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Behavior of circulating endothelin-1 in a group of patients with acute myocardial infarction

S Battistelli1, M Billi, G Manasse

  • 1Istituto di Semeiotica Medica e Geriatria, University of Siena, Italy. battistelli@unisi.it

Angiology
|August 18, 1999
PubMed

Insights

Plasma endothelin-1 (ET-1) is elevated in acute myocardial infarction, especially with left ventricular failure. ET-1 levels correlate inversely with left ventricular ejection fraction, suggesting its utility as a disease marker and systolic function index.

Area of Science:

  • Cardiovascular Medicine
  • Biochemistry
  • Clinical Research

Background:

  • Acute myocardial infarction (AMI) is a leading cause of cardiovascular mortality.
  • Endothelin-1 (ET-1) is a potent vasoconstrictor peptide with potential roles in cardiovascular pathophysiology.
  • Left ventricular (LV) dysfunction is a common complication of AMI, impacting prognosis.

Purpose of the Study:

  • To investigate plasma ET-1 levels in patients with AMI, both complicated and uncomplicated by LV failure.
  • To assess the dynamic changes in ET-1 during the acute phase and recovery.
  • To correlate ET-1 levels with LV systolic function, specifically left ventricular ejection fraction (LVEF), and the impact of thrombolytic therapy.

Main Methods:

  • Plasma ET-1 was measured in 23 AMI patients (complicated/uncomplicated LV failure) and 14 controls on admission, days 2, 3, 5, and discharge.
  • LV function was assessed on discharge, with moderate to severe dysfunction defined as LVEF < 40%.
  • Correlation analyses were performed between ET-1, LV function, and thrombolytic treatment.

Main Results:

  • ET-1 was significantly elevated on admission in both uncomplicated (p < 0.01) and complicated (p < 0.001) AMI patients compared to controls.
  • In complicated patients, ET-1 remained elevated until discharge, unlike the uncomplicated group which normalized by day 5.
  • Plasma ET-1 showed a significant inverse correlation with LVEF (p < 0.001) on discharge, particularly in patients with LVEF < 40% (p < 0.001).
  • ET-1 levels were lower in patients receiving thrombolytic therapy (p < 0.05).

Conclusions:

  • Early elevation of ET-1 in AMI may reflect ischemia, stress, and hemodynamic impairment.
  • Sustained elevation of ET-1 in complicated AMI suggests its role in disease progression.
  • Plasma ET-1 serves as a valuable marker for disease severity and a reliable index of LV systolic function post-MI.

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