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1.
J Hypertens ; 39(8): 1726-1727, 2021 08 01.
Article in English | MEDLINE | ID: covidwho-2103104
2.
Eur Heart J Case Rep ; 5(7): ytab200, 2021 Jul.
Article in English | MEDLINE | ID: covidwho-1294713

ABSTRACT

BACKGROUND: Since the pandemic began in 2020, Remdesivir has been widely used for the treatment of coronavirus disease-2019 (COVID-19). Here, we describe a case of a patient with COVID-19 who developed transient complete atrioventricular (AV) block and bradycardia after initiating treatment with Remdesivir. CASE SUMMARY: A 72-year-old male with a history of atrial fibrillation and lung cancer was hospitalized for COVID-19. Electrocardiogram (ECG) on admission demonstrated atrial fibrillation and right bundle branch block. He was started on a course of Dexamethasone and Remdesivir. Within 24 h of starting Remdesivir, he was noted to be in atrial fibrillation with ventricular rates between 30 and 40 b.p.m. On Day 5 of Remdesivir therapy, ECG demonstrated complete AV block. Having completed the Remdesivir regimen, during the next 48 h, he was closely monitored, and the AV block resolved spontaneously. As he remained asymptomatic and had an adequate chronotropic response with activity, pacemaker implantation was not recommended. DISCUSSION: Despite the widespread use of Remdesivir, there is little known information about its cardiac toxicity. Daily ECGs and close cardiac surveillance of patients who develop severe bradycardia or AV block are essential. Discontinuation of the medication usually results in the resolution of these cardiac disturbances.

3.
Lung ; 199(3): 239-248, 2021 06.
Article in English | MEDLINE | ID: covidwho-1245631

ABSTRACT

BACKGROUND: To date, only dexamethasone has been shown to reduce mortality in coronavirus disease-19 (COVID-19) patients. Tocilizumab has been recently added to the treatment guidelines for hospitalized COVID-19 patients, but data remain conflicting. STUDY DESIGN AND METHODS: Electronic databases such as MEDLINE, EMBASE, and Cochrane central were searched from March 1, 2020, until March 10, 2021, for randomized controlled trials evaluating the efficacy of tocilizumab in hospitalized COVID-19 patients. The outcomes assessed were all-cause mortality, mechanical ventilation, and time to discharge. RESULTS: Nine studies (with 6490 patients) were included in the analysis. In total, 3358 patients received tocilizumab, and 3132 received standard care/placebo. Pooled analysis showed a significantly decreased risk of all-cause mortality (RR 0.89, 95% CI 0.80-0.98, p = 0.02) and progression to mechanical ventilation (RR 0.80, 95% CI 0.71-0.89, p < 0.0001) in the tocilizumab arm compared to standard therapy or placebo. In addition, there was a trend towards improved median time to hospital discharge (RR 1.28, 95% CI 1.12-1.45, p = 0.0002). CONCLUSIONS: Tocilizumab therapy improves outcomes of mortality and need for mechanical ventilation, in hospitalized patients with COVID-19 infection compared with standard therapy or placebo. Our findings suggest the efficacy of tocilizumab therapy in hospitalized COVID-19 patients and strengthen the concept that tocilizumab is a promising therapeutic intervention to improve mortality and morbidity in COVID-19 patients.


Subject(s)
Antibodies, Monoclonal, Humanized/pharmacology , COVID-19 , Receptors, Interleukin-6/antagonists & inhibitors , COVID-19/drug therapy , COVID-19/immunology , COVID-19/mortality , Humans , Immunologic Factors/pharmacology , Outcome Assessment, Health Care , SARS-CoV-2
4.
J Hypertens ; 39(4): 784-794, 2021 04 01.
Article in English | MEDLINE | ID: covidwho-1112117

