Fatal Intruder to The Heart in Covid-19 Pandemic

Introduction: Coronavirus disease (COVID-19) is the disease caused by a new coronavirus called SARS-CoV-2, which commonly demonstrates respiratory complications from mild URTI to severe ARDS. Yet, there is increasing number of patients who presented to our ED with cardiac complaints only. We described a series of 3 COVID 19 cases with cardiovascular involvement which visited to our centre. Case Report: Case 1: A 21-year-old gentleman with no known medical illness complaint of chest discomfort for 1 day, and associated with palpitation and shortness of breath. He had close contact 3 days prior to presentation. Upon arrival at ETD, his heart rate was 62 beats/min and other vital signs were normal. His 1st ECG showed sinus arrhythmia, with no acute ischemic changes (Fig. 1A). Subsequently, he developed bradycardia with heart rate ranged 35-45 beats/min. His 2nd and 3rd ECG showed sinus bradycardia, with no any atrioventricular block (Fig. 1B, 1C). His COVID-19 PCR was positive.   Case 2: A 51-year-old gentleman with underlying hypertension and Type II Diabetes Mellitus, presented with burning sensation over epigastrium for 1 day. Upon arrival at ETD, he was hemodynamically stable. His 1st ECG showed sinus tachycardia; isolated ST elevation over lead V3(3 small boxes); ST depression over lead III and aVF; Q waves over lead III and aVF (Fig. 2A). Subsequently, his 2nd ECG demonstrated sinus rhythm with significant ST elevation over lead V2 (3 small boxes); but complete resolution of ST elevation over lead V3; and ST depression over lead III and aVF (Fig. 2B). His 3rd ECG was same as 2nd ECG, but there is decreased in amplitude of R wave over lead V5 and V6 (Fig. 2C). Troponin I showed negative (<0.05). His COVID-19 PCR was positive.   Case 3: A 64-year-old gentleman with underlying hypertension, Type II Diabetes Mellitus, dyslipidemia, COPD, and IHD presented with left sided chest pain for 1 day, associated with diaphoresis and mild shortness of breath. He also had productive cough for 1 week. Upon arrival at ETD, his blood pressure was 90/54 mmHg and other vital signs were normal. His 1st ECG showed sinus rhythm; ST elevation over II, III, aVF; No ST depression; T inversion over II, III, aVF; Deep Q waves over II, III, aVF and poor R waves progression (Fig. 3A). His 2nd and 3rd ECG showed no evolving changes (Fig. 3B, 3C). His Creatine kinase level was 716. Patient was treated as cardiogenic shock secondary to late presentation MI. Subsequently, patient deteriorated rapidly and was intubated due to unable to maintain his oxygen saturation. His COVID-19 PCR was positive. Discussion: Dawei Wang et al. reported that among 138 hospitalised COVID19 patients, 7.2% had acute myocardial injury, and 16.7% had arrhythmia.(1) In another study, Fei Zhou et al. reported that among 191 hospitalised COVID-19 patients, 17% had acute myocardial injury, and 23% had acute heart failure.(2)   The pathophysiology of myocardial injury in Covid-19 patients is not well known. Angiotensin-converting enzyme-2 (ACE-2) has been identified as a functional receptor for coronaviruses. ACE-2 can be found mainly in lungs and also heart. The binding of SARS-CoV-2 spike protein to ACE-2 causes the down-regulation of ACE-2. This causes the accumulation of Angiotensin-II. Angiotensin-II promotes inflammatory cells activation and thereby causing myocardial injury.  Ashraf Roshdy et al. reported that within the myocardium of 47% of studied hearts, SARS-CoV-2 was detected. Besides chronic cardiac pathologies, postmortem examination demonstrated cardiac dilatation (20%), acute ischemia (8%), intracardiac thrombi (2.5%), pericardial effusion (2.5%), and myocarditis (1.5%).(3)   From all these studies, it showed that COVID-19 infection undeniable causes great impact to our heart. Many COVID-19 patients may able to recover from the COVID-19 infection, but unfortunately left with certain level of cardiovascular injuries and complications.   In JAMA Cardiology study, Valentino O. Puntmann et al. evaluated 100 COVID-19 patients who recovered within the past 3 months via Cardiac Magnetic Resonance (CMR) and cardiac marker. In this study, 67 patients recovered at home, while the remaining 33 patients required hospitalisation. CMR detected cardiac involvement in 78 patients. From CMR, total 60 patients underwent myocardial inflammation (abnormal native T1 and T2).  Among 100 patients, cardiac marker Troponin T was detectable in 71%, while significantly elevated in 5%. Conclusion: In COVID-19 patients, we should not only focus on respiratory complications, yet we should also be aware that they might present only with cardiac manifestations. COVID-19 has shown significant relation with cardiovascular system. However, the pathophysiology of myocardial injury in COVID-19 patients is still unclear and lack of substantial evidences.  COVID-19 infection is a fatal intruder to the heart. It can lead to arrhythmia; myocarditis; heart failure as late consequence, or even death. This will become complicated and more challenging when dealing with COVID-19 patients. Due to its prominent impacts toward the heart, this raises concerns that health screening should become routine for COVID-19 patients to detect any cardiovascular damages.  Further studies and investigations for cardiovascular system are needed in handling COVID-19 patients for early detection, in order to provide better hospitalisation treatment and improve patients’ prognosis, or even post-recovery care.