Articles: myocardial-injury.
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Patients with SARS-CoV-2 infection carry an increased risk of cardiovascular disease encompassing various implications, including acute myocardial injury or infarction, myocarditis, heart failure, and arrhythmias. A growing volume of evidence correlates SARS-CoV-2 infection with myocardial injury, exposing patients to higher mortality risk. SARS-CoV-2 attacks the coronary arterial bed with various mechanisms including thrombosis/rupture of preexisting atherosclerotic plaque, de novo coronary thrombosis, endotheliitis, microvascular dysfunction, vasculitis, vasospasm, and ectasia/aneurysm formation. ⋯ In patients presenting with coronary vasospasm, nitrates and calcium channel blockers are preferred, while treatment of coronary ectasia/aneurysm mandates the use of antiplatelets/anticoagulants, corticosteroids, immunoglobulin, and biologic agents. It is crucial to untangle the exact mechanisms of coronary involvement in COVID-19 in order to ensure timely diagnosis and appropriate treatment. We have reviewed the current literature and provide a detailed overview of the pathophysiology and clinical spectrum associated with coronary implications of SARS-COV-2 infection.
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Acute coronary syndrome remains the leading cause of death in both patients with coronary artery disease and patients with other diseases (such as diabetes mellitus, chronic kidney disease, inflammatory diseases of various etiologies, and others). Early diagnosis of cardiomyocyte damage and necrosis opens up wide opportunities to improve the prognosis of patients with atherosclerotic lesions of the coronary arteries, and also makes it possible to discharge patients without acute cardiovascular pathology from intensive care units with a high degree of probability. The article discusses the evolution of the research and introduction into broad clinical practice of markers of myocardial damage and necrosis, which have largely improved modern clinical practice.
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J. Cardiothorac. Vasc. Anesth. · Oct 2024
ReviewNavigating Cardiovascular Events in Non-Cardiac Surgery: A Comprehensive Review of Complications and Risk Assessment Strategies.
Cardiovascular complications following non-cardiac surgery pose a significant global concern, affecting millions of patients annually. These complications, ranging from asymptomatic troponin elevations to major adverse cardiac events, contribute to heightened morbidity, mortality, and health care expenditures. The underlying mechanisms involve oxygen supply-demand imbalances and acute coronary syndromes precipitated by perioperative stressors. ⋯ An enhanced understanding regarding the standardized approaches is imperative in mitigating these complications effectively. Further research is essential to refine risk prediction models, validate biomarker thresholds, and elucidate the efficacy of preventive measures. Addressing these challenges can eventually lead to improved patient outcomes and more efficient healthcare resource utilization worldwide.
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Review Case Reports
A case of heat stroke with significantly elevated troponin and dynamic ECG changes: Myocardial infarction or Myocardial injury?
We described an 82-year-old man who was taken to our emergency department after being found unconscious. His electrocardiogram (ECG) showed ST-segment elevation in leads V4-V6 and cardiac troponin I (cTnI) was abnormally elevated. In addition to ECG and cTnI changes, this patient was combined with unconsciousness, high fever, abnormal liver function, acute renal failure, and rhabdomyolysis. ⋯ Ca-IMR was 260 mmHg*s/m in the left circumflex artery, indicating the presence of coronary microvascular dysfunction (CMD). After several days of treatment, the patient recovered from multiple organ damage. Therefore, ECG and troponin results should be interpreted carefully in patients with high fever and coma during high temperature seasons.
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Assay-specific increases in circulating cardiac troponin are observed in 20-40% of patients after noncardiac surgery, depending on patient age, type of surgery, and comorbidities. Increased cardiac troponin is consistently associated with excess morbidity and mortality after noncardiac surgery. Despite these findings, the underlying mechanisms are unclear. ⋯ The perioperative period triggers multiple pathological mechanisms that might cause cardiac troponin to cross the sarcolemma. A two-hit model involving two or more triggers including systemic inflammation, haemodynamic strain, adrenergic stress, and autonomic dysfunction might exacerbate or initiate acute myocardial injury directly in the absence of cell death. Consideration of these diverse mechanisms is pivotal for the design and interpretation of interventional perioperative trials.