44 2033180199
All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.
Clinical Cardiology Journal

Sign up for email alert when new content gets added: Sign up

Venkat A*
 
Vaagdevi College of Pharmacy, Telangana, India, Email: [email protected]
 
*Correspondence: Venkat A, Vaagdevi College of Pharmacy, Telangana, India, Email: [email protected]

Received Date: Jul 10, 2021 / Accepted Date: Jul 15, 2021 / Published Date: Jul 20, 2021

Citation: Venkat A. Heart failure in present COVID-19 pandemic. Clin Cardiol J 2021;5(4):5.

This open-access article is distributed under the terms of the Creative Commons Attribution Non-Commercial License (CC BY-NC) (http://creativecommons.org/licenses/by-nc/4.0/), which permits reuse, distribution and reproduction of the article, provided that the original work is properly cited and the reuse is restricted to noncommercial purposes. For commercial reuse, contact [email protected]

Commentary

Patients with cardiovascular disease, including heart failure, are more susceptible to coronavirus disease 2019 (COVID-19), and their clinical course is more severe once infected. Increased troponin plasma levels indicate heart failure and myocardial injury in at least 10% of COVID-19 patients, with greater percentages (25 percent to 35 percent or more) when patients are seriously ill. Multiple mechanisms have been shown in patients with COVID-19 to cause myocardial injury, including those that occur with all severe infections, such as fever, tachycardia, and adrenergic stimulation, as well as those caused by an exaggerated inflammatory response, endotheliitis, and, in some cases, myocarditis.

The renin-angiotensin-aldosterone system may play a vital role. SARSCoV- 2 infects human cells by attaching to angiotensin-converting enzyme 2 (ACE2), an enzyme that converts angiotensin II into angiotensin 1-7, which has vasodilating and anti-inflammatory properties. Downregulation of ACE2 by the virus may boost angiotensin II stimulation and contribute to COVID-19’s harmful hyper-inflammatory response. ACE2 may, on the other hand, be up-regulated in individuals with heart illness who are taking angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. For proper triage and management of these patients, a thorough grasp of the hemodynamic and diagnostic implications is required.

COVID-19 causes abnormal cardiac biomarkers by a variety of methods, including viral entry through the ACE2 receptors, direct cardiac damage, enhanced thrombotic activity, stress cardiomyopathy, and others. Many of the identified mechanisms and manifestations can be attributed to the cytokine storm seen in this pandemic. The two-way interaction between heart failure drugs and infection, as well as the planned COVID-19 medicines and heart failure, can lead to effective management.

Top