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)
references
- Davies MJ, Popple A. Sudden unexpected cardiac death – a practical approach to the forensic problem. Histopathology. 1979; 3:255-277
- Lecomte D, Fornes P, Fouret P, Nicolas G. Isolated myocardial fibrosis as a cause of sudden cardiac death and its possible relation to myocarditis. Journal of Forensic Sciences. 1993; 38(3): 617-621
- Willich SN, Maclure M, Mittleman M et al. Sudden cardiac death – support for a role of triggering in causation. Circulation 1993 87(5):1442-1450