[Left ventricular remodelling and rebuilding of the infarcted area. Morphometric evaluation of the relationships between left ventricular mass, myocyte diameter, capillary density and fibrosis].

Unlabelled: The aim of the study was to assess the structural changes in both the infarcted region and free left ventricular (LV) wall that underly post-infarct LV remodeling in the human heart.

Material And Methods: Morphometric evaluation was performed in 31 human hearts, as follows: group I (control)--non-cardiac death (mean age: 52.4 +/- 11.2) and group II--post-Q-wave myocardial infarction (QMI) death (mean age: 58.8 +/- 9.4). The following morphological parameters were assessed: LV mass, infarct scar extent, stenosis of the infarct-related artery (IRA), myocyte diameter, myocyte nuclear diameter, myocyte nuclear density, density of the coronary network and LV fibrosis. Morphometric measurements were performed with the use of digital image analyser Leica Q500MC.

Results: A significant increase in the LV mass was noted in group II in comparison with the control group (296.0 +/- 81.3 g vs 150.2 +/- 18.6 g; p < 0.00001). LV hypertrophy was associated with: an increase in the myocyte diameter within the infarcted region (increase 61%) and free LV wall (increase 35%), an increase in the myocyte nuclear diameter (increase 28.1% and 11.2%, respectively), a reduction in the myocyte nuclear density (increase 52.9% and 34.4%, respectively), a reduction in the capillary density (48.6% and 4.1%, respectively) and an increase in fibrosis within the free LV wall. Significant linear relationships were observed within the free LV wall between: LV mass and myocyte diameter (r = 0.695; p < 0.001), infarct size and myocyte diameter (r = 0.451; p = 0.046), myocyte diameter and myocyte nuclear diameter (r = 0.551; p = 0.021), myocyte diameter and miocyte nuclear density (r = -0.542; p = 0.011) and miocyte diameter and capillary density (r = -0.569; p = 0.009). Such relationships were not observed within the infarcted area. Conversely, significant relationships between a reduction in the capillary density and IRA stenosis (r(s) = -0.512; p = 0.03) as well as the infarct size (r = -0.616; p = 0.006) were noted.

Conclusions: 1. Left ventricular remodelling post myocardial infarction is a heterogenous process and the observed differences are mainly quantitative in character; 2. Compensatory left ventricular hypertrophy dominates in the areas not affected by necrosis. Rebuilding of the infarcted area is constrained mainly by the changes in the capillary network and depends on the IRA status.