Opinion Article, Int J Cardiol Res Vol: 13 Issue: 6

Cardiovascular Complications of COVID-19: Mechanisms, Diagnosis and Management

Anna Becker^*

¹Department of Cardiology, Charite University Medicine, Berlin, Germany

*Corresponding Author: Anna Becker,
Department of Cardiology, Charite University Medicine, Berlin, Germany
E-mail: anna.becker@charite.de

Received date: 28 November, 2024 Manuscript No. ICRJ-24-156841;

Editor assigned date: 02 December, 2024, PreQC No. ICRJ-24-156841 (PQ);

Reviewed date: 16 December, 2024, QC No. ICRJ-24-156841;

Revised date: 23 December, 2024, Manuscript No. ICRJ-24-156841 (R);

Published date: 30 December, 2024, DOI: 10.4172/2324-8602.1000598.

Citation: Becker A (2024) Cardiovascular Complications of COVID-19: Mechanisms, Diagnosis and Management. Int J Cardiol Res 13:6.

Description

The COVID-19 pandemic, caused by the novel Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), has profoundly impacted global health, challenging clinicians and researchers alike. Beyond its predominant respiratory manifestations, the virus has been shown to cause significant cardiovascular complications, which contribute substantially to morbidity and mortality. These complications range from acute coronary syndromes and myocarditis to thromboembolic events and arrhythmias. Understanding the cardiovascular complications of COVID-19 requires exploring its pathophysiological basis. SARS-CoV-2 gains cellular entry by binding to the Angiotensin-Converting Enzyme 2 (ACE2) receptor, abundantly expressed in the heart, vascular endothelium and lungs. This binding leads to ACE2 downregulation, disrupting the Renin-Angiotensin- Aldosterone System (RAAS) balance and promoting vasoconstriction, inflammation and thrombogenesis. Myocardial injury, defined by elevated cardiac troponin levels, is observed in approximately 20%-30% of hospitalized COVID-19 patients. It is associated with adverse outcomes, including increased mortality. The etiology of myocardial injury is multifactorial, encompassing demand ischemia due to hypoxemia, microvascular thrombosis and stress-induced cardiomyopathy. Acute coronary syndromes, particularly ST-Segment Elevation Myocardial Infarction (STEMI), have been reported, albeit with atypical presentations and delays in care due to devastated healthcare systems.

Myocarditis, characterized by myocardial inflammation, presents with chest pain, dyspnea and arrhythmias. SARS-CoV-2’s direct cardiotropic effects and immune-mediated mechanisms are implicated. Cardiac Magnetic Resonance Imaging (MRI) findings often reveal myocardial edema and late gadolinium enhancement, consistent with myocarditis. Endomyocardial biopsy, although rarely performed, confirms the diagnosis in select cases. COVID-19’s prothrombotic state has resulted in a surge of thromboembolic complications, including Deep Vein Thrombosis (DVT), Pulmonary Embolism (PE) and arterial thrombosis. Stroke, myocardial infarction and limb ischemia have also been reported, particularly in critically ill patients. The pathogenesis involves a combination of endothelial injury, platelet activation and hypercoagulability. Both atrial and ventricular arrhythmias are prevalent in COVID-19, often correlating with disease severity. Hypoxemia, electrolyte imbalances, myocardial injury and systemic inflammation contribute to arrhythmogenesis. Prolonged QT intervals, exacerbated by certain COVID-19 therapies increase the risk of torsades de pointes. Heart failure, both new-onset and exacerbation of pre-existing conditions, is a frequent complication. The mechanisms include direct myocardial injury, high-output states due to systemic inflammation and right ventricular failure secondary to PE or Acute Respiratory Distress Syndrome (ARDS).

Accurate diagnosis of cardiovascular complications requires a combination of clinical evaluation, biomarker assessment and imaging modalities. Cardiac troponins, Brain Natriuretic Peptide (BNP) and Ddimer levels provide valuable prognostic information. Electrocardiography (ECG) and echocardiography are essential for identifying arrhythmias, ventricular dysfunction and structural abnormalities. Advanced imaging techniques such as cardiac MRI and Computed Tomography (CT) angiography offer detailed insights into myocardial and vascular pathology. Prophylactic anticoagulation is recommended for hospitalized COVID-19 patients to reduce VTE risk. Intermediate or therapeutic dosing may be considered in high-risk individuals, balancing the bleeding risk. Corticosteroids have demonstrated mortality benefits in severe COVID-19, likely by attenuating the hyperinflammatory response. Emerging therapies targeting specific cytokines, such as IL-6 inhibitors, show promise in mitigating cardiovascular complications. Continuation of RAAS inhibitors is advised unless contraindicated. Beta-blockers, diuretics and other heart failure therapies should be optimized in patients with cardiac involvement. Oxygen therapy, mechanical ventilation and Extracorporeal Membrane Oxygenation (ECMO) may be required for critically ill patients. Multidisciplinary collaboration is important for managing complex cases. Percutaneous Coronary Intervention (PCI) remains the gold standard for STEMI management. Catheter-based thrombectomy may be considered for large-vessel occlusions in select patients with thromboembolic complications.

Conclusion

COVID-19 cardiovascular complications highlight the complex relation between viral pathogenesis, systemic inflammation and preexisting comorbidities. Early recognition and management are essential for improving patient outcomes. As our understanding of this multifaceted disease continues to evolve, a multidisciplinary approach integrating clinical care, study and public health measures will remain essential in combating the pandemic’s far-reaching effects.