COVID-19 has been the biggest global health threat since world war II. Up to now, the novel coronavirus pneumonia epidemic has resulted in over 300 thousand deaths. Angiotensin-converting enzyme 2 (ACE2), the receptor of SARS-CoV-2, is also the key modulator of renin-angiotensin-aldosterone system (RAAS) axes, which regulates the inflammatory response to maintain internal environment balance. On the contrary, RAAS axes can also regulate the expression of ACE2 which may influence on the susceptibility of SARS-CoV-2. Furthermore, SARS-CoV-2 binds with ACE2 and subsequently down-regulates ACE2 expression, which may exacerbate the inflammatory response due to RAAS imbalance. In this review, we summarized pathogenesis and clinical characteristics of COVID-19 patients, and discussed the potential link between the RAAS axes imbalance and the susceptibility/progression of organ injury in COVID-19. Therefore, we speculate that rebalance of the RAAS axes is the preventive and therapeutic strategy of COVID-19.
Introduction: It is not unusual for temporary transvenous cardiac pacing (TVCP) leads to penetrate and occasionally perforate the right ventricular wall, which generally is asymptomatic. The definition of myocardial injury is evidence of elevated cardiac troponin (cTn) values above the 99th percentile upper reference limit (URL). Myocardial injury is associated with an adverse prognosis. The present study was designed to evaluating myocardial injury complicated by TVCP. Methods: Retrospective study from August 2018 to March 2020, 33 consecutive patients undergo elective TVCP support for non-cardiac procedures, 22 of them had cardiac biomarkers assays before and after TVCP. These 22 eligible patients had a median age of 66 (50-83) years, 6 (27.3%) were women, and all baseline cTn <1 URL. Compare cardiac biomarkers before and after TVCP. Results: 20 (91%, N=22) patients detect cTn >1 URL after pacing. Paired t-test compare before and after pacing leads insertion showed a mean cTn elevation of 3.599 (95% CI, 1.566 to 5.632, P<0.01）URL, and no significantly creatine kinase-MB elevation of 0.1550 (95% CI, -0.01239 to 0.3224, P>0.05 ) URL. Conclusion: This study demonstrates a high incidence of substantial myocardial injury by TVCP, which should be concerned.