Commentary, Int J Cardiol Res Vol: 13 Issue: 1

Pathophysiology and Clinical Implications of Coronary Thrombosis

Yun Chao^*

¹Department of Cardiovascular Medicine, Chongqing Medical University, Chongqing, China

*Corresponding Author: Yun Chao,
Department of Cardiovascular Medicine, Chongqing Medical University, Chongqing, China
E-mail: chaoyun@163.com

Received date: 29 January, 2024, Manuscript No. ICRJ-24-134233;

Editor assigned date: 31 January, 2024, PreQC No. ICRJ-24-134233 (PQ);

Reviewed date: 14 February, 2024, QC No. ICRJ-24-134233;

Revised date: 21 February, 2024, Manuscript No. ICRJ-24-134233 (R);

Published date: 28 February, 2024, DOI: 10.4172/2324-8602.1000543.

Citation: Chao Y (2024) Pathophysiology and Clinical Implications of Coronary Thrombosis. Int J Cardiol Res 13:1.

Abstract

Description

Coronary thrombosis, characterized by the formation of a blood clot within a coronary artery, represents a critical event in the pathogenesis of Acute Coronary Syndromes (ACS), including Myocardial Infarction (MI). Despite advances in cardiovascular medicine, coronary thrombosis remains a significant cause of morbidity and mortality worldwide. The pathogenesis of coronary thrombosis is multifactorial and often involves the interplay of various prothrombotic and proinflammatory factors. Endothelial dysfunction, characterized by impaired nitric oxide bioavailability and increased expression of adhesion molecules, predisposes to platelet activation and adhesion at sites of vascular injury. Subsequent platelet aggregation and activation of the coagulation cascade culminate in the formation of a thrombus within the coronary artery lumen. Rupture or erosion of an atherosclerotic plaque exposes subendothelial components, such as collagen and tissue factor, triggering platelet adhesion and thrombus formation. Additionally, factors such as inflammation, oxidative stress, and shear stress contribute to plaque destabilization and thrombotic events.

The clinical manifestations of coronary thrombosis vary depending on the extent and location of coronary artery occlusion. Patients may present with typical symptoms of ACS, including chest pain or discomfort, dyspnea, diaphoresis, and nausea. The Electrocardiogram (ECG) often reveals ST-segment elevation or depression, T-wave inversions, or Q-wave changes, indicative of myocardial ischemia or infarction. Biomarkers such as cardiac troponins are elevated in the setting of myocardial necrosis and serve as diagnostic markers of MI. However, it is essential to recognize that coronary thrombosis can manifest as a spectrum of clinical syndromes, ranging from STSegment Elevation Myocardial Infarction (STEMI) to Non-STSegment Elevation Myocardial Infarction (NSTEMI) or unstable angina. The diagnosis of coronary thrombosis relies on a combination of clinical evaluation, ECG findings, cardiac biomarkers, and imaging modalities. Coronary angiography remains the gold standard for assessing coronary anatomy and identifying obstructive lesions. The presence of a thrombotic occlusion or significant coronary stenosis on angiography confirms the diagnosis of coronary thrombosis. Intravascular imaging techniques, such as Intravascular Ultrasound (IVUS) and Optical Coherence Tomography (OCT), provide detailed insights into plaque morphology and thrombus composition. Noninvasive imaging modalities, including coronary Computed Tomography Angiography (CTA) and cardiac Magnetic Resonance Imaging (MRI), may also aid in the diagnosis and risk stratification of patients with suspected coronary thrombosis.

The management of coronary thrombosis is guided by the principles of revascularization, antiplatelet therapy, Anticoagulation, And Secondary Prevention. Primary Percutaneous Coronary Intervention (PCI), with the timely restoration of coronary blood flow, is the preferred reperfusion strategy in patients with STEMI. Pharmacological reperfusion therapy, such as fibrinolytic agents, may be considered in settings where primary PCI is not readily available. Dual antiplatelet therapy with aspirin and a P₂Y₁₂ receptor inhibitor, such as clopidogrel, prasugrel, or ticagrelor, is initiated in all patients undergoing PCI to prevent recurrent thrombotic events. Anticoagulation with unfractionated heparin, low molecular weight heparin, or bivalirudin is administered adjunctively during PCI to minimize thrombus formation and procedural complications. Secondary prevention measures, including statin therapy, betablockers, angiotensin-converting enzyme inhibitors, and lifestyle modifications, are instituted to reduce the risk of recurrent ischemic events and improve long-term outcomes.

Conclusion

Coronary thrombosis represents a pivotal event in the pathogenesis of ACS and myocardial infarction. The intricate interplay of prothrombotic and proinflammatory factors precipitates the formation of a thrombus within the coronary artery lumen, leading to myocardial ischemia and infarction. Early recognition and prompt intervention are paramount in mitigating the adverse consequences of coronary thrombosis and improving patient outcomes. Continued efforts aimed at elucidating the underlying mechanisms and novel therapeutic targets hold promise for advancing the management of this critical cardiovascular disorder.