Contextualizing cardiac dysfunction in critically ill patients with COVID-19

Guido Tavazzi, Francesco Corradi, Francesco Mojoli, Francesco Forfori, Gabriele Via

Research output: Contribution to journalReview articlepeer-review

Abstract

Acute cardiac injury incidence in COVID-19 is about 13 times higher in the Intensive Care Unit (ICU)/severely ill than in less critical patients. Patients with cardiovascular comorbidities seem to be more prone to develop higher acuity of the infection, and myocardial injury has been reported amongst them in up to 15% of those hospitalized and up to 30% of ICU-admitted ones. The symptoms of over ischemia/heart failure may be challenging to distinguish as dyspnea and chest discomfort overlap with those due to COVID-19. Therefore, beside close monitoring with electrocardiography, biomarkers and, in case of demonstrated cardiac involvement, echocardiography, strategies to improve myocardial oxygen delivery should be promptly applied. The cytokine release with complement and iNO dysregulation are established mechanisms potentially leading to sepsis-related cardiomyopathy, making sepsis per se one of the potential mechanism leading to acute cardiac injury in COVID-19 patients. Moreover, the hyper-inflammation with endothelial dysfunction is likely be responsible of both pulmonary in-situ platelet aggregation and deep thrombosis potentially leading to severe pulmonary embolism and right ventricular failure. Besides the customary antithrombotic prophylaxis for critical patients, D-dimer levels and tighter coagulation monitoring are recommended and should guide the choice for anticoagulation treatment. We summarize the current knowledge regarding cardiovascular involvement in patient with COVID-19.

Original languageEnglish
Pages (from-to)1340-1345
Number of pages6
JournalMinerva Anestesiol
Volume86
Issue number12
DOIs
Publication statusPublished - Dec 2020

Keywords

  • Angiotensin-Converting Enzyme 2/genetics
  • COVID-19/complications
  • Critical Illness/therapy
  • Heart Diseases/etiology
  • Humans
  • Ventricular Dysfunction, Right/etiology

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