Clinical characteristics and outcomes of 112 cardiovascular disease patients infected by 2019-nCoV / 中华心血管病杂志

Objective: To explore the clinical characteristics and prognosis of the new coronavirus 2019-nCoV patients combined with cardiovascular disease （CVD). Methods: A retrospective analysis was performed on 112 COVID-19 patients with CVD admitted to the western district of Union Hospital in Wuhan, from January 20, 2020 to February 15, 2020. They were divided into critical group (ICU, n=16) and general group (n=96) according to the severity of the disease and patients were followed up to the clinical endpoint. The observation indicators included total blood count, C-reactive protein (CRP), arterial blood gas analysis, myocardial injury markers, coagulation function, liver and kidney function, electrolyte, procalcitonin (PCT), B-type natriuretic peptide (BNP), blood lipid, pulmonary CT and pathogen detection. Results: Compared with the general group, the lymphocyte count (0.74 (0.34, 0.94)×109/L vs. 0.99 (0.71, 1.29)×109/L, P=0.03) was extremely lower in the critical group, CRP (106.98 (81.57, 135.76) mg/L vs. 34.34 (9.55,76.54) mg/L, P<0.001) and PCT (0.20 (0.15,0.48) μg/L vs. 0.11 (0.06,0.20) μg/L, P<0.001) were significantly higher in the critical group. The BMI of the critical group was significantly higher than that of the general group (25.5 (23.0, 27.5) kg/m2 vs. 22.0 (20.0, 24.0) kg/m2，P=0.003). Patients were further divided into non-survivor group (17, 15.18%) group and survivor group (95, 84.82%). Among the non-survivors, there were 88.24% (15/17) patients with BMI> 25.0 kg/m2, which was significantly higher than that of survivors (18.95% (18/95), P<0.001). Compared with the survived patients, oxygenation index (130 (102, 415) vs. 434 (410, 444), P<0.001) was significantly lower and lactic acid (1.70 (1.30, 3.00) mmol/L vs. 1.20 (1.10, 1.60) mmol/L, P<0.001) was significantly higher in the non-survivors. There was no significant difference in the proportion of ACEI/ARB medication between the critical group and the general group or between non-survivors and survivors （all P>0.05). Conclusion: COVID-19 patients combined with CVD are associated with a higher risk of mortality. Critical patients are characterized with lower lymphocyte counts. Higher BMI are more often seen in critical patients and non-survivor. ACEI/ARB use does not affect the morbidity and mortality of COVID-19 combined with CVD. Aggravating causes of death include fulminant inflammation, lactic acid accumulation and thrombotic events.

Association of IL33/ST2 signal pathway gene polymorphisms with myocardial infarction in a Chinese Han population / 华中科技大学学报（医学）（英德文版）

This study investigated the relationship between IL-33/ST2 signal pathway gene polymorphisms and myocardial infarction (MI) in Han Chinese. A case-control association analysis was performed on a total of 490 MI patients (MI group) and 929 normal subjects (NC group). Sequenom Mass Array and Taqman genotyping technique were used to analyze the tag single nucleotide polymorphisms (SNPs) in the genes encoding IL-33, ST2, and IL-1RaP (rs11792633, rs1041973 and rs4624606). The results showed that the frequencies of rs4624606 genotypes AA, TT, AT were 0.031, 0.647, 0.322 in MI group and 0.026, 0.712, 0.263 in NC group, and the allele frequencies of A and T were 0.192, 0.808 in MI group and 0.157, 0.843 in NC group. There were significant differences in rs4624606 genotypes and allele frequencies between MI group and NC group (P<0.05). For rs11792633, the allele frequencies of C and T were 0.45, 0.55 in MI group and 0.454, 0.546 in NC group with no significant differences found between the two groups. Compared with genotype CC+TC, rs11792633 genotype TT had an increased risk of hypertension (P<0.05). However, there were no significant differences in the frequencies of rs11792633 genotypes between the two groups. No significant differences were noted in the frequencies of rs1041973 genotype and allele between the two groups. Logistic regression analysis showed that rs4624606 genotypes AT and AA+AT were both significantly associated with MI (AT: OR=1.325, P=0.029, 95% CI=1.03-1.705; AA+AT: OR=1.316, P=0.028, 95% CI=1.03-1.681) after factors such as age, gender, smoking, drinking, body mass index (BMI), triglyceride (TG) and cholesterol were adjusted. Those carrying rs4624606 genotype AT or AA+AT had an increased risk of MI. No associations were found between the polymorphisms of the other two loci with MI. It was concluded that, in the IL33/ST2 signal pathway, the A allele of rs4624606 polymorphism of IL-1RaP gene is a potential independent risk factor for MI, and the genotypes AA+AT and AT are associated with the incidence of MI.

