Prognostic value of myocardial injury in patients with COVID-19 / 中华心血管病杂志

Objective: To analyze the prognostic value of myocardial injury in patients with COVID-19. Method: Confirmed cases of COVID-19 patients admitted from January 31st to February 5th at isolation ward of Renmin Hospital of Wuhan University were divided into non-survival group （33 cases）and survival group (169 cases)according to the clinical outcomes 5 weeks after admission. Data including demographics, comorbidities, vital signs, laboratory results were obtained. Cardiac injury was defined as serum concentration of high sensitivity cardiac troponin I (hs-cTnI) above 0.04 μg/L. Univariate and multivariate Cox regression were used to analyze the prognostic value of myocardial injury in patients with COVID-19. Kaplan-Meier analysis was used to plotted survival curve and analyze the impact of myocardial injury on the survival outcome of COVID-19 patients. Results: A total of 202 patients were included, the age was 63 (51, 70) years old, 88 (43.6%) of them were male, 85 (42.1%) of them had comorbidities, 125 (61.9%) of them were severely to critically ill. Till March 11, 33 patients died, all of them were critically ill patients. The age, proportion of males, comorbidities, respire rate, serum levels of hs-cTnI and incidence of heart failure in the non-survival group were significantly higher than those in the survival group (all P<0.05). The hospitalization time of non-survival group was significantly shorter than that of survival group (6(4, 9) vs. 32(23, 36), P<0.001). Myocardial injury was an important prognostic factor of COVID-19 (HR=5.382, 95%CI 2.404-12.050, P<0.001). Kaplan-Meier survival analysis showed that the presence of myocardial injury was significantly associated with the reduced survival rate among COVID-19 patients (P<0.001). Conclusion: Myocardial injury is an important prognostic factor of COVID-19, COVID-19 patients with myocardial injury face a significantly higher risk of death.

Inhibitory effect of the paraoxonase gene on the formation of rabbit coronary atherosclerosis

OBJECTIVE@#To observe the effect on the inhibition of coronary atherosclerosis hardening of the paraoxonase gene (PON-1) which transfected to the rabbit epicardial adipose tissue.@*METHODS@#Rabbit coronary atherosclerosis model was established by high-fat feeding, liposome-encapsulated recombinant plasmid pEGFP-PON-1 50 μ L was injected to the rabbit pericardial cavity, and was harvested 4 weeks after transfection.@*RESULTS@#The epicardial fat transfected PON-1 gene had effect on the high lipid level. It significantly increased expression of PON-1 in peripheral arterial vascular tissue (P <0.05); and significantly reduced total cholesterol and low-density lipoprotein cholesterol levels (P<0.05), and the thickness ratio of coronary artery intima/media (P <0.05).@*CONCLUSIONS@#The injection of the PON-1 gene in the pericardial cavity can effectively suppress the formation of coronary atherosclerosis.

High mobility group box 1 protein: possible pathogenic link to atrial fibrillation / 中华医学杂志(英文版)

Atrial fibrillation (AF) is the most common sustained dysrhythmia in clinical practice. The bulk of evidence suggests that inflammatory processes, oxidative stress and matrix metalloproteinase are associated with development of AF. However, these agents may be involved in high mobility group box 1 protein (HMGB1). We hypothesized that HMGB1 may be a possible pathogenic link to AF. A growing body of evidence supports these hypotheses. First, the level of serum HMGB1 is significantly increased in patients with AF including paroxysmal and persistent AF. Second, HMGB1 has been identified as a new pro-inflammatory cytokine in cardiovascular diseases, along with tumor necrosis factor (TNF)-α, interleukin (IL)-6, and C-reactive protein, and there is cross-talk between HMGB1 and inflammatory cytokines. Third, oxidative stress is involved in the release of the pro-inflammatory cytokine, HMGB1, indicating there is cross-talk between oxidative stress and inflammation, and oxidative stress may reinforce the effect of inflammation on the pathogenesis of AF and inflammation may play a more important role in the pathogenesis of AF. Fourth, HMGB1 can promote matrix metalloproteinase-9 upregulation and activation. Fifth, HMGB1 receptors (receptor for advanced glycation end products, Toll-like receptor-2,4) may mediate the atrial structural remodeling or be up-regulated in patients with non-valvular AF. These results suggest that HMGB1 may participate in the pathogenesis of AF and provide a potential target for pharmacological interruption of AF.

Effects of antiarrhythmic drug use on atrial fibrillation recurrence in atrial fibrillation patients post circumferential pulmonary vein ablation / 中华心血管病杂志

<p><b>OBJECTIVE</b>This prospective and randomize-controlled trial was designed to investigate the effects of antiarrhythmic drug use (AADs) on atrial fibrillation (AF) recurrence in atrial fibrillation patients post circumferential pulmonary vein ablation (CAPV).</p><p><b>METHODS</b>Seventy-four consecutive AF patients underwent CAPV (41 paroxysmal and 33 drug refractory AF) were randomly assigned to receive placebo (Group A) or AADs (Group B) for 3 months. Monthly standard electrocardiograms (ECG) and Holter monitoring were performed to assess AF recurrences during 17 - 28 months follow-up.</p><p><b>RESULTS</b>CAPV was successful in all patients. The recurrence rate of AF in Group B was significantly lower than that in Group A at 3 months post CAPV (13.5% vs. 37.8%, P < 0.01) and similar thereafter (29.7% vs. 24.3% at 12 months and 8.1% vs. 8.1% at more than 12 months, all P > 0.05). There was also no significant difference in terms of total recurrence rate between the two groups (37.8% vs. 32.4%, P > 0.05).</p><p><b>CONCLUSION</b>Post CAPV antiarrhythmic drug therapy could only decrease the early AF recurrence rate but was not effective for decreasing AF recurrence rate on later stage.</p>