Increased Epicardial Adipose Tissue Thickness is Associated With Angiographic Thrombus Burden in the Patients With

Eftal Murat Bakirci1, Husnu Degirmenci2, Hakan Duman3

  • 1Department of Cardiology, Faculty of Medicine, Erzincan University, Erzincan, Turkey eftalka@yahoo.com.

Insights

Epicardial adipose tissue (EAT) thickness and neutrophil to lymphocyte ratio (NLR) predict coronary thrombus and no-reflow in myocardial infarction patients. Higher EAT thickness is linked to increased thrombus burden and poorer outcomes.

Area of Science:

  • Cardiology
  • Biomedical Engineering
  • Medical Imaging

Background:

  • Non-ST-segment elevation myocardial infarction (NSTEMI) is a critical cardiovascular condition.
  • Epicardial adipose tissue (EAT) is metabolically active and influences coronary artery health.
  • The no-reflow phenomenon is a complication of percutaneous coronary intervention (PCI) associated with adverse outcomes.

Purpose of the Study:

  • To investigate the relationship between EAT thickness, coronary thrombus presence, and the no-reflow phenomenon in NSTEMI patients undergoing primary PCI.
  • To determine if EAT thickness is an independent predictor of coronary thrombus formation and no-reflow.

Main Methods:

  • A study involving 229 NSTEMI patients undergoing primary PCI.
  • Echocardiography was used to measure EAT thickness.
  • Coronary angiography assessed thrombus presence and reflow.
  • Neutrophil to lymphocyte ratio (NLR) and waist circumference were also analyzed.

Main Results:

  • EAT thickness and NLR were significantly higher in patients with coronary thrombus compared to those without.
  • Patients experiencing no-reflow had significantly higher EAT thickness and NLR than those with reflow.
  • EAT thickness positively correlated with thrombus burden, NLR, and waist circumference, and negatively with HDL cholesterol.
  • Multivariate analysis confirmed EAT thickness and NLR as independent predictors of coronary thrombus and no-reflow.

Conclusions:

  • EAT thickness is a significant predictor of coronary thrombus formation and the no-reflow phenomenon in NSTEMI patients.
  • EAT may play a crucial role in the pathophysiology of coronary thrombus and no-reflow.
  • EAT thickness could serve as a valuable imaging biomarker in managing NSTEMI patients undergoing PCI.

Related Concept Videos

Acute Coronary Syndrome III: Diagnostic Studies01:30

Acute Coronary Syndrome III: Diagnostic Studies

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...
484
Atherosclerosis II: Clinical Manifestations and Diagnostic Tests01:27

Atherosclerosis II: Clinical Manifestations and Diagnostic Tests

Atherosclerosis is a progressive disorder that leads to the thickening and narrowing of arterial walls due to plaque buildup. This condition can cause various symptoms depending on the arteries affected:Coronary Artery Disease (CAD): This condition affects the coronary arteries and may lead to chest pain (angina), shortness of breath (dyspnea), heart attacks, and other heart disease symptoms.Cerebrovascular Disease: This affects blood flow to the brain, causing transient ischemic attacks (TIAs)...
863
Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations01:19

Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations

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...
813