myocardial fibrosis

Myocardial fibrosis can develop as a consequence of myocardial ischaemia and is present in 16-55% of sudden cardiac deaths (Davies and Popple 1979).


Mechanisms of myocardial ischaemia

Reduced oxygen perfusion leads to;

  • Reduced pH
  • Raised interstitial potassium ion concentration
  • Raised intracellular calcium concentration
  • Slowed conduction
  • Reduced excitability
  • Prolonged refractory period
  • Cell-to-cell uncoupling
  • Generation of spontaneous electrical activity


Risks of myocardial fibrosis

  • Predisposition to electrical instability
    • Infarcted muscle produces regional cardiac sympathetic/ parasympathetic dysfunction in the infarcted area and in regions apical to the infarct (fibres crossing infarcted area disrupted). Denervated regions are more sensitive to catecholamines, resulting in differential conduction/ refractoriness, predisposing to arrhythmias.
    • This creates regional changes in automaticity – electrical heterogeneity favouring the development of VF/ fatal arrhythmias. (Willich 1993; Lecomte 1993)


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