Association of IL33/ST2 signal pathway gene polymorphisms with myocardial infarction in a Chinese Han population / 华中科技大学学报（医学）（英德文版）

This study investigated the relationship between IL-33/ST2 signal pathway gene polymorphisms and myocardial infarction (MI) in Han Chinese. A case-control association analysis was performed on a total of 490 MI patients (MI group) and 929 normal subjects (NC group). Sequenom Mass Array and Taqman genotyping technique were used to analyze the tag single nucleotide polymorphisms (SNPs) in the genes encoding IL-33, ST2, and IL-1RaP (rs11792633, rs1041973 and rs4624606). The results showed that the frequencies of rs4624606 genotypes AA, TT, AT were 0.031, 0.647, 0.322 in MI group and 0.026, 0.712, 0.263 in NC group, and the allele frequencies of A and T were 0.192, 0.808 in MI group and 0.157, 0.843 in NC group. There were significant differences in rs4624606 genotypes and allele frequencies between MI group and NC group (P<0.05). For rs11792633, the allele frequencies of C and T were 0.45, 0.55 in MI group and 0.454, 0.546 in NC group with no significant differences found between the two groups. Compared with genotype CC+TC, rs11792633 genotype TT had an increased risk of hypertension (P<0.05). However, there were no significant differences in the frequencies of rs11792633 genotypes between the two groups. No significant differences were noted in the frequencies of rs1041973 genotype and allele between the two groups. Logistic regression analysis showed that rs4624606 genotypes AT and AA+AT were both significantly associated with MI (AT: OR=1.325, P=0.029, 95% CI=1.03-1.705; AA+AT: OR=1.316, P=0.028, 95% CI=1.03-1.681) after factors such as age, gender, smoking, drinking, body mass index (BMI), triglyceride (TG) and cholesterol were adjusted. Those carrying rs4624606 genotype AT or AA+AT had an increased risk of MI. No associations were found between the polymorphisms of the other two loci with MI. It was concluded that, in the IL33/ST2 signal pathway, the A allele of rs4624606 polymorphism of IL-1RaP gene is a potential independent risk factor for MI, and the genotypes AA+AT and AT are associated with the incidence of MI.

Study on the association of -689C/T polymorphism in the PPARgamma2 promoter with myocardial infarction / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To investigate the association of -689C/T polymorphism in the peroxisome proliferator-activated receptor-gamma2 (PPARgamma2) promoter with myocardial infarction (MI).</p><p><b>METHODS</b>This is a case-control study, which included 194 subjects with MI and 693 subjects without MI in nondiabetic Han population in Wuhan. Polymerase chain reaction-restriction fragment length polymorphism was used to determine the -689C-->T substitution.</p><p><b>RESULTS</b>The CC,CT, and TT genotype frequencies of -689C/T polymorphism were 88.1%,11.9%,and 0.0 in MI patients and 93.1%,6.6%,and 0.3% in controls, respectively (CC vs. CT+TT, P=0.025). The -689T allele was an independent risk factor for MI (OR=2.125, 95%CI: 1.206-3.744, P=0.009) after adjusting for age,sex,waist circumference,body mass index, smoking, alcohol drinking, physical activities, systolic blood pressure, diastolic blood pressure, fasting blood glucose, total cholesterol, triglyceride, level. The -689T allele carriers had significantly higher TC levels than noncarriers [(5.05+/-1.16) mmol/L vs. (4.78+/-1.05) mmol/L, P=0.004] in the total population.</p><p><b>CONCLUSION</b>The PPARgamma2 promoter -689C/T polymorphism is associated with an increased risk of MI.</p>

Role of apoptosis of neutrophils and vascular endothelial cells and changes of relative factors in the pathogenesis of traumatic sepsis at the advanced stage / 中华创伤杂志

Objective To explore the role of apoptosis of neutrophils and vascular endothelial cells and changes of relative cytokines and thrombotic factors in the pathogenesis of traumatic sepsis at the advanced stage.Methods The venous blood was collected from the patients with traumatic sepsis at advanced stage and traumatic patients without sepsis and healthy subjects.The peripheral hlood mononu- clear cells(PBMC)and neutrophils were isolated and cultured.The apoptosis of neutrophils and vascular endothelial cells was assayed,and the level of IL-4,IL-10 in PBMC culture supernatants were deter- mined,and the tissue factor(TF)and vW factor(vWF)of peripheral plasma were measured.Results The percentages of apoptosis of neutrophils and numbers of apoptotic circulating vascular endothelial cells were higher than that of traumatic patients without sepsis and healthy controls significantly.And the levels of anti-inflammatory cytokines IL-4,IL-10 and thrombotic factors TF,vWF in traumatic sepsis were elevated than that of traumatic patients without sepsis and controls too.Conclusion Immune suppres- sion and abnormal thrombotic state may be one characteristic of traumatic sepsis at advanced stage,which perhaps involveds in the pathogenesis of traumatic sepsis at the advanced stage and multiple organ dys- function syndrome.

