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Acute Coronary Syndrome III: Diagnostic Studies01:30

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Diagnosing acute coronary syndrome or ACS begins with a thorough patient history. Notable symptoms include central, crushing chest pain radiating to the left arm, neck, jaw, or back, along with shortness of breath, sweating (diaphoresis), nausea, vomiting, dizziness, and palpitations.It is crucial to note any history of cardiac illnesses and assess risk factors, including age, gender, smoking, hypertension, diabetes, hyperlipidemia, and a sedentary lifestyle.During physical examination, vital...
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Acute Coronary Syndrome I: Introduction01:30

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Acute Coronary Syndrome (ACS) encompasses a spectrum of heart conditions caused by sudden obstruction of coronary arteries, typically resulting from the rupture of an atherosclerotic plaque and subsequent thrombus (blood clot) formation. This obstruction can lead to partial or complete blockage of blood flow, causing varying degrees of myocardial ischemia or infarction.ACS includes the following clinical entities:Unstable Angina (UA)Non-ST-Elevation Myocardial Infarction (NSTEMI)ST-Elevation...
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The pathophysiology of Acute Coronary Syndrome [ACD] involves several key processes:The main underlying cause of ACD is atherosclerosis, a chronic inflammatory disease characterized by the buildup of lipid-laden plaques within the coronary arteries.As the atherosclerotic plaque grows in the coronary artery, it may become unstable due to the formation of a lipid-rich core and a thin fibrous cap. Inflammatory cells within the plaque, such as macrophages, secrete enzymes that degrade the...
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Coronary Artery Disease I: Introduction01:30

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Coronary Artery Disease (CAD): An Overview with Scientific InsightsCoronary Artery Disease (CAD), often referred to as C-A-D, is a prevalent blood vessel disorder classified under the broader category of atherosclerosis. Atherosclerosis is a pathological process characterized by the hardening and narrowing of arteries due to the accumulation of atherosclerotic plaques. These plaques are composed of cholesterol, fatty substances, inflammatory cells, calcium, and fibrin, reducing blood flow to...
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Dynamic changes in sRAGE levels and relationship with cardiac function in STEMI patients.

Louise J N Jensen1, Søren Lindberg2, Søren Hoffmann2

  • 1The Medical Research Laboratory, Department of Clinical Medicine, Aarhus University, Noerrebrogade 44, DK-8000 Aarhus C, Denmark; Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Noerrebrogade 44, DK-8000 Aarhus C, Denmark.

Clinical Biochemistry
|January 7, 2015
PubMed
Summary

Soluble receptor of advanced glycation end-products (sRAGE) levels rise early in acute myocardial infarction (AMI), even before Troponin I. Elevated sRAGE is linked to long-term cardiac dysfunction after treatment.

Keywords:
Acute myocardial infarctionBiomarkerLeft ventricular ejection fractionPrimary percutaneous coronary interventionSoluble receptor of advanced glycation end-productssRAGE

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Area of Science:

  • Cardiovascular Medicine
  • Biomarker Research
  • Acute Myocardial Infarction

Background:

  • Soluble receptor of advanced glycation end-products (sRAGE) is a potential biomarker in coronary artery disease (CAD).
  • Patients with acute myocardial infarction (AMI) exhibit elevated sRAGE levels compared to healthy individuals.

Purpose of the Study:

  • To investigate dynamic changes in sRAGE levels during AMI.
  • To determine the relationship between sRAGE levels and cardiac dysfunction post-AMI.

Main Methods:

  • Prospective study of 80 ST-elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (pPCI).
  • sRAGE concentrations measured pre-pPCI, immediately post-pPCI, and on days 1 and 2 post-pPCI.
  • Left ventricular ejection fraction (LVEF) and infarct size assessed via echocardiography and cardiac MRI.

Main Results:

  • sRAGE levels significantly increased post-pPCI compared to pre-pPCI (median ratio: 1.25), preceding Troponin I elevation.
  • sRAGE levels decreased substantially by day 1 post-pPCI (median ratio: 0.34).
  • Peak sRAGE independently correlated with long-term cardiac dysfunction (LVEF) and infarct size.

Conclusions:

  • sRAGE levels peak early in AMI and post-pPCI, decreasing thereafter.
  • The rise in sRAGE precedes detectable Troponin I changes.
  • sRAGE is an independent predictor of long-term cardiac dysfunction following AMI.