Impact of COVID-19 vaccination in post-COVID cardiac complications.

BACKGROUND: After the acute infection, COVID-19 can produce cardiac complications as well as long-COVID persistent symptoms. Although vaccination against COVID-19 represented a clear reduction in both mortality and ICU admissions, there is very little information on whether this was accompanied by a decrease in the prevalence of post-COVID cardiac complications. The aim of this study was to analyze the relationship between COVID-19 vaccination and the prevalence of post-COVID cardiac injury assessed by echocardiogram, and long-COVID persistent cardiac symptoms. METHODS: All patients who consulted for post-COVID evaluation 14 days after discharge from acute illness were included. Patients with heart disease were excluded. The relationship between complete vaccination scheme (at least two doses applied with 14 days or more since the last dose) and pathological echocardiographic findings, as well as the relationship of vaccination with persistent long-COVID symptoms, were evaluated by multivariate analysis, adjusting for age, sex and clinical variables that would have shown significant differences in univariate analysis. RESULTS: From 1883 patients, 1070 patients (56.8%) suffered acute COVID-19 without a complete vaccination scheme. Vaccination was associated with lower prevalence of cardiac injury (1.35% versus 4.11%, adjusted OR 0.33; 95% CI 0.17-0.65, p=0.01). In addition, vaccinated group had a lower prevalence of persistent long-COVID symptoms compared to unvaccinated patients (10.7% versus 18.3%, adjusted OR 0.52; 95% CI 0.40-0.69, p<0.001). CONCLUSION: Vaccination against COVID-19 was associated with lower post-COVID cardiac complications and symptoms, reinforcing the importance of fully vaccinating the population.

Rol del bloqueo aldosterónico en el tratamiento de la hipertensión arterial refractaria y estados de hiperaldosteronismo / Role of aldosterone blockade in the treatment of refractory arterial hypertension and hyperaldosteronism / Papel do bloqueio da aldosterona no tratamento da hipertensão arterial refratária e hiperaldosteronismo

El bloqueo de los efectos adversos del sistema renina-angiotensina-aldosterona (SRAA) ha sido un foco importante en el desarrollo de drogas para el tratamiento de la enfermedad cardiovascular en los últimos 30 años. Los niveles plasmáticos de aldosterona disminuyen en forma transitoria luego del inicio del tratamiento con inhibidores de la enzima convertidora de angiotensina (IECA) y se ha demostrado que la aldosterona ejerce efectos adversos sobre el sistema cardiovascular en forma independiente de la angiotensina II. En dos reuniones consecutivas 50 líderes de opinión se reunieron para discutir en forma crítica la evidencia actualmente disponible. El presente documento sintetiza las conclusiones que surgieron por consenso de la mesa: "Rol del bloqueo aldosterónico en el tratamiento de la hipertensión arterial refractaria y estados de hiperaldosteronismo". El interés clínico en el bloqueo aldosterónico en pacientes tratados con IECA o antagonistas de los receptores de angiotensina (ARA) fue estimulado por el Estudio RALES (Randomized Aldactone Evaluation Study), que demostró que el antagonista de los receptores mineralocorticoides (RMC), espironolactona, redujo el riesgo de mortalidad de toda causa así como de hospitalizaciones por insuficiencia cardíaca (IC), en pacientes con IC severa (clase funcional III-IV, NYHA) y fracción de eyección disminuida. La hipertensión arterial refractaria (HTAR) es un problema médico común que afecta entre el 10% al 30% de los pacientes hipertensos, según la población evaluada. Los estudios en HTAR se ven limitados por el alto riesgo cardiovascular de estos pacientes. El rol de la aldosterona en perpetuar la refractariedad a través de su conocido efecto de retención de sodio y agua y la producción de disfunción endotelial han motivado el uso de bloqueantes de receptores mineralocorticoides, demostrándose una drástica reducción de la presión arterial sistólica y diastólica, por lo que actualmente su empleo es recomendado como cuarta línea de tratamiento en pacientes con HTAR que no respondieron a una terapia adecuada previamente (Guía de la Sociedad Europea de Hipertensión/Sociedad Europea de Cardiología 2007).