Dependence of ventricular wallstress-induced refractoriness changes on pacing cycle lengths and its mechanism / 生理学报

The aim of this article was to investigate the dependence of ventricular wallstress-induced refractoriness changes on pacing cycle lengths and its mechanism in anaesthetized rabbits. The rabbit heart preparation was used. The left ventricular afterload was increased by partially clipping the root of the ascending aorta. The changes in effective refractory periods (ERP) induced by the left ventricular afterload rising were examined at different pacing cycle lengths (1000, 500, 300 and 200 ms). In addition, the effect of streptomycin on these changes was also observed. The results are as follows: (1) The rising of left ventricular afterload led to marked changes in ERP at rapidly pacing cycle lengths (300 ms, 21+/-5 ms, 17.0%; 200 ms, 19+/-3 ms, 18.8%. P<0.01) than at slow ones (1000 ms, 3+/-2 ms, 1.5%; 500 ms, 7+/-3 ms, 4.0%. P>0.05); (2) Streptomycin inhibited the changes caused by the left ventricular afterload rising at pacing cycle lengths 300 ms and 200 ms (P>0.05). It is suggested that ventricular wallstress-induced refractoriness changes are pacing cycle length-dependent, and the effect of streptomycin appears to be consistent with the inhibition of stretch-activated ion channels.

Adenosine protects cardiomyocytes from hypoxia/reoxygenation injury / 生理学报

The aim of this study was to investigate the protective effect of adenosine (ADO) on cardiomyocytes following hypoxia/reoxygenation (H/R) and its molecular mechanism. Primary cultured cardiomyocytes of neonatal rats were divided into two groups, namely H/R (control) and ADO (1.0 micromol/L) groups. The morphologic changes in cardiomyocytes were observed under an inverted phase-contrast microscope. The following parameters of the two groups were determined: lactate dehydrogenase (LDH) activity, intracellular calcium concentration and malondialdehyde (MDA) content. Tumor necrotic factor (TNF-alpha) assay was performed using an ELISA kit and NF-kappaB in the nucleus was analyzed by electrophoretic mobility shift assay (EMSA). The results are as follows: (1) after H/R injury, cardiomyocytes contracted, tending to get round in shape and its pseudopods decreased, while marked morphological changes were not observed in ADO group; (2) LDH leakage maintained at a lower level in ADO group than that in the control group during H/R (both P<0.01); (3) ADO significantly reduced the concentration of calcium in cells and prevented calcium overload during H/R (both P<0.01); (4) ADO markedly reduced the content of MDA during H/R (both P<0.01); (5) ADO inhibited the production of TNF-alpha during H/R (both P<0.01); and (6) ADO down-regulated NF-kappaB binding activity of cardiomyocytes during H/R (both P<0.01) The results suggest that (1) exogenous ADO attenuates H/R injury of cultured cardiomyocytes; (2) exogenous ADO inhibits the production of TNF-alpha after H/R injury; (3) exogenous ADO prevents the activation of NF-kappaB, which may be the molecular mechanism of down-regulation of TNF-alpha expression.

Effect of tetradrine on electrophysilogic changes caused by rising of left ventricular preload in guinea pigs / 中国中药杂志

<p><b>OBJECTIVE</b>To investigate the changes of guinea pig heart electrophysiological properties caused by increasing left ventricular preload, and to assess the effects of tetradrine on these changes.</p><p><b>METHOD</b>Working model preparation of guinea pig hearts in vitro was used, and the preload of left ventricle was increased by adjusting the prefusion pressure of left atria. The changes of heart electrophysiologic parameters including monophasic action potential duration (MAPD90), monophasic action potential amplitude (MAPA), effective refractory period (ERP) and ventricular fibrillation threshold (VFT) were observed before and after altering the preload of left ventricle, and compared in the absence and presence of tetradrine, streptomycin or verapamil.</p><p><b>RESULT</b>The rising of left ventricular preload led to shortening of MAPD90, ERP, and to descent of MAPA, VFT (all P<0.01). Both Tetradrine and streptomycin inhibited these changes of heart electrophysiologic parameters caused by elevation of left ventricular afterload (all P<0.01). In contrast, verapamil had no effects on the preload-related electrophysiological changes (all P>0.05).</p><p><b>CONCLUSION</b>Electrophysiologic changes caused by increasing left ventricular preload may be inhibited by tetrandrine, through inhibition of stretch-activated ion channels.</p>