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Idiopathic inflammatory myopathy (IIM) comprises a group of rare systemic diseases characterized by progressive weakness of the symmetrical proximal limb muscles, elevated muscle enzymes, inflammation or necrosis on muscle biopsy. IIM may impair the function of multiple organs, particularly the heart. However, it rarely manifests as acute myocardial infarction (AMI) at initial presentation. The present study described the case of a 39-year-old woman with AMI, whose muscle biopsy on the left arm conformed to polymyositis. Coronary arteriography showed irregularities in the left descending and right coronary artery (25% diameter reduction in middle segment). It was concluded that AMI was the chief manifestation of IIM at initial presentation. Furthermore, to the best of our knowledge, the present study was the first to provide a systematic literature review to assess AMI in IIM patients and discuss the possible causes of AMI. [ABSTRACT FROM AUTHOR]

Previous studies have described the beneficial effects of overexpressing integrin-linked kinase (ILK) after myocardial infarction (MI) in small animal models. However, the effects of ILK in pre-clinical large animals are not known. To move closer to clinical translation, we examined the effects of ILK gene transfer in a swine model of ischemic heart disease. Swine received percutaneous intracoronary injections of adenoviral vector expressing ILK (n=10) or empty ad-null (n=10) in the left anterior descending coronary artery (LAD) following LAD occlusion. Four weeks after transfection, we confirmed that transgene expression was restricted to the infarcted area in the cardiac tissue. Imaging studies demonstrated preserved cardiac function in the ILK group. ILK treatment was associated with reduced infarcted scar size and preserved left ventricular (LV) geometry (LV diameter and LV wall thickness). Enhanced angiogenesis was preserved in the ILK animals, along with reduction of apoptosis. ILK gene therapy improves cardiac remodeling and function in swine following MI associated with increased angiogenesis, reduced apoptosis, and increased cardiomyocyte proliferation with no signs of toxicity. These results may deliver a new approach to treat post-infarct remodeling and subsequent heart failure. [ABSTRACT FROM AUTHOR]

Myocardial infarction (MI) remains the leading cause of cardiovascular-associated mortality and morbidity. Improving the retention rate, survival and cardiomyocyte differentiation of mesenchymal stem cells (MSCs) is important in improving the treatment of patients with MI. In the present study, temperature-responsive chitosan hydrogel, an injectable scaffold, was used to deliver MSCs directly into the infarcted myocardium of rats following MI. Histopathology and immunohistochemical staining were used to evaluate cardiac cell survival and regeneration, and cardiac function was assessed using an echocardiograph. It was demonstrated that chitosan hydrogel increased graft size and cell retention in the ischemic heart, promoted MSCs to differentiate into cardiomyocytes and increased the effects of MSCs on neovasculature formation. Furthermore, chitosan hydrogel enhanced the effect of MSCs on the improvement of cardiac function and hemodynamics in the infarcted area of rats following MI. These findings suggest that chitosan hydrogel is an appropriate material to deliver MSCs into infarcted myocardium. [ABSTRACT FROM AUTHOR]

Acute myocardial infarction (AMI) is a major cause of morbidity and mortality worldwide. The highest risk of fatality occurs within the initial hours of onset of AMI. Thus, early diagnosis of cardiac ischemia is critical for the effective management of patients with AMI. Improper diagnosis of patients with chest pain often leads to inappropriate admission of patients without AMI and vice versa. In addition to clinical history, physical examination, accurate electrocardiogram findings and assessment of cardiac biomarkers have an important role in the early diagnosis of acute ischemia. The present review discusses in detail the various cardiac biomarkers released during the event of an AMI. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the effect of different routes of tirofiban injection on the function of the left ventricle and the prognosis of patients with myocardial infarction (MI) treated with percutaneous coronary intervention (PCI). Ninety-five patients with MI treated with PCI were divided into two groups [coronary (n=49) and intravenous (n=46)] according to the injection route. A comparison of the left ventricular function and prognosis was made between the two groups following PCI. The success rate of PCI in the coronary group was 97.96%, which was higher than that in the intravenous group (P<0.05). No significant differences were identified in the platelet count (PLT) and platelet aggregation rate (PAR) between the two groups prior to the tirofiban injection. Following the tirofiban injection, the PLT decreased markedly in both groups, with no significant differences between them. The PAR also decreased significantly in the two groups; however, the value in the coronary group was lower than that in the intravenous group (P<0.05). The improvements in the thrombolysis in MI grades, left ventricular ejection fraction and left ventricular diastolic function were greater in the coronary group than those in the intravenous group (P<0.05). All patients received follow-up for 30 days and the incidence of bleeding in the coronary group was lower than that in the intravenous group (P<0.05). No significant differences were recorded in the recurrence rates of MI, arrhythmia, myocardial ischemia, thrombocytopenia and mortality between the two groups. In conclusion, the administration of tirofiban into the coronary artery could effectively improve the blood flow, left ventricular function and prognosis of patients with MI treated with PCI. [ABSTRACT FROM AUTHOR]

Ischemia or hypoxia-induced myocardial injury is closely associated with oxidative stress. Scavenging free radicals and/or enhancing endogenous antioxidative defense systems may be beneficial for the impediment of myocardial ischemic injury. Hydrogen (H2) gas, as a water- and lipid-soluble small molecule, is not only able to selectively eliminate hydroxyl (.OH) free radicals, but also to enhance endogenous antioxidative defense systems in rat lungs and arabidopsis plants. However, thus far, it has remained elusive whether H2 gas protects cardiomyocytes through enhancement of endogenous antioxidative defense systems. In the present study, the cardioprotective effect of H2 gas against ischemic or hypoxic injury was investigated, along with the underlying molecular mechanisms. H9c2 cardiomyoblasts (H9c2 cells) were treated in vitro with a chemical hypoxia inducer, cobalt chloride (CoCl2), to imitate hypoxia, or by serum and glucose deprivation (SGD) to imitate ischemia. Cell viability and intracellular .OH free radicals were assessed. The role of an endogenous antioxidative defense system, the NF-E2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) signaling pathway, was evaluated. The findings revealed that treatment with CoCl2 or SGD markedly reduced cell viability in H9c2 cells. H2 gas-rich medium protected against cell injury induced by SGD, but not that induced by CoCl2. When the cells were exposed to SGD, levels of intracellular .OH free radicals were markedly increased; this was mitigated by H2 gas-rich medium. Exposure of the cells to SGD also resulted in significant increases in HO-1 expression and nuclear Nrf2 levels, and the HO-1 inhibitor ZnPP IX and the Nrf2 inhibitor brusatol aggravated SGD-induced cellular injury. H2 gas-rich medium enhanced SGD-induced upregulation of HO-1 and Nrf2, and the HO-1 or Nrf2 inhibition partially suppressed H2 gas-induced cardioprotection. Furthermore, following genetic silencing of Nrf2 by RNA interference, the effects of H2 gas on the induction of HO-1 and cardioprotection were markedly reduced. In conclusion, H2 gas protected cardiomyocytes from ischemia-induced myocardial injury through elimination of .OH free radicals and also through activation of the Nrf2/HO-1 signaling pathway. [ABSTRACT FROM AUTHOR]