MANAGEMENT OF COVID-19 IN PERSPECTIVE OF CARDIOLOGISTS
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 un...
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Veröffentlicht in: | Pakistan heart journal (Karachi) 2020-04, Vol.53 (1) |
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Sprache: | eng |
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Zusammenfassung: | 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 abnormalit |
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ISSN: | 0048-2706 2227-9199 |
DOI: | 10.47144/phj.v53i1.1907 |