Treatment Of Myocardial Damage Research Articles

Clinical Observation of Trimetazidine Combined With Coenzyme Q10 in the Treatment of Myocardial Damage Caused by COVID-19.

Clinical Observation of Trimetazidine Combined With Coenzyme Q10 in the Treatment of Myocardial Damage Caused by COVID-19.

Treatment of myocardial damage past the coronary intervention—what can be salvaged?

Treatment of myocardial damage past the coronary intervention—what can be salvaged?

Treatment of myocardial damage past the coronary intervention—what can be salvaged?

In the report by Li et al . in this issue of Journal of Xiangya Medicine ( JXYM ), 80 rats underwent either permanent ligation of the left anterior descending coronary artery or a sham operation. The animals that underwent ligation, and therefore developed an acute myocardial infarction, were subsequently treated with either placebo, low-dose salidroside or high dose salidroside. Treatment with salidroside has been previously reported to be beneficial in cerebral ischemia (1) and cancer (2). These effects are partly attributed to the anti-apoptotic properties of salidroside. Li et al . studied whether this effect could also be beneficial in the heart, following myocardial infarction after 2 weeks. Using a combination of TUNEL staining and immunoblotting and myocardial mitochondria isolation, the authors elegantly show that treatment with salidroside significantly improves survival rates and limits myocardial cell apoptosis, 2 weeks after myocardial infarction. Furthermore, Li et al . deliver evidence that this effect could be attributed to alterations in expression of genes that are known to be involved in cell apoptosis, such as Bcl-2 and cytochrome-c. Besides this they show also that salidroside limits the release of cleaved caspase-3 and -9. These two proteins play an important role in the caspase cascade, which leads to apoptosis (3). Taken together, treatment with salidroside seems to be beneficial in preserving myocardial tissue following myocardial infarction by limiting ischemia and induced cell death.

The establishment of pediatric reference intervals for creatine kinase-MB and troponin I

Objective To establish the pediatric reference intervals for Troponin I and Creatine kinase-MB (CK-MB). Methods Healthy children (223 boys and 162 girls) aged from 7 months to 12 years old were studied.Blood specimens were collected and centrifuged, all serum samples were kept refrigerated below -70 ℃.Troponin I and CK-MB were measured on the UniCel DxI 800 immunoassay system (Beckman Coulter) on the same day.Nonparametric statistics was used to estimate the 99th percentile reference intervals. Results The children were divided into three groups (group A 128 cases；group B 128 cases；group C 129 cases) according to age.The upper reference limits for CK-MB were dependent of age, and the group A (7 months-1 years) was shown to be 13.41 μg/L, the group B (2-3 years) was shown to be 9.35 μg/L, the group C (4-12 years) was shown to be 5.48 μg/L.The upper reference limit for Troponin I was independent of age or gender and shown to be 0.01 μg/L among 385 children. Conclusions Pediatric reference intervals for Troponin I and CK-MB have been defined in healthy children at a relevant age group (7 months-12 years).It is effective for clinical diagnosis and treatment of myocardial damage for children by determining reference intervals for Troponin I and CK-MB.（Chin J Lab Med，2012,35：1142-1145） Key words: Troponin I; Creatine kinase; Isoenzymes; Reference values; Child

Abstract 5599: Secreted Frizzled Protein 2, a Cardioprotective Gene is Upregulated in Mesenchymal Stem Cells Following Engraftment in the Injured Myocardium

