SARS-Cov-2 and Associated Heart Failure: An Overview of the Possible Mechanisms

SARS-Cov-2 and Associated Heart Failure: An Overview of the Possible Mechanisms

Abdelmohcine Aimrane, Bilal El-Mansoury, Said Sabir, Soraia El Baz, Nadia Zouhairi, Mohamed Echchakery, Ahmed Draoui, Chatoui Hicham, Naima Fdil, Souad Sellami, Abdesslam Ferssiwi, Abdelali Bitar, Hanane Rais
Copyright: © 2022 |Pages: 17
DOI: 10.4018/978-1-7998-8225-1.ch010
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Abstract

The newly emerged pandemic of coronavirus-induced disease of the year 2019 (COVID-19) has become the utmost health concern worldwide. Patients with COVID-19 are highly susceptible to develop hypercoagulable state increasing the risk of causing venous and arterial thrombosis at both small and large vessels. Additionally, in patients showing co-morbidities, for instance patients with inborn errors of metabolism linked to heart failure, the complications and mortalities are even higher than in any other case. In such frail patients already showing health concerns, the COVID-19-induced pneumonia may cause acute or chronic cardiovascular complications. Indeed, several reports of thrombotic complications in association with other complications has been presented, such as large vessels storks, clotting of catheters, and myocardial injury. Nevertheless, knowledge on the COVID-19-associated cardiovascular diseases remains scarce. Thus, in this chapter, the authors represent an overview of the available data on the induced heart failure related to COVID-19.
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Evidence On The Interplay Between Cardiovascular Complications And Covid19

COVID19 infection and fatality increase in patients with comorbidities, especially of cardiovascular concerns. In fact, cardiovascular disease (CVD) is the most common co-morbidity associated with COVID-19 and the fatality rate in COVID-19 patients with CVD is higher compared to other comorbidities, such as hypertension (HTN) and diabetes (Unudurthi, Luthra, Bose, Mccarthy, & Irene, 2020). Conversely and interestingly, cardiovascular diseases may precipitate from the infection with COVID19(Freaney et al., 2020). In order to understand such interplay between cardiovascular complications and COVID19 infection, several studies has put the line on the probable interacting factors with various viewpoints.

The mortality rate among patients with elevated a cardiac injury biomarker Troponin T (TnT), was ~60%, whereas the mortality rate in patients with normal TnT levels was ~9% (Unudurthi et al., 2020), and it was demonstrated that high levels of troponin are associated with higher mortality rates of up to 50% (Kermali, Khalsa, Pillai, Ismail, & Harky, 2020). In addition, COVID-19 patients with CVD have a higher mortality rate (around 10.5%) as compared to other comorbidities such as hypertension (6%), diabetes (7.3%), or chronic respiratory disease (6.3%) (Yang et al., 2020a). In severe cases, direct acute myocardial injury characterized by concentric left ventricular hypertrophy with a dilated, severely hypokinetic right ventricle and cardiac amyloidosis has been reported(Hu et al., 2004). In addition, preliminary autopsy reports from patients that succumbed to severe COVID-19 infection show severe right ventricular dilation, cardiac necrosis and infiltration of immune cells into the myocardium (Unudurthi et al., 2020).

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