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The pathophysiology of peri-operative myocardial infarction

B M Biccard1, R N Rodseth

  • 1Department of Anaesthetics, Nelson R Mandela School of Medicine, University of KwaZulu-Natal, Inkosi Albert Luthuli Central Hospital, South Africa. biccardb@ukzn.ac.za

Anaesthesia
|June 10, 2010
PubMed

Insights

Myocardial oxygen supply-demand imbalance, not plaque rupture, is the main driver of early peri-operative myocardial infarction. Future research should focus on predicting and treating flow stagnation and thrombus formation.

Area of Science:

  • Cardiology
  • Cardiovascular Surgery
  • Critical Care Medicine

Background:

  • Peri-operative myocardial infarction (PMI) is a significant complication.
  • Plaque rupture and myocardial oxygen supply-demand imbalance are considered equal contributors to PMI.

Purpose of the Study:

  • To critically analyze data on PMI etiology.
  • To determine the predominant mechanism of early postoperative myocardial infarction.

Main Methods:

  • Review of post-mortem data.
  • Analysis of pre-operative coronary angiography and non-invasive investigations.
  • Evaluation of troponin surveillance and peri-operative hemodynamic predictors.

Main Results:

  • Myocardial oxygen supply-demand imbalance is predominant in the early postoperative period.
  • Flow stagnation and thrombus formation are key pathways in PMI.
  • Plaque rupture is a more random event throughout the peri-operative period.

Conclusions:

  • Myocardial oxygen supply-demand imbalance is the primary cause of early PMI.
  • Therapeutic interventions should target flow stagnation and thrombus formation.
  • Plaque rupture's role is less significant in the early postoperative phase.
Abstract

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