A variety of stem cells including Mesenchymal Stem Cells (MSCs) have been shown to have therapeutic potential in the treatment of myocardial damage. While the mechanism of action still remains unknown, MSCs have been shown to produce and secrete a broad variety of cytokines, chemokines and growth factors that may potentially be involved in cardiac repair. This has been confirmed by reports that human MSCs can exert favourable cardiac effects after myocardial infarction (MI) without persistence, engraftment, transdifferentation or cell fusion. Thus, the mechanisms responsible for their functional benefits appear to be attributable to paracrine effects. Secreted frizzled protein 2 (SFRP2) is expressed in MSCs following Akt gene transfer and has been shown to have paracrine protective effects. The objective of this study was to determine the effect of the ischemic environment on the engrafted MSC in order to understand the host - stem cell interaction. Using laser microdissection (LMD), the engrafted MSCs were retrieved from the injured myocardium 1 week post MI. To determine if SFRP2 was upregulated in our retrieved MSC population, RT PCR analysis of the retrieved MSCs Vs control MSCs was performed. SFRP2 was found to be 5,700 fold upregulated in MSCs exposed to the infarcted myocardium compared to control MSCs. Subsequent in vitro cardioprotection assays identified SFRP2 as a potent protector of cardiomyocytes during hypoxia treatment. Mitochondrial activity increased by 52% when neonatal rat cardiomyocytes were treated with SFRP2 recombinant protein during hypoxia treatment when compared to hypoxia alone. Caspase activity was also decreased in cardiomyocytes treated with SFRP2 during hypoxia. Cells also showed a healthy morphology and maintained beating after exposure to hypoxia. These data suggest that the injured host can induce MSCs to express cytoprotective factors such as SFRP2 and identify the host - stem cell interaction as an important determinant of the therapeutic effect of stem cell administration.

Transfection of antisense p38α gene ameliorates myocardial cell injury mediated by hypoxia and burn serum

Backgroud Myocardial damage occurs immediately following severe burns even before significant reduction in blood volume. This phenomenon is called postburn “shock heart” (“cardiac shock”), the pathogenesis of which is unclear. This study was designed to investigate the role of antisense p38α gene transfection in ameliorating hypoxia and burn serum-mediated myocardial cell injury. Methods A model of myocardial cells cultured under hypoxia and with burn serum was established. The cells were divided into control group (group C), the group cultured under hypoxia plus burn serum (group HS), and the group treated with antisense p38α gene transfection (group A-p38α) and cultured under hypoxia plus burn serum. Burn serum was collected from Wistar rats with 40% TBSA III degree burns. Hypoxia was produced using a mixed gas with 1% O 2. Antisense p38α gene recombinants were constructed and expression of p38α kinase, and NF-κB subunits p50, p65 and IκBα in myocardial cells were detected by Western blot. Myocardial viability was determined by tetrazolium colorimetry (MTT). Apoptosis was detected by flow cytometry. Lactate dehydrogenase (LDH) activity in cell culture supernatants was determined. Changes in TNFα and IL-1β mRNA expression were detected by RT-PCR. Results Activation of p38α kinase, expression of NF-κB p50, NF-κB p65 and IκB protein, and TNFα and IL-1β were downregulated significantly following antisense p38α gene transfection into myocardial cells treated with hypoxia plus burn serum. Myocardial apoptosis and LDH activity in cell culture supernatants decreased markedly and myocardial viability increased significantly in the antisense p38α gene treated group. Conclusions Results demonstrated that transfection of antisense p38α gene diminishes myocardial cell injury mediated by hypoxia and burn serum, suggesting a new target for the prevention and treatment of myocardial damage after burn.

The frequency, impact, and management of mitral regurgitation in patients with heart failure

Management of severe chronic mitral regurgitation (MR) in severe heart failure is challenging. There are controversies over the efficacy of surgical correction of MR in the presence of severely depressed left ventricular (LV) function. The etiology of MR plays an important role in clinical decision making. In organic MR, surgical correction should be performed even if patients have an LV ejection fraction of less than or equal to 30%. In functional MR, treatment of myocardial damage should be considered as the priority. The long-term mortality benefit of surgical correction of functional MR associated with severe LV dysfunction caused by cardiomyopathy (ischemic or dilated) likely depends on whether myocardial dysfunction can be reversed or improved by treatments (eg, coronary artery revascularization, pharmacologic treatment). Preoperative examination of viable myocardium (ischemic and hibernating myocardium) helps to identify a surgical candidate with ischemic MR associated with ischemic cardiomyopathy. The role of device treatment of MR in heart failure needs further investigation with outcome data.