Comparing In-Hospital Outcomes for Acute Myocardial Infarction Patients in High-Volume Hospitals Performing Primary Percutaneous Coronary Intervention vs. Regional General Hospitals.

Background: It has been reported that patients with acute myocardial infarction (AMI) transferred to low-volume primary percutaneous coronary intervention (PCI) hospitals (<115/year) in low population density areas experience higher in-hospital mortality rates. This study compared in-hospital outcomes of patients admitted to high-volume primary PCI hospitals (≥115/year) with those for other regional general hospitals.

Methods and results: Retrospective analysis was conducted on data obtained from 2,453 patients with AMI admitted to hospitals in Iwate Prefecture (2014-2018).

Role of Toll like receptor signaling pathway in ischemic coronary artery disease.

Inflammatory process plays a fundamental role in ischemic coronary artery disease (CAD) in terms of both the etiology of atherosclerosis and the pathophysiology of CAD. In particular, chronic inflammation plays a key role in coronary artery plaque instability and subsequent occlusive thrombosis. It is therefore important to clarify the mechanism underlying the activation of the immune response in the pathogenesis of CAD.

Local expression of Toll-like receptor 4 at the site of ruptured plaques in patients with acute myocardial infarction.

Several reports suggest that a chronic inflammatory process plays a key role in coronary artery plaque instability and subsequent occlusive thrombosis. In a previous study, we found that TLR4 (Toll-like receptor 4) mediates the synthesis of cytokines in circulating monocytes of patients with AMI (acute myocardial infarction); however, it remains unclear whether TLRs are expressed at the site of the ruptured plaque in these patients. The aim of the present study was to determine whether TLR2 and TLR4 are expressed at the site of ruptured plaques in patients with AMI and to compare this with systemic levels.

Association between oxidative DNA damage and telomere shortening in circulating endothelial progenitor cells obtained from metabolic syndrome patients with coronary artery disease.

Metabolic syndrome (MS) induces an increase in oxidative stress and may be an important contributory factor for coronary artery disease (CAD). Telomere shortening of endothelial progenitor cells (EPCs) may be the key factor in endothelial cell senescence. The rate of telomere shortening is highly dependent on cellular oxidative damage.

Association between toll-like receptor 8 expression and adverse clinical outcomes in patients with enterovirus-associated dilated cardiomyopathy.

Background: In recent reports, human toll-like receptor (TLR) 8 mediates the antiviral response by recognizing single-stranded RNA. The inflammatory response against enteroviral (EV) RNA replication may play an important role in dilated cardiomyopathy (DCM). The purpose of this study was to determine whether TLR8 was expressed with EV replication in patients with enterovirus-associated DCM.

Elevated circulating levels of heat shock protein 70 are related to systemic inflammatory reaction through monocyte Toll signal in patients with heart failure after acute myocardial infarction.

Background: Recent studies have shown that heat shock protein (HSP) 70 may serve as a "damage signal" to the immune system and could be the endogenous ligand for Toll-like receptor (TLR) 4 mediating synthesis of inflammatory cytokines.

Aims: To explore the relationship between circulating HSP70 levels and activation of monocyte TLR4 and myocardial damage after AMI.

Methods And Results: This study examined circulating HSP70 and monocyte TLR4 levels in 52 patients with AMI and 20 controls, and analyzed ex vivo inflammatory cytokine productions using HSP70-stimulated monocytes.

Activated toll-like receptor 4 in monocytes is associated with heart failure after acute myocardial infarction.

Peripheral monocytosis may affect the development of heart failure (HF) after acute myocardial infarction (AMI). Activated toll-like receptor (TLR) 4 in monocytes plays an important role in the synthesis of proinflammatory cytokines. We examined TLR4 expression in monocytes, which may be a possible source of proinflammatory cytokines in AMI.