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Objective:To investigate the effect of curcumin on the nucleotide-binding oligomerization domain-like receptor protein (NLRP3) inflammasome in cardiomyocytes of rats with early sepsis and its mechanism.Methods:Twenty-four male SD rats were randomly divided into three groups: the sham-operated group (sham group, n=8), the sepsis group ( n=8), and the curcumin intervention group (Cur group, n=8). A rat model of sepsis was prepared by cecal ligation and perforation (CLP). After modeling, 100 mg/kg of curcumin was intraperitoneally injected and repeated 24 h later. Rats in the sepsis group were injected with normal saline. The levels of myocardial injury-specific troponin T (cTnT) in rat plasma were detected by ELISA at 6, 24, and 48 h. Hematoxylin-eosin (HE) staining was used to observe the pathological injury of the myocardium in the myocardial tissue of rat at 48 h. The apoptosis of cardiomyocytes was detected by TUNEL assay. The expression levels of Cleaved caspase-1, NLRP3 and IL-1β protein were detected by Western blot, and the ultrastructural changes of the cardiomyocytes were observed under a transmission electron microscope. Results:The levels of cTnT in rat plasma at 6, 24, and 48 h in the Cur group were significantly lower than those in the sepsis group ( P<0.05). HE staining showed infiltration, cell edema and necrosis of myocardial inflammatory cells in the sepsis group, while only partial cell edema and necrosis were observed in the Cur group. TUNEL assay showed that the apoptosis of cardiomyocytes in the Cur group was significantly lower than that in the sepsis group [(28.4±2.3)% vs. (43.6±3.8)%, P<0.05]. The expression levels of Cleaved caspase-1, NLRP3 and IL-1β in the Cur group were lower than those in the sepsis group and higher than those in the sham-operated group ( P<0.05). Under transmission electron microscopy, the nuclei in the sham-operated group had intact membranes and uniform chromatin distribution; in the sepsis group chromatin margination, pyknosis, mitochondrial cristae breakage, cavitation, and partial breakage of sarcomere were observed; while in the Cur group partial chromatin margination, slightly edema and dilation of mitochondria, with basically complete morphology were observed. Conclusions:Curcumin inhibits NLRP3-mediated acute myocardial injury in septic rats, and its mechanism may be related to pyroptosis induced by the down-regulation of the expression of Cleaved caspase-1 and IL-1β protein.
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OBJECTIVE@#To investigate the risk factors for acute myocardial injury in coronavirus disease 2019 (COVID-19) patients.@*METHODS@#This is a retrospective analysis of a COVID-19 cohort, in which 149 confirmed COVID-19 patients enrolled were divided into the group of myocardial injury (19 cases) and the group of non-myocardial injury (130 cases). Myocardial injury was defined according to Fourth universal definition of myocardial infarction released by European Society of Cardiology (ESC) in 2018, that cardiac troponin (cTn) was above 99th percentile of the reference level. Clinical information and results of laboratory tests of the eligible patients were collected. Factors associated with myocardial injury in COVID-19 patients were evaluated.@*RESULTS@#Compared with the group of non-injury, the patients in the group of injury were older and had a larger proportion of severe or critical cases (P < 0.05), higher respiratory rate and lower percutaneous oxygen saturation (SpO2) without oxygen therapy on admission (P < 0.05). All inflammatory indexes except for tumor necrosis factor α (TNF-α) showed significant elevation in the patients of the group of injury (P < 0.05). Analyzed by Spearman correlation test, we showed that the levels of circulatory cTnI were in positive correlation with the levels of high-sensitivity C-reactive protein (hs-CRP), ferritin, receptor of interleukin-2 (IL-2R), interleukin-6 (IL-6) and interleukin-8 (IL-8) (ρ > 0, P < 0.05). Lower SpO2 without oxygen therapy on admission (OR: 0.860, 95%CI: 0.779-0.949, P=0.003) and higher plasma IL-6 levels (OR: 1.068, 95%CI: 1.019-1.120, P=0.006) were independent risk factors for acute myocardial injury in the patients with COVID-19 by multivariate Logistic regression analyses.@*CONCLUSION@#Hypoxic state and inflammation may play a key role in the pathogenesis of acute myocardial injury in COVID-19 patients.
