Beta-blocker and calcium-channel blocker therapy in patients with cardiovascular pathologies during post-COVID period

С начала 2020 г. в мире распространилась инфекция, вызванная вирусом SARS-CoV-2, что в дальнейшем привело к пандемии COVID-19. Долгое время вопросы ведения пациентов с новой коронавирусной инфекцией в остром периоде рассматривались как первоочередные. По мере накопления клинического опыта и данных о возбудителе новой коронавирусной инфекции стало очевидно, что проблема последствий перенесенного COVID-19 и ведения пациентов на постгоспитальном этапе является такой же важной. В силу прямой и опосредованной кардиотоксичности вируса SARS-CoV-2 особую группу риска на всех этапах составляют пациенты с сердечно-сосудистыми заболеваниями. Поэтому одной из важных задач мирового медицинского сообщества стала разработка способов улучшения качества и прогноза жизни пациентов с сердечно-сосудистыми заболеваниями в постковидном периоде. В статье сделан обзор наиболее крупных исследований, включая данные регистра «Анализ динамики коморбидных заболеваний пациентов, перенесших инфицирование SARS-CoV-2 (AКТИВ SARS-CoV-2)», по вопросу медикаментозной терапии пациентов с сердечно-сосудистыми заболеваниями с акцентом на бета-адреноблокаторы и блокаторы кальциевых каналов. В представленных работах терапия бета-адреноблокаторами продемонстрировала благоприятное влияние на тяжесть течения новой коронавирусной инфекции у пациентов с сердечно-сосудистыми заболеваниями, снижение смертности на госпитальном и в отдаленном постгоспитальном периодах. Данные по применению блокаторов кальциевых каналов изучены в меньшей степени, но можно отметить, что данная группа препаратов является одной из самых часто назначаемых в терапии пациентов с сохранением стойких жалоб на повышение артериального давления на постгоспитальном этапе. Требуется дальнейшее изучение влияния отдельных классов антигипертензивных препаратов на прогноз пациентов с сердечно-сосудистыми заболеваниями и COVID-19. Early in 2020, the infection caused by SARS-CoV-2 emerged and caused the COVID-19 pandemic. For a long time, management of patients with the acute novel coronavirus infection was of primary importance. With accumulation of clinical information and data on the causative agents of novel coronavirus infection it became obvious that the COVID-19 consequences and post-hospital follow-up of patients are important as well. Due to the direct and mediated cardiac toxicity of SARS-CoV-2 virus, cardiovascular patients are at high risk at any stage of the disease. Therefore, one of the priorities for healthcare professionals is development of the ways to improve the quality and prognosis of life for cardiovascular patients in the post-COVID period. The article discusses large-scale studies including the data from the International Register «Analysis of Chronic Non-infectious Diseases Dynamics After COVID-19 Infection in Adult Patients» (AСTIV-SARS-CoV-2), as regards drug therapy of cardiovascular patients with a focus on beta-blockers and calcium-channel blockers. In mentioned publications, beta-blocker therapy demonstrated favourable impact on the novel coronavirus infection severity in cardiovascular patients, reduction in mortality rates during the hospital and post-hospital periods. Data on the use of calcium-channel blockers have been studied to a lesser extent; however, calcium-channel blockers are thought to be one of the most commonly prescribed groups in the therapy of patients with persistent complaints of high blood pressure at the post-hospital period. A study of the impact of some categories of antihypertensives on the outcome for cardiovascular patients with COVID-19 is warranted.

Effect of angiotensin II receptor blocker therapy on markers of fibrosis and immune inflammation in hypertensive patients with chronic kidney disease after ischemic stroke

Aim. To compare the effect of angiotensin II receptor blocker therapy (azilsartan, telmisartan) on fibrosis and immune inflammation markers in hypertensive patients with chronic kidney disease (CKD) after ischemic stroke (IS).Material and methods. The study included 76 hypertensive patients aged 60-74 years (mean age, 66±5 years) with CKD after IS. Patients were randomly divided into following pharmacotherapy groups: 38 patients — telmisartan group; 36 patients — azilsartan group. The control group consisted of 20 hypertensive people (mean age, 63±2 years) without a history of CKD and IS. The levels of matrix metalloproteinase 9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) were determined by enzyme-linked immunosorbent assay (ELISA Kit, USA). The levels of interleukin-1β (IL-1β), tumor necrosis factor α (TNF-α), interferon γ (INF-γ), monocytic chemoattractant protein 1 (MCP-1) were assessed using Vector-Best kit (Russia).Results. Six-month azilsartan therapy led to a decrease in the levels of MMP-9 by 19,9% (p<0,01), TIMP-1 by 7,5% (p<0,05), IL-1β by 7,8%, TNF-α by 13,5%, INF-γ by 7,1%, MCP-1 by 13% (p<0,05). Telmisartan therapy was associated with a decrease in the levels of MMP-9 by 39,1% (p<0,01), TIMP-1 by 16,4%, IL-1β by 10,1% (p<0,05), TNF-α by 20,8% (p<0,01), INF-γ by 14,6% (p<0,05), MCP-1 by 21,3% (p<0,01). Intergroup comparison revealed more pronounced changes in the levels of MMP-9 by 19,2% (p<0,01), TIMP-1 by 7,2% (p<0,05), TNF-α by 7,3% (p<0,05), INF-γ by 7,5% (p<0,05), and MCP-1 by 8,3% (p<0,05) when using telmisartan compared to azilsartan. When using telmisartan, the increase in glomerular filtration rate (GFR) was 14,2% (p<0,05) higher compared to azilsartan.Conclusion. Six-month telmisartan therapy in hypertensive patients with CKD after stroke was accompanied by a more pronounced decrease in markers of myocardial fibrosis (MMP-9, TIMP-1) and immune inflammation (TNF-α, INF-γ, MCP-1) compared with azilsartan, as well as with more pronounced improvement in renal function.

