<p>COVID-19 primarily affects the lungs, but it can also cause neurological, psychological, and cardiovascular complications. Myocardial injury and myocarditis are of significant concerns that are often indicated by elevated troponin levels, a marker of cardiac involvement. This study analyzed risk factors and outcome of elevated troponin-I levels in COVID-19 patients compared to those with normal levels. We included 766 COVID-19 patients of which 50.6% were female, and 74.2% having co-morbidities. Patients were divided into two groups: 383 with elevated troponin levels and 383 with normal levels. We compared their demographics, clinical characteristics and outcome to identify the risk factors for cardiac injury during COVID-19 infection. Data was analyzed through SPSS V.24. Patients with elevated troponin were predominantly male (63.7%) and younger (mean age 58.42 years) than those with normal levels (64.86 years). Despite having fewer co-morbidities and milder COVID-19 cases, participants with raised troponin had lower ICU admission (37.02% vs. 60.2%) and ARDS rates (38.78% vs. 61.2%), yet mortality rates were similar. Ejection fraction remained stable across groups, but Pro-BNP levels were significantly lower in those with raised troponin (8.4% vs. 91.5%). This study highlights significant associations between elevated troponin levels in COVID-19 patients and factors like male gender, comorbid conditions, and ARDS. However, contrary to other studies, higher troponin levels were often found in patients with less severe COVID-19 with negative association with pro-BNP levels. The findings suggest that elevated troponin in COVID-19 does not directly correlate with disease severity or mortality. Further research with longitudinal follow-up and more granular biomarker analysis is recommended to fully elucidate the relationship between troponin levels and cardiac outcomes in COVID-19 patients.</p>