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1.
Clin Drug Investig ; 42(9): 763-774, 2022 Sep.
Article in English | MEDLINE | ID: covidwho-1990812

ABSTRACT

BACKGROUND AND OBJECTIVES: Remdesivir is an antiviral drug used to treat coronavirus disease 2019 (COVID-19) with a relatively obscure cardiac effect profile. Previous studies have reported bradycardia associated with remdesivir, but few have examined its clinical characteristics. The objective of this study was to investigate remdesivir associated bradycardia and its associated clinical characteristics and outcomes. METHODS: This is a single-institution retrospective study that investigated bradycardia in 600 patients who received remdesivir for treatment of COVID-19. A total of 375 patients were included in the study after screening for other known causes of bradycardia (atrioventricular [AV] nodal blockers). All patients were analyzed for episodes of bradycardia from when remdesivir was initiated up to 5 days after completion, a time frame based on the drug's putative elimination half-life. Univariate and multivariate statistical tests were conducted to analyze the data. RESULTS: The mean age of the sample was 56.63 ± 13.23 years. Of patients who met inclusion criteria, 49% were found to have bradycardia within 5 days of remdesivir administration. Compared to the cohort without a documented bradycardic episode, patients with bradycardia were significantly more likely to experience inpatient mortality (22% vs 12%, p = 0.01). The patients with bradycardia were found to have marginally higher serum D-dimer levels (5.2 vs 3.4 µg/mL, p = 0.05) and were more likely to undergo endotracheal intubation (28% vs 14%, p = 0.008). Male sex, hyperlipidemia, and bradycardia within 5 days of completing remdesivir were significant predictors of inpatient mortality. No significant differences in length of stay were found. CONCLUSIONS: Bradycardia that occurs during or shortly after remdesivir treatment in COVID-19 patients may be associated with an increased rate of in-hospital mortality. However, COVID-19 and its cardiac complications cannot be excluded as potential contributors of bradycardia in the present study. Future studies are needed to further delineate the cardiac characteristics of COVID-19 and remdesivir.


Subject(s)
COVID-19 Drug Treatment , Adenosine Monophosphate/analogs & derivatives , Adult , Aged , Alanine/adverse effects , Alanine/analogs & derivatives , Antiviral Agents/adverse effects , Bradycardia/chemically induced , Bradycardia/drug therapy , Bradycardia/epidemiology , Humans , Male , Middle Aged , Retrospective Studies , SARS-CoV-2
3.
Case Rep Cardiol ; 2022: 9943937, 2022.
Article in English | MEDLINE | ID: covidwho-1816872

ABSTRACT

Background. Currently, the literature regarding the management of COVID-19 induced cardiomyopathy with reduced ejection fraction is limited. In this case report, we present the first documented case of COVID-19 induced myocardial stunning leading to severely reduced LV systolic function that was reversed by the administration of corticosteroids and tocilizumab. Case Summary. A 39-year-old female with well controlled systemic hypertension, tested positive for SARS-CoV-2 RNA and underwent self-isolation for 14 days. Patient presented to our facility a month later with one-week history of progressively worsening generalized body aches, chills, fever, watery diarrhea, nausea with associated mild dry nonproductive cough, shortness of breath and nonspecific chest pain. Initial labs demonstrated that she was COVID-19 positive, elevated troponin (4.295 ng/ml), and elevated BNP (2,291 pg/ml). Her initial Transthoracic echocardiography demonstrated an Left ventricular ejection fraction (LVEF) of 20-25% with apical akinesis. After administration of tocilizumab and corticosteroids, patient demonstrated interval improvement with LVEF improving to 50-55% within days. Her labs confirmed these findings with improved troponin (0.858 ng/ml) and BNP (209 pg/ml). Discussion. This case demonstrates that it can be safe and efficacious to use tocilizumab and corticosteroids in patients with COVID-19 induced cardiomyopathy. These finding suggest that cytokine storm is the predominant mechanism by which COVID-19 induced cardiomyopathy occurs. Additional studies are required to determine the role of corticosteroids and tocilizumab in management of this condition.

4.
Case Rep Cardiol ; 2022: 9371818, 2022.
Article in English | MEDLINE | ID: covidwho-1770051

ABSTRACT

Background. Coronavirus 2019 (COVID-19) was initially identified approximately in December 2019 at Wuhan, China, as patients presented with vague prodromal and respiratory symptoms. With the developing investigation of its clinical manifestation, cardiac symptoms have been widely reported including acute coronary syndromes, myocarditis, arrhythmias, heart failure, and cardiac arrest. Case Summary. An 84 year-old male with history of coronary artery disease, hypertension, and hyperlipidemia presented to an outside urgent care with prodromal symptoms. The patient had received the second Pfizer vaccine three months prior. This presentation, he was found to be COVID-19 positive as well as bradycardic with a complete AV block. He was transferred to a tertiary center for further evaluation and management. However, after transfer, the patient refused further invasive cardiac interventions and after medical therapy was discharged home in complete AV block. Discussion. We report a novel case of a Pfizer-vaccinated patient whose initial presenting symptoms of COVID-19 included a complete AV block as well as the challenges and difficulties in approaching such patients. Although this patient's etiology of his complete AV block may result from multiple factors, given the acuity in setting of concurrent COVID-19 infections, top differentials include viral myocarditis, COVID-19-induced Takotsubo cardiomyopathy complicated by a complete AV-block, or a direct conduction pathway infection. Management of patients should focus on a multidisciplinary approach, and prevention is critical via vaccination.

5.
Journal of the American College of Cardiology (JACC) ; 79(9):2946-2946, 2022.
Article in English | Academic Search Complete | ID: covidwho-1751489
6.
Journal of the American College of Cardiology (JACC) ; 79(9):2373-2373, 2022.
Article in English | Academic Search Complete | ID: covidwho-1751451
8.
Eur Heart J Case Rep ; 5(6): ytab217, 2021 Jun.
Article in English | MEDLINE | ID: covidwho-1286559

ABSTRACT

BACKGROUND: Heart transplant recipients represent a particularly vulnerable patient population to the novel coronavirus disease 2019 (COVID-19) due to chronic immunosuppression and high rates of comorbidities. Currently, data are limited and evidence to guide management of heart transplant recipients with COVID-19 is sparse. In this case report, we provide a summary of the current literature as well as an in-depth analysis of our clinical decision-making. CASE SUMMARY: A 67-year-old female who underwent cardiac transplantation 1 year prior was found to have acute hypoxic respiratory failure due to COVID-19. Her immunosuppressant medications were modulated with discontinuation of mycophenolate and titration of tacrolimus troughs with a goal of 6-10 ng/dL. She was administered supportive treatment including convalescent plasma, remdesivir, and dexamethasone, in addition to antibiotic treatment that resulted in resolution of her symptoms within a matter of days despite her precarious disposition. DISCUSSION: This case demonstrates that it can be safe and efficacious to modulate immunosuppressant medications in cardiac transplant recipients in accordance with recommendations made by the International Society of Heart and Lung Transplantation. This case additionally demonstrates that aspects of the current literature regarding the management of COVID-19 can be safely extrapolated to cardiac transplant recipients. Providing supportive care with dexamethasone, remdesivir, and convalescent plasma as indicated can be beneficial in cardiac transplant recipients; although, the current literature regarding convalescent plasma and remdesivir is conflicting.

9.
Journal of the American College of Cardiology ; 77(18, Supplement 1):2028, 2021.
Article in English | ScienceDirect | ID: covidwho-1213661
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