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Curr Probl Cardiol ; : 101870, 2023 Jun 09.
Article in English | MEDLINE | ID: covidwho-20239221

ABSTRACT

BACKGROUND: COVID-19 pandemic hampered operational efficiency of heart transplant (HT) programs worldwide. Little is known about the global and country-specific changes in HT volumes during the pandemic years 2020-2021. We aimed to describe the global and country-level impact of the COVID-19 pandemic on HT volumes in 2020-2021. METHODS: This is a cross-sectional study of the Global Observatory on Donation and Transplantation, including the years 2019 to 2021. Among 60 countries that reported HT data in the years 2019-2020, we analyzed 52 countries with ≥1 transplant during each year. RESULTS: Overall, the number of HTs decreased during 2020 by 9.3% (1.82 to 1.65 PMP). While 75% (n=39/52) of countries experienced a decrease in HT volumes in 2020, volumes were maintained/increased in the remaining countries. Countries with maintained HT volumes had a higher organ donation rate in 2020 compared to those with decreased volumes (P=.03), the only significant predictor of change in HT volumes (P=.005). In 2021, a 6.6% recovery from the previous year's drop in global HT rate was noticed, reaching 1.76 HT PMP. Only one in five countries with reduced volumes in 2020 recovered their baseline volumes in 2021. Only 30.8% of countries with maintained volumes in 2020 had continued growth in HT volumes in 2021. CONCLUSION: Further work should define underlying causes of this heterogeneity in HT volume during the pandemic. Identifying policies and practices that helped certain countries mitigate the effect of the pandemic on HT activities may help other countries during similar health crises in the future.

3.
Biomed Pharmacother ; 146: 112518, 2022 Feb.
Article in English | MEDLINE | ID: covidwho-1562447

ABSTRACT

SARS-CoV-2 causes respiratory illness with a spectrum of systemic complications. However, the mechanism for cardiac infection and cardiomyocyte injury in COVID-19 patients remains unclear. The current literature supports the notion that SARS-CoV-2 particles access the heart either by the circulating blood cells or by extracellular vesicles, originating from the inflamed lungs, and encapsulating the virus along with its receptor (ACE2). Both cardiomyocytes and pericytes (coronary arteries) express the necessary accessory proteins for access of SARS-CoV-2 particles (i.e. ACE2, NRP-1, TMPRSS2, CD147, integrin α5ß1, and CTSB/L). These proteins facilitate the SARS-CoV-2 interaction and entry into the pericytes and cardiomyocytes thus leading to cardiac manifestations. Subsequently, various signaling pathways are altered in the infected cardiomyocytes (i.e. increased ROS production, reduced contraction, impaired calcium homeostasis), causing cardiac dysfunction. The currently adopted pharmacotherapy in severe COVID-19 subjects exhibited side effects on the heart, often manifested by electrical abnormalities. Nonetheless, cardiovascular adverse repercussions have been associated with the advent of some of the SARS-CoV-2 vaccines with no clear mechanisms underlining these complications. We provide herein an overview of the pathways involved with cardiomyocyte in COVID-19 subjects to help promoting pharmacotherapies that can protect against SARS-CoV-2-induced cardiac injuries.


Subject(s)
COVID-19/metabolism , Heart Diseases/metabolism , Myocardium/metabolism , Myocytes, Cardiac/metabolism , SARS-CoV-2/metabolism , Animals , Antiviral Agents/administration & dosage , Antiviral Agents/metabolism , COVID-19/epidemiology , COVID-19 Vaccines/administration & dosage , COVID-19 Vaccines/metabolism , Heart Diseases/drug therapy , Heart Diseases/epidemiology , Humans , Myocytes, Cardiac/drug effects , SARS-CoV-2/drug effects , COVID-19 Drug Treatment
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