Association between kaolin-induced maximum amplitude and slow-flow/no-reflow in ST elevation myocardial infarction

Qing Li1, Enmin Xie2, Yimin Tu2

  • 1Department of Cardiology, Peking University China-Japan Friendship School of Clinical Medicine, Beijing 100029, China; Department of Cardiology, China-Japan Friendship Hospital, Beijing 100029, China.

Insights

Maximum amplitude during thrombin activation (MAthrombin) predicts slow-flow/no-reflow in ST-segment elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention. Higher MAthrombin levels are linked to increased risk of adverse cardiovascular events.

Area of Science:

  • Cardiology
  • Hematology
  • Interventional Cardiology

Background:

  • High thrombus burden in ST-segment elevation myocardial infarction (STEMI) increases slow-flow/no-reflow risk.
  • The association between kaolin-induced maximum amplitude (MAthrombin) and slow-flow/no-reflow remains underexplored.

Purpose of the Study:

  • To investigate the predictive value of MAthrombin for slow-flow/no-reflow in STEMI patients.
  • To assess MAthrombin as a risk factor for long-term adverse cardiovascular events.

Main Methods:

  • Retrospective enrollment of 690 STEMI patients undergoing primary percutaneous coronary intervention (PCI).
  • MAthrombin measurement via thromboelastography before PCI.
  • Analysis using logistic regression and restricted cubic spline regression (RCS).
  • Follow-up for adverse cardiovascular events.

Main Results:

  • MAthrombin was an independent risk factor for slow-flow/no-reflow (TIMI flow grade ≤2).
  • RCS revealed a nonlinear relationship between MAthrombin and slow-flow/no-reflow.
  • A MAthrombin cutoff of 68 mm predicted slow-flow/no-reflow.
  • Elevated MAthrombin and slow-flow/no-reflow independently predicted long-term adverse cardiovascular events.

Conclusions:

  • MAthrombin is a significant independent risk factor for predicting slow-flow/no-reflow in STEMI patients post-primary PCI.
  • MAthrombin may serve as a valuable biomarker for risk stratification in STEMI management.
Abstract

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