Respiratory Muscle Weakness in Thyrotoxic Periodic Palsy: A Lesson to Remember

Thyrotoxic periodic palsy (TPP) is a sporadic form of hypokalemic periodic palsy that may occur in association with hyperthyroidism mostly with Graves’ disease. Acute thyrotoxic periodic palsy is a disorder most commonly seen in Asian men and characterized by abrupt onset of hypokalemia and paralysis. The disorder primarily affects the lower extremities and can involve all four limbs and presents as acute flaccid paralysis. The diagnosis of thyrotoxic periodic palsy is not difficult, but the disease's low incidence and many differentials for acute flaccid paralysis delay and complicate the diagnosis. TPP is not related to the etiology, severity, and duration of thyrotoxicosis. The treatment is similar to hypokalemic periodic palsy with potassium supplementation and initiation of antithyroid drugs and beta-blocker therapy. Here a similar case of quadriparesis is reported, which got precipitated after abrupt cessation of carbimazole in a young male. This initially was thought to be a case of hypokalemic periodic palsy and was later diagnosed to be TPP and recovered after initiating antithyroid drugs and potassium supplementation.

Digoxin vs. beta-blocker therapy in atrial fibrillation: analysis from the ESC-EHRA EORP Atrial Fibrillation General Long-Term (AFGen LT) Registry

Background There is a long-standing and unresolved controversy over the effects of digoxin on mortality. Furthermore, there is scarce evidence comparing the use of digoxin to beta-blocker in the general population with atrial fibrillation (AF). In this study, we aimed to evaluate the effects of digoxin over beta-blocker therapy among patients with AF. Methods Patients from the EORP-AF General Long-Term Registry with AF who were treated with either digoxin or beta-blocker were included. All patients were over 18 years old and had documented evidence of AF within 12 months prior to enrolment. The outcomes of interest were all-cause mortality, cardiovascular (CV) mortality, non-CV mortality and number of patients with unplanned hospitalisation (total and AF-related). These were recorded until the last known follow-up available. Results Of 6377 patients, 549 (8.6%) and 5828 (91.4%) were treated with digoxin and beta-blockers, respectively. Patients in the digoxin group were older (73 vs. 71 years, p&lt;0.001) with reduced renal function (eGFR 65.4 vs. 68.7 mL/min/1.73m2, p=0.002), and had (in general) greater burden of comorbidities in terms of chronic kidney disease, chronic obstructive pulmonary disease, heart failure, hypertension and peripheral artery disease. Nonetheless, the use of anticoagulation therapy was comparable between both groups (p=0.112). Over 24 months follow-up, there were 550 (8.6%) all-cause mortality and 1304 (23.6%) patients with unplanned emergency hospitalisation. Digoxin use was associated with increased all-cause mortality (hazard ratio [HR] 1.90 [95% CI, 1.48–2.44]), both from CV and non-CV causes (CV: HR 2.21 [95% CI, 1.49–3.26]); non-CV: HR 1.70 [95% CI, 1.04–2.79]). There was no statistical difference in terms of unplanned emergency hospitalisation (HR 0.99 [95% CI, 0.80–1.21]) and AF-related hospitalisation (HR 0.78 [95% CI, 0.58–1.06]) between both groups. Using multivariable cox regression analysis, digoxin compared to beta-blocker therapy was independently linked to increased all-cause mortality (HR 1.52 [95% CI, 1.11–2.09]) and CV mortality (HR 1.82 [95% CI, 1.11–2.97]), but was not related to non-CV mortality (HR 1.31 [95% CI, 0.71–2.41]), emergency hospitalisation (HR 0.91 [95% CI, 0.71–1.16]) or AF-related hospitalisation (HR 0.88 [95% CI, 0.62–1.24]), after adjustment for known risk factors. Conclusion We demonstrated that the use of digoxin was independently associated with excess all-cause mortality, driven by CV death, but was non-inferior to beta-blocker in terms of preventing unplanned emergency or AF-related hospitalisation, after accounting for important risk factors. FUNDunding Acknowledgement Type of funding sources: None.