MANAGEMENT OF COVID-19 IN PERSPECTIVE OF CARDIOLOGISTS

Abstract

After influenza Coronavirus Disease 2019 (COVID-19) is pandemic. The outbreak of the disease started in China and the number of cases exceeded in the world as of March 15, 2020 and the rate is multiplicating tremendously.¹ COVID-19 has its effect on cardiovascular system increasing morbidity with underlying cardiovascular condition and causing myocardial infarction and dysfunction.²

COVID-19 is caused by severe acute respiratory syndrome Coronavirus-2 (SARS-COV-2). It is believed that SARS-COV-2 entered in humans after it shifted from cats to an intermediate host (Malayan Pangolin).³

SARS-COV-2 spread by respiratory droplets and can be found in stool. The secondary infection rates range from 0.5-5%.^4,5 The most common symptoms are fever (88%), dry cough (67.7%), rhinorrhea (4.8%) less frequent is gastrointestinal symptoms (diarrhea 4-14%, nausea/emesis 5%).⁵ Chinese reports presented with more significant symptoms in which 14% presented with dyspnea, respiratory rate ≥ 30 bpm blood oxygen saturation ≤ 93%, PO2 to fraction of impaired oxygen ratio < 300 and/or lung infiltrates >50% within 24 to 48 hours and 5% with respiratory failure, septic shock, and/or multiple organ dysfunction or failure.⁶

COVID-19 caused myocardial injury as presented in Wuhan China with elevated high sensitivity troponin I (hs-CTNI) or new ECG changes in 7.2% and 2.2% required ICU care.⁷ There is an elevation of other inflammatory biomarkers (D-dimer, ferritin, interleukin-6, lactate dehydrogenase) reflects cytokine storm or secondary hemophagocytic lymphohistiocytosis. The presentation of cardiac problem misleads viral myocarditis or stress cardiomyopathy. There is left ventricular dysfunction (EF 27%, LVEDD 5.8cm) and elevated cardiac biomarkers.⁸

The exact mechanism of cardiac involvement is not known. It is postulate that myocardial involvement may be via ACE2 or cytokine storm with T helper cells or hypoxia induced excessive intracellular calcium leading to cardiac myocyte apoptosis.^9-11

Preventive measure are best strategy for COVID-19. Vaccines and monoclonal antibodies against SARS-CoV-2 are in investigation stages. Recombinant human ACE2 (APN01) has been proposed as treatment to prevent SARS-COV-2. ^12-13 Remdesevir and Chloroquineare other drugs that may add clinical benefits in reduction of pneumonia and hospital stay.^14-17

In mild to severe cases of COVD-19 typical imaging findings are not different (e.g. ground-glass opacification with or without consolidative abnormalities, consistent with viral pneumonia, minimal or no pleural effusions).¹⁸

CT chest was performed in Chinese cohort, though one should avoid its use unless necessary.  If it is mandatory to use as a diagnostic tool it should be balanced with risk to other patients and health care workers during process of patient transport and time that is spent in diagnostic area. An alternative approach on bedside is use of lung ultrasound that presents with thickening of the pleural line and B line supporting alveolar consolidation. Pleural effusions are unusual.¹⁹

In a study of 1014 patients in Wuhan who underwent reverse transcription polymerase chain reaction (RT-PCR) testing and chest CT for evaluation of COVID-19 a posterior chest CT for COVID-19 had sensitivity of 97% and specificity of 25% using PCR test as a reference.²⁰ Chest CT abnormalities has also been identified in development of symptoms and even prior to detection of viral RNA from upper respiratory symptoms.²¹