A comprehensive review on the interconnection of C-reactive protein, cardiac troponins, and cytokine storm in cardiovascular manifestations of COVID-19

The COVID-19 pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been associated with substantial cardiovascular morbidity and mortality, both during acute infection and in the post-recovery phase. Identifying and understanding key biomarkers is critical for elucidating underlying mechanisms, guiding risk stratification, and informing therapeutic strategies. This literature review was conducted with the aim to synthesize current evidence on the role of major cardiovascular biomarkers C-reactive protein (CRP), cardiac troponins, and pro-inflammatory cytokines in the pathophysiology, prognosis, and long-term sequelae of COVID-19. The authors have gone through various databases such as - PubMed, Scopus, Web of Science, and Google Scholar. This review evaluates peer-reviewed clinical and mechanistic studies examining the association between COVID-19 between January 2020 to June 2025 with keywords and MeSH terms such as “C-Reactive Protein” OR “CRP” and “Cardiac Troponins” or “Troponin I″ or “Troponin T″ and “Cytokine Storm” and “COVID-19″ or “SARS-CoV-2″ and “Cardiovascular Complications” and cardiovascular complications, with a focus on inflammatory and myocardial injury biomarkers. CRP, an acute-phase reactant and sensitive indicator of systemic inflammation, is markedly elevated in severe COVID-19 and correlates with endothelial dysfunction and disease severity. Cardiac troponins, highly specific markers of myocardial injury, are significantly increased in affected patients, predicting adverse clinical outcomes and higher mortality risk. Elevated levels of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and other cytokines characteristic of the COVID-19–induced “cytokine storm” play a pivotal role in the pathogenesis of acute cardiac injury, myocarditis, arrhythmias, and thromboembolic events. Persistent elevation of these biomarkers in some patients after acute illness suggests ongoing myocardial stress and chronic inflammation, potentially contributing to post-acute sequelae of SARS-CoV-2 infection, including long COVID and late cardiovascular complications. Biomarkers such as CRP, cardiac troponins, and cytokines are integral to understanding the cardiovascular impact of COVID-19, offering prognostic value for both acute and long-term outcomes. Ongoing research into targeted anti-inflammatory and cardioprotective therapies holds promise for mitigating these complications and improving patient survival and quality of life. • In this review, the authors discuss the complex interplay between C-reactive protein (CRP), cardiac troponins (cTnI, cTnT), and pro-inflammatory cytokines (IL-6, IL-1β, TNF-α), highlighting their synergistic involvement in acute and post-COVID-19 cardiovascular complications. • The dual role of CRP is explored-not only as a marker of systemic inflammation but also as a mediator of endothelial dysfunction, thrombosis, and atherogenesis, contributing to disease progression and adverse cardiac events. • This review underscores how elevated cardiac troponins serve as definitive biomarkers of myocardial injury, closely associated with myocarditis, acute coronary syndromes, heart failure, and increased mortality in COVID-19 patients. • We examine the pathophysiological impact of the cytokine storm, where excessive immune activation leads to myocardial inflammation, vascular permeability, fibrosis, and microvascular thrombosis in severe cases. • The authors summarize therapeutic and prognostic implications, emphasizing the clinical utility of CRP and troponin monitoring, the role of immunomodulators and the urgent need for long-term cardiovascular surveillance in post-COVID-19 care.