The aim of the study was to assess the relationship between the left ventricle (LV) hypertrophy and the effect of different morphological and clinical parameters in patients after Q-wave myocardial infarction (QMI).
Material and methods: A morphometric evaluation was performed in 21 patients after QMI (the mean age was 58.8 +/- 9.4). Samples from infarcted region and the free wall of LV obtained during autopsy were measured. Results were compared to parameters observed in the control group that comprised 10 patients who died due to non-cardiac causes (the mean age 52.4 +/- 11.2). The following morphological parameters were assessed: heart weight, LV mass, infarct scar extent, myocytes diameter, myocytes nuclei' diameter, myocytes nuclei' density, coronary capillaries density (immunohistochemical staining for CD34), LV fibrosis. Morphometric measurements were performed with the use of digital image analyser Leica Q500MC. Clinical characteristics such as patients age, duration of the disease, sex and prevalence of hypertension were also evaluated.
Results: Postmortem pathological studies showed significant increase in the LV mass in the investigated group when compared to control group (296.0 +/- 81.3 g vs. 150.2 +/- 18.6 g; p < 0.0003). LV hypertrophy was associated with different structural alterations: increase in the myocytes diameter both in the infarcted region (increase 61%) and free LV wall (increase 35%), increase in the myocytes nuclei diameter (increase 28.1% and 11.2%, respectively), reduction in the myocytes nuclei' density (decrease, 52.9% and 34.4%, respectively), reduction in the coronary capillaries density (decrease 48.6% and 4.1%; respectively) and the increase in fibrosis in the free wall of LV (increase 91%). Multiple regression analysis showed the increase in the myocytes' diameter in the infarcted region (beta = 0.355; p = 0.048) and the increase in the myocytes' diameter in the free LV wall (beta = 0.787; p = 0.015) as the only two factors affecting the degree of LV hypertrophy. A linear relationship between the LV mass and the increase in the myocytes' diameter was observed only in the free LV wall (r = 0.695; p < 0.001). Moreover, the increase in myocytes' diameter within the free wall of LV correlated to the infarct scar extent (r = 0.451; p = 0.046).
Conclusions: (1) Compensatory increase in the LV mass following MI is proportionate to the loss of contractility of necrotic myocardium. (2) Increase in the LV mass that occurred after MI is mainly determined by the degree of myocytes' hypertrophy. The significance of correlations between the two parameters depends on the myocytes location (free wall of LV vs. infarcted region).