Subject(s)
Humans , Biomarkers , COVID-19 , Hypoxia , Inflammation , Retrospective Studies , Risk Factors , SARS-CoV-2ABSTRACT
ObjectiveTo study the relationship between acute myocardial injury（AMI） and coagulation function in patients with COVID-19.MethodsA retrospective study was carried out to record the general and laboratory data of 133 patients diagnosed with COVID-19 who were hospitalized in Wuhan TongJi Guanggu Hospital, Wuhan, Hubei Province from February 10 to February 29, 2020. The laboratory data includes blood routine, liver and renal function, myocardial infarction tests, coagulation function, inflammatory factors, hypersensitive C-reactive protein, procalcitonin etc. The patients were divided into two groups according to cardiac troponin I（TNI）34.2 ug/L. The differences of general conditions and laboratory data between the two groups were compared. Besides, the correlation between coagulation function and coagulation function, and the ROC curve of D-dimer in AMI were conducted .ResultsAmong the 133 patients, 9 (6.77%) had cTnI greater than 34.2 μg/L, and 124 (93.23%) had normal cTnI. There were significant differences between the two groups in age, COPD history, blood routine (neutrophil count, lymphocyte count, platelet count), myoglobin, liver function (direct bilirubin, indirect bilirubin), cytokines (IL-2 receptor, IL-6, IL-8, IL-10, TNF-α), coagulation function (PT, PTA, D-dimer). D-dimer level was positively correlated with TnI, CK-MB and myoglobin levels. The cut off value of D-dimer was 2.35 μg/ml in acute myocardial injury.ConclusionAcute myocardial injury in COVID-19 patients may be related to coagulation dysfunction. Therefore, monitoring of coagulation function dynamically, screening of thrombus and starting anticoagulant and antiplatelet therapy timely help to reduce acute myocardial injury.
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ObjectiveTo study the relationship between acute myocardial injury（AMI） and coagulation function in patients with COVID-19.MethodsA retrospective study was carried out to record the general and laboratory data of 133 patients diagnosed with COVID-19 who were hospitalized in Wuhan TongJi Guanggu Hospital, Wuhan, Hubei Province from February 10 to February 29, 2020. The laboratory data includes blood routine, liver and renal function, myocardial infarction tests, coagulation function, inflammatory factors, hypersensitive C-reactive protein, procalcitonin etc. The patients were divided into two groups according to cardiac troponin I（TNI）34.2 ug/L. The differences of general conditions and laboratory data between the two groups were compared. Besides, the correlation between coagulation function and coagulation function, and the ROC curve of D-dimer in AMI were conducted .ResultsAmong the 133 patients, 9 (6.77%) had cTnI greater than 34.2 μg/L, and 124 (93.23%) had normal cTnI. There were significant differences between the two groups in age, COPD history, blood routine (neutrophil count, lymphocyte count, platelet count), myoglobin, liver function (direct bilirubin, indirect bilirubin), cytokines (IL-2 receptor, IL-6, IL-8, IL-10, TNF-α), coagulation function (PT, PTA, D-dimer). D-dimer level was positively correlated with TnI, CK-MB and myoglobin levels. The cut off value of D-dimer was 2.35 μg/ml in acute myocardial injury.ConclusionAcute myocardial injury in COVID-19 patients may be related to coagulation dysfunction. Therefore, monitoring of coagulation function dynamically, screening of thrombus and starting anticoagulant and antiplatelet therapy timely help to reduce acute myocardial injury.
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Pheochromocytoma may cause anatomic and functional cardiac abnormalities. Various echocardiographic abnormalities have been observed, including systolic anterior movement, global hypokinesis as well as hypokinesis of the base and the apex of LV. There are no previous reports of serial echocardiographic finding in patients with pheochromocytoma. We experienced a 38-year-old woman with pheochromocytoma who suffered from acute myocardial injury. Echocardiography revealed that the acute myocardial injury started in the base in the early phase and subsequently extended to the mid-portion of left ventricule. The injury persisted longer in the base than the mid-portion. than 1.5 times the adjacent normal coronary artery.