Evaluation of myocardial injury patterns and ST changes among critical and non-critical patients with coronavirus-19 disease

Abstract

Novel coronavirus disease (COVID-19) has led to a major public health crisis globally. Currently, myocardial damage is speculated to be associated with COVID-19, which can be seen as one of the main causes of death of patients with COVID-19. We therefore, aim to investigate the effects of COVID-19 disease on myocardial injury in hospitalized patients who have been tested positive for COVID-19 pneumonia in this study. A prospective study was conducted among 201 patients with COVID-19 in the Pakistan Military Hospital from April 1 to August 31, 2020, including non-critical cases and critical cases. COVID-19 patients were stratified as critical and non-critical according to the signs and symptoms severity; with those requiring intensive care and invasive mechanical ventilation as critical, and those did not requiring invasive mechanical ventilation as non-critical. A total of 201 COVID-19 patients with critical and non-critical categories presented with myocardial injury. All patients with myocardial injury had an elevation in CKMB and Troponin-I levels. Of these patients, 43.7% presented with new electrocardiography (ECG) changes, and ST depression was typically observed in 36.3% patients. In addition, 18.7% patients presented with abnormal echocardiography findings, with right ventricular dilatation and dysfunction commonly seen among critical group patients. Results analyzed by a logistic regression model showing COVID-19 direct contribution to myocardial injury in these patients. COVID-19 disease directly leads to cardiovascular damage among critical and non-critical patients. Myocardial injury is associated not only with abnormal ECG changes but also with myocardial dysfunction on echocardiography and more commonly observed among critical patients.

Prevalence of right ventricular dysfunction and impact on all-cause death in hospitalized patients with COVID-19: a systematic review and meta-analysis

“…29 studies reported data about the prevalence of RVD 14 – 42 , while 7 reported about all-cause mortality according to RVD status 17 , 19 , 20 , 30 , 33 , 35 , 36 . 11 studies were held in Europe 16 , 18 – 21 , 33 – 36 , 38 , 40 , 8 in North America 23 , 25 , 26 , 28 , 29 , 37 , 41 , 42 , 3 in Asia 30 – 32 , and 7 in other geographical locations 14 , 15 , 17 , 22 , 24 , 27 , 39 , including 2 multinational studies 24 , 27 . Cohorts included were quite homogeneous in terms of mean age of the included patients (ranging from 52 years old to 68 years old); among sex, males were generally more represented than females (up to 84%).…”

“…The definition of RVD was heterogeneous across studies, both in terms of parameters and cut-offs used to defined RVD. 13 studies used a combination of several parameters 15 , 18 , 19 , 21 , 24 , 28 , 30 , 33 – 35 , 38 , 40 , 42 , 8 studies defined RVD according to TAPSE cut-off 14 , 16 , 22 , 23 , 31 , 32 , 36 , 39 , while other or unclear definitions of RVD was used in 8 studies 17 , 20 , 25 – 27 , 29 , 37 , 41 . In one study, a surrogate of Right Ventricular-Arterial uncoupling, which in turn relates the degree of RVD to the increase of pulmonary pressure, was addressed 20 .…”

A Complicated Case of COVID-19-Induced Inferolateral Wall Myocardial Infarction Successfully Treated With Streptokinase

“…According to a study "in 201 COVID-19 patients with myocardial injury, elevation in CKMB and troponin I levels was found in all of them; 43.7% presented with new electrocardiography (ECG) changes, 36.3% had ST depression, and 18.7% of the patients had abnormal echocardiography findings, and right ventricular dilatation and dysfunction were commonly seen in the critical group patients" [12]. cTnI, cardiac troponin (cTnT), and BNP have shown remarkable potential in predicting COVID-19 outcomes and deteriorating health.…”

Coronavirus Disease 2019 (COVID-19) Coronary Vascular Thrombosis

“…Hospitalized patients with SARS CoV-2 infection have an increased risk of developing myocardial injury, determined by elevated cardiac troponin concentrations in the blood [1] , [2] , [3] , [4] . Patients with prior cardiovascular disease or risk factors such as myocardial infarction (MI) or hypertension are more likely to develop cardiac injury, but even individuals without a past history of cardiovascular disease can develop myocardial injury, increasing the risk for acute cardiac complications such as heart failure or potentially chronic cardiomyopathy [5] , [6] , [7] , [8] , [9] , [10] . Initial considerations of mechanisms included direct viral infection of cardiac myocytes, endothelial cells (ECs), or other cells; autoimmune T cell-mediated injury resulting in myocarditis; autoantibody-mediated injury through complement activation and/or antibody-dependent cellular cytotoxicity 11 .…”