Highlights The usage of antihypertensive drugs is not associated with the risk and severity of COVID-19. Hypertensive patients with COVID-19 benefit from prior usage of angiotensin-converting enzyme inhibitors/angiotensin receptor blockers.

BackgroundCataracts are the main cause of poor vision and blindness worldwide. The effects of statin administration on cataracts remain debated. Therefore, we conducted a systematic review and meta‐analysis to determine whether statin use affects the risk of cataracts.Methods and ResultsWe performed a systematic search of the electronic databases PubMed, EMBASE, and the Cochrane Library through January 2016. Weighted averages were reported as relative risk values with 95% CIs. Statistical heterogeneity scores were assessed with the standard Cochran's Q test and the I2 statistic. A total of 6 cohort studies, 6 case–control studies, and 5 randomized controlled trials, together involving more than 313 200 patients, were included in our study. The pooled estimates of cohort studies indicated that the use of statins moderately increases the risk of cataracts (relative risk, 1.13; 95% CI, 1.01–1.25). The pooled estimates of case–control studies (relative risk=1.10, 95% CI, 0.99–1.23) and randomized controlled trials (relative risk, 0.89; 95% CI, 0.72–1.10) indicated that the use of statins does not increase the risk of cataracts. The sensitivity analysis confirmed the stability of the results. Heterogeneity was found among the cohort and case–control studies.ConclusionsBased on the present meta‐analysis of these studies, we could only conclude that there is no clear evidence showing that statin use increases the risk of cataracts. The most likely case is that there is no association between statin use and cataracts. Because of the considerable benefits of statins in cardiovascular patients, this issue should not deter their use.

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Background Transesophageal echocardiography (TEE) has been considered the gold standard for left atrial appendage (LAA) thrombus detection. Nevertheless, TEE may sometimes induce discomfort and cause complications. Cardiac computed tomography has been studied extensively for LAA thrombus detection. We performed this systemic review and meta‐analysis to assess the diagnostic accuracy of cardiac computed tomography for LAA thrombus detection compared with TEE. Methods and Results A systemic search was conducted in the PubMed, Embase, and Cochrane Library databases from January 1977 to February 2021. Studies performed for assessment diagnostic accuracy of cardiac computed tomography on LAA thrombus compared with TEE were included. Summary sensitivity, specificity, and posterior probability of LAA thrombus was calculated by using bivariate random‐effects model. The Quality Assessment of Diagnostic Accuracy Studies‐2 tool was used for the quality assessment. A total of 27 studies involving 6960 patients were included in our study. The summary sensitivity of early imaging studies was 0.95 (95% CI, 0.79–0.99), and the specificity was 0.89 (95% CI, 0.85–0.92). The positive posterior probability was 19.11%, and the negative posterior probability was 0.16%. The summary sensitivity of delayed imaging studies was 0.98 (95% CI, 0.92–1.00), and the specificity was 1.00 (95% CI, 0.98–1.00). The positive posterior probability was 95.76%, and the negative posterior probability was 0.12%. The delayed imaging method significantly improved the specificity (1.00 versus 0.89; P <0.05) and positive posterior probability (95.76% versus 19.11%; P <0.05). Conclusions Cardiac computed tomography with a delayed imaging is a reliable alternative to TEE. It may save the patient and health care from an excess TEE. Registration URL: https://www.crd.york.ac.uk/PROSPERO ; Unique identifier: CRD42021236352.

Late sodium current (I) is a small sustained inward current observed during the cardiac action potential plateau phase following decay of the early peak I. The endogenous I is relatively small in normal hearts but exerts functionally significant effects on cardiomyocyte repolarization with potentially pro-arrhythmic effects in hearts with reduced repolarization reserve. Enhanced I occurs in long QT syndrome 3 (LQTS 3) patients, and under a number of pathological and pharmacological cardiovascular conditions, including bradycardia, myocardial ischemia, reperfusion injury, and heart failure. It may there play important roles in arrhythmogenesis and mechanical dysfunction. Experimental and clinical research suggests that I inhibition may prevent and treat cardiac arrhythmias and improve ventricular pump function. Selective I inhibitors, exemplified by ranolazine, GS-967 and GS-458967 have little or no effect on peak sodium current and/or I, and carry no or minimal pro-arrhythmic risk compared to those associated with administration of classical class I or III antiarrhythmic drugs, particularly in patients with ischemic heart disease. This increased understanding of I may be encouraging to clinicians in use of I inhibitors to treat cardiac arrhythmias and mechanical dysfunction directly associated with enhanced I such as LQTS type 3, and myocardial ischemia. This review discusses the roles of endogenous and enhanced I in arrhythmogenesis and mechanical dysfunction, and the basic and clinical research of I inhibitors.

HUA inhibits endothelial cell migration via miR-663, which regulates PTEN by targeting TGF-β1.

Cardiac arrhythmias associated with intracellular calcium inhomeostasis are refractory to antiarrhythmic therapy. We hypothesized that late sodium current (I Na) contributed to the calcium-related arrhythmias. Monophasic action potential duration at 90% completion of repolarization (MAPD90) was significantly increased and ventricular arrhythmias were observed in hearts with increased intracellular calcium concentration ([Ca2+]i) by using Bay K 8644, and the increase became greater in hearts treated with a combination of ATX-II and Bay K 8644 compared to Bay K 8644 alone. The prolongations caused by Bay K 8644 and frequent episodes of ventricular tachycardias, both in absence and presence of ATX-II, were significantly attenuated or abolished by late I Na inhibitors TTX and eleclazine. In rabbit ventricular myocytes, Bay K 8644 increased I CaL density, calcium transient and myocyte contraction. TTX and eleclazine decreased the amplitude of late I Na, the reverse use dependence of MAPD90 at slower heart rate, and attenuated the increase of intracellular calcium transient and myocyte contraction. TTX diminished the phosphorylation of CaMKII-δ and Nav 1.5 in hearts treated with Bay K 8644 and ATX-II. In conclusion, late I Na contributes to ventricular arrhythmias and its inhibition is plausible to treat arrhythmias in hearts with increased [Ca2+]i

Background/Aims: Reports have suggested that the traditional Chinese medicine Smilacis Glabrae Rhizoma attenuates hyperuricemia, but its mechanism is unclear. Our previous study demonstrated that uric acid could induce the generation of reactive oxygen species(ROS), which subsequently cause endothelial dysfunction. Therefore, we focused on the oxidative stress process. In this study, we would use LC-MS and bioinformatic analysis to investigate the underlying mechanism. Methods: We utilized LC-MS to reveal the differential protein expression in the kidneys of rats in the hyperuricemia group and the Smilacis Glabrae Rhizoma treatment group and then subjected the differentially expressed proteins to bioinformatic analysis. We also determined the serum ROS level of the two groups. According the above results, we built our hypothesis and performed in vitro experiments to validate this hypothesis. Results: We found that catalase was upregulated in the group treated with Smilacis Glabrae Rhizoma, and the level of reactive oxygen species was higher in the hyperuricemia group. Thus, we speculated that Smilacis Glabrae Rhizoma could alleviate oxidative stress by upregulating catalase. In vitro experiments, we found that high concentrations of uric acid reduced catalase expression in endothelial cells, which was alleviated by Smilacis Glabrae Rhizoma and resulted in a reduction of reactive oxygen species. Knockdown of catalase led to an increase in reactive oxygen species. Conclusion: We demonstrated that Smilacis Glabrae Rhizoma could alleviate the oxidative stress caused by hyperuricemia by upregulating catalase expression. This finding could represent a new application for Smilacis Glabrae Rhizoma in the treatment of hyperuricemia.