ABSTRACT

AIMS: We sought to evaluate the association of angiotensin-converting-enzyme inhibitors (ACEI) or AT1 blockers (ARB) therapy with clinical outcomes in patients with coronavirus disease 2019 (COVID-19). METHODS AND RESULTS: Electronic databases were searched to identify published studies that reported clinical outcomes in patients with COVID-19 who were or were not taking an ACEI/ARB. We studied all-cause mortality and/or severe disease outcomes. Fully adjusted effect estimates from individual studies were pooled using a random-effects model. In total, 34 (31 cohort-based and three case-control) studies met our eligibility criteria. Due to the inherent differences between cohort and case-control studies, we did not combine results of these studies but used them to identify the consistency of their results. The 31 cohort studies provided outcome data for 87 951 patients with COVID-19, of whom 22 383/83 963 (26.7%) were on ACEI/ARB therapy. In pooled analysis, we found no association between the use of ACEI/ARB and all-cause mortality/severe disease [relative risk: 0.94, 95% confidence interval (CI): 0.86-1.03, I2 = 57%, P = 0.20] or occurrence of severe disease (relative risk: 0.93, 95% CI: 0.74-1.17, I2 = 56%, P = 0.55). Analysis of three population-based case-control studies identified no significant association between ACEI/ARB (pooled odds ratio: 1.00, 95% CI: 0.81-1.23, I2 = 0, P = 0.98) and all-cause mortality/severe disease. In 13 of the 31 cohort studies as well as in three case-control studies that reported outcomes separately for ACEI and ARB, there was no differential effect for mortality/severe disease outcomes. CONCLUSION: In patients with COVID-19, we found no association between ACEI/ARB treatment and mortality/severe disease. ACEI/ARB should not be discontinued, unless clinically indicated.


Subject(s)
Angiotensin Receptor Antagonists/therapeutic use , Angiotensin-Converting Enzyme Inhibitors/therapeutic use , COVID-19 , Observational Studies as Topic , Renin-Angiotensin System/drug effects , COVID-19/mortality , Case-Control Studies , Cohort Studies , Humans , SARS-CoV-2
5.
Prog Cardiovasc Dis ; 63(5): 682-689, 2020.
Article in English | MEDLINE | ID: covidwho-974476

ABSTRACT

The Coronavirus Disease 2019 (COVID-19) is now a global pandemic with millions affected and millions more at risk for contracting the infection. The COVID-19 virus, SARS-CoV-2, affects multiple organ systems, especially the lungs and heart. Elevation of cardiac biomarkers, particularly high-sensitivity troponin and/or creatine kinase MB, is common in patients with COVID-19 infection. In our review of clinical analyses, we found that in 26 studies including 11,685 patients, the weighted pooled prevalence of acute myocardial injury was 20% (ranged from 5% to 38% depending on the criteria used). The plausible mechanisms of myocardial injury include, 1) hyperinflammation and cytokine storm mediated through pathologic T-cells and monocytes leading to myocarditis, 2) respiratory failure and hypoxemia resulting in damage to cardiac myocytes, 3) down regulation of ACE2 expression and subsequent protective signaling pathways in cardiac myocytes, 4) hypercoagulability and development of coronary microvascular thrombosis, 5) diffuse endothelial injury and 'endotheliitis' in several organs including the heart, and, 6) inflammation and/or stress causing coronary plaque rupture or supply-demand mismatch leading to myocardial ischemia/infarction. Cardiac biomarkers can be used to aid in diagnosis as well as risk stratification. In patients with elevated hs-troponin, clinical context is important and myocarditis as well as stress induced cardiomyopathy should be considered in the differential, along with type I and type II myocardial infarction. Irrespective of etiology, patients with acute myocardial injury should be prioritized for treatment. Clinical decisions including interventions should be individualized and carefully tailored after thorough review of risks/benefits. Given the complex interplay of SARS-CoV-2 with the cardiovascular system, further investigation into potential mechanisms is needed to guide effective therapies. Randomized trials are urgently needed to investigate treatment modalities to reduce the incidence and mortality associated with COVID-19 related acute myocardial injury.


Subject(s)
COVID-19/virology , Heart Diseases/virology , Heart/virology , Hospitalization , SARS-CoV-2/pathogenicity , COVID-19/complications , COVID-19/diagnosis , Diagnosis, Differential , Heart/physiopathology , Heart Diseases/diagnosis , Heart Diseases/physiopathology , Heart Diseases/therapy , Host-Pathogen Interactions , Humans , Predictive Value of Tests , Prognosis , Risk Factors
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