Blocking the adverse effects of the rennin-angiotensin system has been a major focus of drug development for the treatment of cardiovascular disease over the last 30 years. Plasma aldosterone levels are only transiently decreased suppressed after the initiation of angiotensin-converting enzyme (ACE) inhibitors treatment and has been shown that aldosterone causes adverse effects on the cardiovascular system independent of angiotensin II. In two consecutive meetings, 50 experts critically reviewed the available evidence. The present document reflects the consensus of the subject: "Role of aldosterone blockade in the treatment of refractory arterial hypertension and hyperaldosteronism". Clinical interest in blocking aldosterone in patients treated with ACE inhibitors or angiotensin receptor blockers (ARBs) was stimulated by the Randomized Aldactone Evaluation Study (RALES), which demonstrated that the mineralocorticoid (MC) antagonist spironolactone reduced the risk of all-cause mortality as well as hospitalizations for heart failure (HF) in patients with severe NYHA Class III-IV HF and a reduced left ventricular ejection fraction (LVEF). The refractory arterial hypertension (RAH) is a common medical problem that affects from 10% to 30% of hypertensive patients, according to the study population. Studies in RAH are limited by the high cardiovascular risk of these patients. The role of aldosterone perpetuate refractoriness through its known effect of sodium and water retention and production of endothelial dysfunction have motivated the use of mineralocorticoid receptor blockers, demonstrating a dramatic reduction in the systolic and diastolic blood pressure, by what use is currently recommended as a fourth-line treatment in patients with RAH who did not respond to appropriate therapy previously (Guide to the European Society of Hypertension / European Society of Cardiology 2007).

O bloqueio dos efeitos adversos do sistema renina-angiotensina-aldosterona (SRAA) tem sido o foco principal no desenvolvimento de drogas para o tratamento de doença cardiovascular nos últimos 30 anos. Os níveis plasmáticos da aldosterona temporariamente diminuem depois de início do tratamento com inibidores da enzima conversora da angiotensina (IECA) e tem mostrado-se que a aldosterona ter efeitos adversos sobre o sistema cardiovascular independente da angiotensina II. Em duas reuniões consecutivas, 50 líderes de opinião se reuniram para discutir criticamente as evidências atuais. O presente documentoreflete o consensosobre o assunto: "Papel do bloqueio da aldosterona no tratamento da hipertensão arterial refratária e hiperaldosteronismo". Interesse clínico no bloqueio da aldosterona em pacientes tratados com IECA ou antagonistas do receptor de angiotensina (ARA) foi estimulado pelo estudo RALES (Randomized Aldactone Evaluation Study), que demonstrou que o antagonista receptor mineralocorticóide (RMC), espironolactona, reduziu o risco de mortalidade por qualquer causa e hospitalizações por insuficiência cardíaca (IC) em pacientes com IC severa (classe funcional III-IV, NYHA) e fração de ejeção diminuída. A hipertensão arterial refratária (HTAR) é um problema médico comum que afeta entre 10% a 30% dos pacientes hipertensos, de acordo com a população em estudo. Os estudos em HTAR são limitados pelo elevado risco cardiovascular desses pacientes. O papel da aldosterona em perpetuar a refratariedade através do seu efeito conhecido de retenção e produção de disfunção endotelial de sódio e água tem motivado o uso de bloqueadores dos receptores mineralocorticóides, demonstrando uma redução drástica na pressão arterial sistólica e diastólica, por o uso é atualmente recomendada como quarta linha de tratamento em pacientes com HTAR, que não respondem à terapia apropriada anteriormente (Guia da Sociedade Europeia de Hipertensão/Sociedade Europeia de Cardiologia 2007).