortality after acute myocardial infarction.

Background: Previous studies showed that nicorandil can reduce coronary events in patients with coronary artery disease. However, it is unclear whether oral nicorandil treatment may reduce mortality following acute myocardial infarction (AMI).

Methods And Results: We examined the impact of oral nicorandil treatment on cardiovascular events in 1846 AMI patients who were hospitalized within 24 h after AMI onset, treated with emergency percutaneous coronary intervention (PCI), and discharged alive.

Effect of intracoronary thrombectomy on 30-day mortality in non-diabetic patients with acute hyperglycemia after acute myocardial infarction.

Background: There is limited evidence about useful therapeutic interventions for patients with acute hyperglycemia (AH) after acute myocardial infarction (AMI).

Methods: We studied 2433 consecutive non-diabetic AMI patients who underwent percutaneous coronary intervention (PCI) within 24h after the onset. Patients were divided into two groups according to the presence or absence of AH (admission serum glucose level ≥ 11.

Impact of diabetes mellitus on rehospitalization for heart failure among survivors of acute myocardial infarction in the percutaneous coronary intervention era.

Background: There is little data regarding the clinical impact of diabetes mellitus (DM) on heart failure (HF) among survivors of acute myocardial infarction (AMI) in the percutaneous coronary intervention (PCI) era.

Methods And Results: The present study group comprised 4,035 survivors who underwent PCI within 24 h of the onset of symptoms. DM was an independent predictor of rehospitalization for HF by multivariate analysis (hazard ratio (HR) 1.

Lymphotoxin-alpha3 mediates monocyte-endothelial interaction by TNFR I/NF-kappaB signaling.

We recently reported that the single nucleotide polymorphisms of the lymphotoxin-(LT)alpha gene, a member of the tumor necrosis factor (TNF) family, are closely related to acute myocardial infarction; however, the precise mechanism of LTalpha signaling in atherogenesis remains unclear. We investigated the role of LTalpha3, a secreted homotrimer of LTalpha, in monocyte-endothelial cell adhesion using cultured human umbilical vein endothelial cells (HUVEC). We found that LTalpha3 induced cell adhesion molecules and activated NF-kappaB p50 and p65.

Up-regulation of cell adhesion molecule genes in human endothelial cells stimulated by lymphotoxin alpha: DNA microarray analysis.

Background: We recently reported that the A252G polymorphism of the Lymphotoxin-alpha (LTA) gene, a member of the tumor necrosis factor family, is strongly related with the onset of acute myocardial infarction; however, the roles of LTA in the development of atherosclerosis remain unclear.

Methods And Results: Changes in gene expression profile in cultured human umbilical vein (HUVEC) and coronary artery endothelial cells (HCAEC) treated with LTA were analyzed with high density oligonucleotide arrays comprised of 8,500 genes. LTA stimulation at 10 ng/mL for 2 hours profoundly induced gene expression associated with signal transduction, cell adhesion and chemoattraction, such as the nuclear factor of kappa light polypeptide gene enhancer in B-cells (NFkB), endothelial adhesion molecule 1 (E-Selectin), vascular cell adhesion molecule 1 (VCAM1), and monocyte chemotactic protein 1 (MCP1) (2.

Structural confirmation of ostreocin-D by application of negative-ion fast-atom bombardment collision-induced dissociation tandem mass spectrometric methods.

Negative-ion fast-atom bombardment collision-induced dissociation tandem mass spectrometric (FAB-CID-MS/MS) methodology was successfully applied to verify the highly complex structure of ostreocin-D (MW 2633), a new palytoxin analog isolated from the marine dinoflagellate Ostreopsis siamensis and proposed to be 42-hydroxy-3,26-didemethyl-19,44-dideoxypalytoxin based on NMR data. The charge-remote fragmentations were facilitated by a negative charge introduced to a terminal amino group or to a hydroxyl group at the other terminus by a reaction with 2-sulfobenzoic acid cyclic anhydride. Product ions generated from the [M - H](-) ions provided information on the structural details of ostreocin-D.