Cardiac Manifestation of COVID-19
By Dr. Shkelzen Badivuku
On December 31, 2019, Chinese health officials reported to the World Health Organization (WHO) cases of unknown pneumonia not responsive to traditional treatment, in Wuhan, Hubei Province7. Chinese scientist isolated the novel coronavirus on January 7 and pathogen identified was severe acute respiratory syndrome corona virus 2, SARS-CoV-2 which causes COVID-19. (CO for corona, VI for virus, D for disease and 19 for the year the outbreak was reported).
In March of 2020 the WHO declared the outbreak a Public Health Emergency of International Concern (PHEIC). The full spectrum of COVID-19 ranges from mild, self-limited respiratory disease associated with multiorgan failure, thromboembolic event and death, (WHO, 2020). SARS-CoV-2 is primarily transmitted by respiratory droplets exhaled by infected individuals. These droplets can be in spectrum of, respiratory droplets in diameter 5-10 μm and droplet less then <5μm in diameter are referred to as droplet nuclei or aerosols. Larger droplet falls out of the air relatively quickly while close to source, usually within 6-foot distance. Smaller droplet referred as aerosols may remain in the air over the time and greater distances decreasing in concentration from their source, (WHO, 2020).
The CDC recently updated its guidance to acknowledge this potential for airborne spread of SARS-CoV-2. COVID-19 has incubation period of 2 to 14 days, with potential asymptomatic transmission. Recent evidence suggests that up to 40-45% of people infected with SARS CoV-2 may never be symptomatic but still transmit the virus. Viral spread from asymptomatic may account for more than 50% of transmission event in COVID-19. Approximately 15-20% of patient develop acute respiratory syndrome coronavirus 2, SARS CoV-2 and about 5% become critically ill. The effects of acute respiratory syndrome corona virus 2 infection are attributed to hypoxia and inflammatory response resulting in cardiac damage worsening of prognosis, irrelevant to preexisting conditions.
There is increasing awareness of cardiovascular manifestation of COVID-19 disease and adverse impact of cardiovascular implications in prognostic aspect of the disease.
The goal of this article is reviewing the importance of EKG abnormalities as a leading tool to assess the extent of cardiovascular implications in COVID19 confirmed patient and discus potential cardiac complications.
Cardiac complications in COVID19 patient are classified into five categories:
– cardiac injury, due to ischemia and myocarditis
– new-onset or worsening of pre-existing heart failure
– thromboembolic disease and
– cardiac abnormalities induced by medical treatment
Cardiac injury: patient presenting with cardiac symptoms and EKG changes should be carefully assessed by clinician to recognize COVID-19 cardiac complications i.e., myocarditis, tachyarrhythmias and/or bradyarrhythmia’s. In Myocarditis, sinus tachycardia and bundle branch block pattern were observed. Other cases of Myocarditis demonstrated nonspecific conduction delay and ST segment elevation in Lead III and avF. Recommendations of Task Force for Universal Definition of Myocardial Infarction applies to any patient whose cardiac Troponin (cTn) I/T is above 99 percentile of upper reference limit, meaning every healthy person should have cTn a value of Troponin below the upper reference limit. The percentage of COVID-19 with myocardial injury ranges from 7.2% to 12% and much higher in critically ill patient, (Haseeb. 2020)4.
COVID-19 and cardiac arrhythmia: recent study published (Wang, 2020)9 cardiac arrhythmia represented leading complications and were more common to critically ill patient. Among 187 patients with confirmed COVID-19, 5.9% of the patient experienced malignant arrhythmia. Similar study reported critically ill patient with COVID-19 experienced cardiac arrest with pulseless electrical activity or ventricular arrhythmias during their recovery. Cardiac arrhythmias in COVID-19 confirmed cases presented 16.9% while malignant arrhythmias presented 11.5%, (Wang, 2020) 9. In critically ill COVID-19 confirmed patient with fever will have bradycardia which prolongs QT interval and triggers Torsade’s de pointes. Atrial tachycardia or atypical atrial flutter with wide QRS morphology was reported.
For the measurement of QT interval, it is recommended use of lead II and V5 and V6.
Antiviral and other medications can potentially exacerbate or initiate new onset cardiac arrhythmia in COVID-19 confirmed cases. COVID-19 antiviral associated medications such as Lopinavir and Ritonavir are associated with QT interval prolongations. Cases of QT interval prolongation and Torsade’s de pointes due to hydroxychloroquine/chloroquine (HCQ/CQ) are reported. The largest reported cohort study treated with HCQ/CQ and Azithromycin, no instances of Torsade’s de pointes or arrhythmogenic death was reported. QT prolongation was present but there was no need to discontinue therapy. Azithromycin per se is associated with risk of QT prolongation and TdP and sudden cardiac death, however the absolute risk is low. 3. 8
Thromboembolic events: patient with COVID-19 are at higher risk for thromboembolic event. Thrombotic event occurred in 16% of COVID-19 patient. 6.2% were venous, (3.2% pulmonary embolism and 3.9% deep vein thrombosis) and 11.1% arterial (1.6% ischemic stroke, 8.9% MI and 1% systemic thromboembolism 2. The S1, Q3, T3 was observed in another patient whose infection was complicated by pulmonary embolism, (Haseeb, 2020)4.
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Dr. Shkelzen Badivuku is a Professor of Physiology at Berkely. Professor Badivuku is a regular contributor of articles and consultant for the National Telemetry Association.