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Complete atrioventricular block (CAVB) is a common complication of ST‐segment elevation myocardial infarction (STEMI). Although STEMI patients complicated with CAVB had a higher mortality in the thrombolytic era, little is known about the impact of CAVB on STEMI patients who underwent primary percutaneous coronary intervention (PCI). The study aimed at evaluating the clinical impact of CAVB on STEMI patients in the primary PCI era. We consecutively enrolled 1295 STEMI patients undergoing primary PCI within 24 hours from onset. Patients were divided into two groups according to the infarct location: anterior STEMI (n = 640) and nonanterior STEMI (n = 655). The outcomes were all‐cause death and major adverse cardiocerebrovascular events (MACCE) with a median follow‐up period of 3.8 (1.7–6.6) years. Eighty‐one patients (6.3%) developed CAVB. The incidence of CAVB was lower in anterior STEMI patients than in nonanterior STEMI (1.7% vs 10.7%, p < .05). Anterior STEMI patients with CAVB had a higher incidence of all‐cause deaths (82% vs 20%, p < .05) and MACCE (82% vs 25%, p < .05) than those without CAVB. Although higher incidence of all‐cause deaths was found more in nonanterior STEMI patients with CAVB compared with those without CAVB (30% vs 18%, p < .05), there was no significant difference in the incidence of MACCE (24% vs 19%). Multivariate analysis showed that CAVB was an independent predictor for all‐cause mortality and MACCE in anterior STEMI patients, but not in nonanterior STEMI. CAVB is rare in anterior STEMI patients, but remains a poor prognostic complication even in the primary PCI era.

Background Although PAR‐1 (protease‐activated receptor‐1) exerts important functions in the pathophysiology of the cardiovascular system, the role of PAR ‐1 signaling in heart failure development remains largely unknown. We tested the hypothesis that PAR ‐1 signaling inhibition has protective effects on the progression of cardiac remodeling induced by chronic renin–angiotensin system activation using renin‐overexpressing hypertensive (Ren‐Tg) mice. Methods and Results We treated 12‐ to 16‐week‐old male wild‐type ( WT ) mice and Ren‐Tg mice with continuous subcutaneous infusion of the PAR ‐1 antagonist SCH 79797 or vehicle for 4 weeks. The thicknesses of interventricular septum and the left ventricular posterior wall were greater in Ren‐Tg mice than in WT mice, and SCH 79797 treatment significantly decreased these thicknesses in Ren‐Tg mice. The cardiac fibrosis area and monocyte/macrophage deposition were greater in Ren‐Tg mice than in WT mice, and both conditions were attenuated by SCH 79797 treatment. Cardiac mRNA expression levels of PAR ‐1, TNF‐α (tumor necrosis factor‐α), TGF‐β1 (transforming growth factor‐β1), and COL3A1 (collagen type 3 α1 chain) and the ratio of β‐myosin heavy chain (β‐ MHC ) to α‐ MHC were all greater in Ren‐Tg mice than in WT mice; SCH 79797 treatment attenuated these increases in Ren‐Tg mice. Prothrombin fragment 1+2 concentration and factor Xa in plasma were greater in Ren‐Tg mice than in WT mice, and both conditions were unaffected by SCH 79797 treatment. In isolated cardiac fibroblasts, both thrombin and factor Xa enhanced ERK1/2 (extracellular signal‐regulated kinase 1/2) phosphorylation, and SCH 79797 pretreatment abolished this enhancement. Furthermore, gene expression of PAR ‐1, TGF ‐β1, and COL 3A1 were enhanced by factor Xa, and all were inhibited by SCH 79797. Conclusions The results indicate that PAR ‐1 signaling is involved in cardiac remodeling induced by renin–angiotensin system activation, which may provide a novel therapeutic target for heart failure.

Background: Little is known about the clinical outcomes of acute myocardial infarction (AMI) in patients with a history of malignant tumor (MT). Patients and Methods: We retrospectively studied 1,295 consecutive patients with AMI who underwent primary percutaneous coronary intervention within 24 hours of onset. The patients were divided into two groups: those with a history of MT (MT group, n=50) and those without n=1,245). Results: The MT group was older, and had lower hemoglobin, total protein, and albumin levels. All-cause mortality and re-admission rates due to acute decompensated heart failure (ADHF) were significantly higher in the MT group. Multivariate analysis showed that a history of MT was an independent predictor for all-cause mortality and re-admission due to ADHF. Conclusion: The clinical outcomes of patients with AMI with a history of MT are poor, and a history of MT is an independent predictor for all-cause mortality and re-admission due to ADHF. These patients may need careful risk management for heart failure to avoid re-admissions due to ADHF.Acute myocardial infarction (AMI) is a life-threatening disease that is common in developed countries. Although prognosis has improved dramatically since the development of primary percutaneous coronary intervention (PCI) in the early 1990s, ST elevation myocardial infarction (STEMI) still has a poor prognosis, with an in-hospital mortality rate of 7.1% in Japan (1). Another fatal disease is the development of a malignant tumor (MT) (2). Previous studies have shown a close relation between MTs and cardiovascular disease. MTs themselves cause venous or arterial thrombosis due to abnormal coagulation, platelet activation, and endothelial dysfunction (3). Regarding the treatment for MT, modern treatment strategies have improved relapse-free survival but they often induce the development of cardiovascular disease. Chemotherapy, such as with classical therapeutic drugs and molecular targeted drugs, and radiotherapy sometimes cause heart failure, thrombosis, ischemic heart disease, valvular disease, and hypertension (4, 5). Previous studies have reported that MTs adversely affect the development of cardiovascular disease but only few reports have investigated the clinical outcomes of AMI patients with a history of MT. In the present study, we investigated the clinical characteristics and outcomes of patients with AMI with a history of MT. Patients and MethodsStudy population. We retrospectively studied 1,295 consecutive patients with AMI who were admitted to our hospital and underwent primary PCI within 24 hours from the onset of symptoms between January 2007 and December 2016. The patients who were admitted to our hospital after 24 hours from onset or those who did not undergo primary PCI were excluded. The patients were divided into two groups as follows: those who had a history of MT and those without. The MT group consisted of patients who had a past history of MT and those who were diagnosed during hospitalization for AMI treatment. Moreover, we included...