Background Microvascular dysfunction, serum cytokines and chemokines may play important roles in pathophysiology of coronavirus disease 2019 (COVID-19), especially in severe cases. Methods Patients with COVID-19 underwent non-invasive evaluation of systemic endothelium-dependent microvascular reactivity - using laser Doppler perfusion monitoring in the skin of the forearm - coupled to local thermal hyperemia. Maximal microvascular vasodilatation (44° C thermal plateau phase) was used as endpoint. A multiplex biometric immunoassay was used to assess a panel of 48 serum cytokines and chemokines. Severe COVID-19 (S-COVID) was defined according to WHO criteria, while all other cases of COVID-19 were considered mild to moderate (M-COVID). A group of healthy individuals who tested negative for SARS-CoV-2 served as a control group and was also evaluated with LDPM. Results Thirty-two patients with COVID-19 (25% S-COVID) and 14 controls were included. Basal microvascular flow was similar between M-COVID and controls (P=0.69) but was higher in S-COVID than in controls (P=0.005) and M-COVID patients (P=0.01). The peak microvascular vasodilator response was markedly decreased in both patient groups (M-COVID, P=0.001; S-COVID, P<0.0001) compared to the healthy group. The percent increases in microvascular flow were markedly reduced in both patient groups (M-COVID, P<0.0001; S-COVID, P<0.0001) compared to controls. Patients with S-COVID had markedly higher concentrations of dissimilar proinflammatory cytokines and chemokines, compared to patients with M-COVID. Conclusions In patients with COVID-19, especially with S-COVID, endothelium-dependent microvascular vasodilator responses are reduced, while serum cytokines and chemokines involved in the regulation of vascular function and inflammation are increased.

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BackgroundCoronary computed tomography angiography (CCTA) allows for noninvasive coronary artery disease (CAD) phenotyping. Factors related to CAD progression are epidemiologically valuable.ObjectiveTo identify factors associated with CAD progression in patients undergoing sequential CCTA testing.MethodsWe retrospectively analyzed 384 consecutive patients who had at least two CCTA studies between December 2005 and March 2013. Due to limitations in the quantification of CAD progression, we excluded patients who had undergone surgical revascularization previously or percutaneous coronary intervention (PCI) between studies. CAD progression was defined as any increase in the adapted segment stenosis score (calculated using the number of diseased segments and stenosis severity) in all coronary segments without stent (in-stent restenosis was excluded from the analysis). Stepwise logistic regression was used to assess variables associated with CAD progression.ResultsFrom a final population of 234 patients, a total of 117 (50%) had CAD progression. In a model accounting for major CAD risk factors and other baseline characteristics, only age (odds ratio [OR] 1.04, 95% confidence interval [95%CI] 1.01-1.07), interstudy interval (OR 1.03, 95%CI 1.01-1.04), and past PCI (OR 3.66, 95%CI 1.77-7.55) showed an independent relationship with CAD progression.ConclusionsA history of PCI with stent placement was independently associated with a 3.7-fold increase in the odds of CAD progression, excluding in-stent restenosis. Age and interstudy interval were also independent predictors of progression.

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Introdução A doença cardiovascular está associada a COVID-19 grave. Nosso objetivo foi descrever características clínicas e laboratoriais (incluindo eletrocardiográficas e ecocardiográficas) e desfechos de pacientes com doença cardíaca hospitalizados com COVID-19, laboratorialmente confirmada através de RT-PCR de teste swab nasofaríngeo internados em instituto de referencia para cirurgia cardíaca. Métodos Trata-se de um estudo observacional retrospectivo de pacientes adultos consecutivos internados, entre março e setembro de 2020, com infecção confirmada por SARS-CoV-2. Os dados foram coletados de acordo com o formulário de relato de caso ISARIC e complementados com variáveis relacionadas às cardiopatias. Resultados Foram incluídos 121 pacientes cuja média de idade foi 60 ± 15,2 anos; 80/121 (66,1%) eram do sexo masculino. Dois terços dos pacientes (80/121, 66,1%) apresentavam COVID-19 no momento da admissão hospitalar e COVID-19 foi o motivo da internação em 42 (34,7%). Outros motivos de internação foram síndrome coronariana aguda (26%) e insuficiência cardíaca descompensada (14,8%). Doenças cardíacas crônicas foram encontradas em 106/121 (87,6%), principalmente doença arterial coronariana (62%) ou doença valvar (33,9%). Ecocardiograma transtorácico foi realizado em 93/121 (76,8%) e aumento das câmaras cardíacas foram encontradas em 71% (66/93); ECG de admissão foi feito em 93 casos (93/121, 76,8%) e 89,2% (83/93) estavam alterados. A aquisição hospitalar de COVID-19 ocorreu em 20 (16,5%) dos pacientes e a mortalidade nesse grupo foi de 50%, enquanto a mortalidade nos demais foi de 18,8%(p = 0,003). Na análise bivariada para mortalidade de todo o grupo, os níveis de BNP e os níveis de troponina NÃO foram associados à mortalidade. Na análise multivariada, apenas os níveis de proteína C reativa e creatinina foram associados de modo significativo à mortalidade. Conclusões O COVID-19 impactou o perfil das admissões hospitalares em pacientes cardíacos. Os níveis de BNP e troponina não foram associados à mortalidade e podem não ser bons discriminadores de prognóstico em cardiopatas.