Background: It has been proved in animal models that postconditioning (PC) could attenuate reperfusion injury. But there are not many clinical studies on the application of PC. Hypothesis: Four cycles of 1-minute balloon inflation and deflation, following initial balloon reperfusion in ST-segment elevation myocardial infarction (MI) but before stenting, might improve clinical outcomes compared with primary percutaneous coronary intervention (PCI) alone. Methods: Forty-three patients diagnosed with acute MI were randomly assigned to 2 groups: the control group (n = 20) and the PC group (n = 23). Blood samples were obtained and assayed for creatine kinase MB (CK-MB) and high-sensitive C-reactive protein. Electrocardiogram, echocardiography, and rest technetium Tc 99m-sestamibi (99mTc-MIBI) myocardial perfusion single-photon emission computed tomography (SPECT) were performed.
Results:The control group presented with higher peak CK-MB as compared with the PC group (351.9 ± 153.6 vs 247.7 ± 118.3 U/L, P = 0.028) as well as the area under the curve (AUC) of CK-MB (8040 ± 3358 vs 5955 ± 2509, P = 0.04). After PCI, PC was associated with a lower level of hs-CRP in comparison with the control group (5.5 ± 4.5 vs 9.5 ± 5.2 mg/L, P = 0.019). More patients in the PC group had complete ST-segment resolution than did patients in the control group (82.6% vs 45.0%, P = 0.049). Left ventricle ejection fraction was better in the PC group than in the control group (0.57 ± 0.09 vs 0.47 ± 0.11, P = 0.002). Compared with the control group, PC greatly reduced infarct size, by 46% as measured by SPECT (13 ± 11.2% vs 24.2 ± 10.6%, P = 0.002). Conclusions: This study indicated that PC in emergent PCI was a valuable modification of primary PCI.
IntroductionCoronary heart disease will become the leading cause of death worldwide by 2020. 1 Acute myocardial infarction (AMI) is a major cause of such mortality. Early and successful myocardial reperfusion with the use of thrombolytic therapy or percutaneous coronary intervention (PCI) is the most effective strategy for reducing the size of a myocardial infarct and improving the clinical outcome. But at the same time, the process of restoring blood flow to the ischemic myocardium can induce additional lethal injuries that are termed myocardial reperfusion injury. 2 Studies in animal models of AMI suggest that 50% of the final size of an MI is caused by myocardial reperfusion injury. 3 So new strategies for preventing reperfusion injury should be explored.Postconditioning (PC), defined as a cycle of brief interruptions of reperfusion applied at the onset of reperfusion after a prolonged ischemic insult, has been found to attenuate reperfusion injury in several animal experiments. 4 -7 In our study we applied this cardioprotective intervention at the time of myocardial reperfusion in 23 Chinese AMI patients receiving emergent PCI.
Lactate dehydrogenase A (LDHA), a critical component of the glycolytic pathway, relates to the development of various cancers, including thyroid cancer. However, the regulatory mechanism of LDHA inhibition and the physiological significance of the LDHA inhibitors in papillary thyroid cancer (PTC) are unknown. Long non-coding RNA (lncRNA) plays a vital role in tumor growth and progression. Here, we identified a novel lncRNA LINC00671 negatively correlated with LDHA, downregulating LDHA expression and predicting good clinical outcome in thyroid cancer. Moreover, hypoxia inhibits LINC00671 expression and activates LDHA expression largely through transcriptional factor STAT3. STAT3/LINC00671/LDHA axis regulates thyroid cancer glycolysis, growth, and lung metastasis both in vitro and in vivo. In thyroid cancer patients, LINC00671 expression is negatively correlated with LDHA and STAT3 expression. Our work established STAT3/LINC00671/LDHA as a critical axis to regulate PTC growth and progression. Inhibition of LDHA or STAT3 or supplement of LINC00671 could be potential therapeutic strategies in thyroid cancer.
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