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2.
J Appl Physiol (1985) ; 131(3): 1136-1137, 2021 09 01.
Article in English | MEDLINE | ID: covidwho-1438133
4.
EXCLI J ; 20: 252-275, 2021.
Article in English | MEDLINE | ID: covidwho-1102721

ABSTRACT

New coronavirus SARS-CoV-2 (COVID-19) has caused chaos in health care systems. Clinical manifestations of COVID-19 are variable, with a complex pathophysiology and as yet no specific treatment. It has been suggested that the renin-angiotensin-aldosterone system has a possible role in the severity of cases and the number of deaths. Our hypothesis is that drugs with inverse agonist effects to the angiotensin-1 receptor can be promising tools in the management of patients with COVID-19, possibly avoiding complications and the poor evolution in some cases. Any risk factors first need to be identified, and the most appropriate time to administer the drugs during the course of the infection also needs to be established. Several angiotensin receptor blockers (ARB) have a favorable profile and are important candidates for the treatment of COVID-19. In this review we discussed a set of compounds with favorable profile for COVID-19 treatment, including azilsartan, candesartan, eprosartan, EXP3174, olmesartan, telmisartan, and valsartan. They are effective as inverse agonists and could reduce the "cytokine storm" and reducing oxidative stress. As COVID-19 disease has several evolution patterns, the effectiveness of ARB therapy would be related to infection "timing", patient risk factors, previous use of ARBs, and the specific molecular effects of an ARB. However, controlled studies are needed to identify whether ARBs are beneficial in the treatment of patients with COVID-19.

5.
Arq Bras Cardiol ; 115(2): 273-277, 2020 Aug 28.
Article in Portuguese, English | MEDLINE | ID: covidwho-910595

ABSTRACT

BACKGROUND: SARS-CoV-2 is an emerging RNA virus associated with a severe acute respiratory disease known as COVID-19. Although COVID-19 is predominantly a pulmonary disease, some patients have severe cardiovascular damage. We performed a quantitative evidence synthesis of clinical data, myocardial injury biomarkers, and cardiac complications associated with in-hospital death in patients with COVID-19. METHODS: We searched the databases PubMed, Embase, and Google Scholar to identify studies comparing clinical data, myocardial injury biomarkers, and cardiac complications between non-survivors and survivors of COVID-19. Effect sizes were reported as mean difference or standardized mean difference for continuous variables and risk ratio for dichotomous variables with 95% confidence intervals. A random effects model was used to pool the results. RESULTS: Six retrospective studies reporting data from 1,141 patients (832 survivors and 309 non-survivors) were included. We found that underlying cardiovascular conditions; elevation of high-sensitivity cardiac troponin I, N-terminal pro-B-type natriuretic peptide, and creatine kinase-MB; and cardiac complications were associated with increased risk of death for patients with SARS-CoV-2 infection. CONCLUSIONS: The confirmation that underlying cardiovascular conditions, elevation of myocardial injury biomarkers during COVID-19 infection, and acute cardiovascular decompensation are predictors for mortality in SARS-CoV-2 infection must encourage new research to clarify potential mechanisms and test appropriate treatments. (Arq Bras Cardiol. 2020; 115(2):273-277).


FUNDAMENTO: O SARS-CoV-2 é um vírus de RNA emergente associado à doença respiratória aguda grave conhecida como COVID-19. Embora a COVID-19 seja predominantemente uma doença pulmonar, alguns pacientes apresentam graves danos cardiovasculares. Realizamos uma síntese de evidências quantitativas de dados clínicos, biomarcadores de lesão miocárdica e complicações cardíacas associadas ao óbito hospitalar em pacientes com COVID-19. MÉTODOS: Buscamos nas bases de dados PubMed, Embase e Google Scholar para identificar estudos que comparassem dados clínicos, biomarcadores de lesão miocárdica e complicações cardíacas entre pacientes sobreviventes e não sobreviventes da COVID-19. Os tamanhos dos efeitos foram apresentados como diferença média ou diferença média padronizada para variáveis contínuas e razão de risco para variáveis dicotômicas, com intervalos de confiança de 95%. Foi utilizado um modelo de efeitos aleatórios para agrupar os resultados. RESULTADOS: Foram incluídos seis estudos retrospectivos que relataram dados de 1.141 pacientes (832 sobreviventes e 309 não sobreviventes). Verificamos que condições cardiovasculares subjacentes; elevação de troponina cardíaca I de alta sensibilidade; N-terminal do pró-hormônio do peptídeo natriurético do tipo B e creatina quinase-MB; e complicações cardíacas foram associadas ao aumento do risco de óbito em pacientes com infecção por SARS-CoV-2. CONCLUSÕES: A confirmação de que condições cardiovasculares subjacentes, elevação de biomarcadores de lesão miocárdica durante a infecção por COVID-19 e descompensação cardiovascular aguda são preditores de mortalidade na infecção por SARS-CoV-2 deve incentivar novas pesquisas para esclarecer possíveis mecanismos e testar tratamentos adequados. (Arq Bras Cardiol. 2020; 115(2):273-277).


Subject(s)
Cardiovascular Diseases/mortality , Cardiovascular Diseases/virology , Coronavirus Infections/complications , Coronavirus Infections/mortality , Pneumonia, Viral/complications , Pneumonia, Viral/mortality , Betacoronavirus , Biomarkers/blood , COVID-19 , Humans , Myocardium/pathology , Pandemics , Retrospective Studies , SARS-CoV-2
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