gms | German Medical Science

Question: Experiments using coronary artery occlusion to produce partial-thickness ischemia in dogs have shown both ST-segment depression and elevation in overlying epicardial leads. Recent computer simulations with realistic anisotropic models predict local epicardial ST elevation and remote depression [Ref. 1]. Changes in tissue conductivity modify the ST deviation pattern [Ref. 2]. Reperfusion after ischemia is followed by a redistribution of connexins towards the lateral sides of the myocytes. It is not known if the "lateralized" connexins form gap junctions. If they do, anisotropy of intracellular conductivity would be reduced. We hypothesized that this change of conductivity would account for local epicardial ST depression during a subsequent ischemia.

Method Used: A computer model of the human heart and torso was used to compute differences between ST and TQ segment potentials on the epicardial and thoracic surfaces. The model included a realistic cardiac anatomy, anisotropic ventricles with transmural fiber rotation, ventricular blood, and thoracic inhomogeneities. ST deviation patterns were computed for normal and reduced intracellular anisotropy ratio, the latter representing gap junctional remodeling.

Results: The assumedly normal conductivity values lead to ST elevation on the epicardium and in surface leads overlying the ischemia. However, a reduced intracellular anisotropy would lead to ST depression in the same region.

Conclusion: Connexins are lateralized following reperfusion. Our results show that, if lateralized connexins form sufficient gap junctions, this would influence ST deviation during a subsequent ischemia. This effect could account for local epicardial ST depression. Direct measurements of the changes in anisotropic bidomain conductivities are needed to validate this hypothesis.