Relation of early mononuclear and polymorphonuclear cell infiltration to late scar thickness after experimentally induced myocardial infarction in the rat

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Abstract
This report describes the relationship between the intensity of early inflammation after acute myocardial infarction and the later thickness of the left ventricular (LV) scar. Histologic sections of hearts from methylprednisolone-treated (MP), cobra venom factor-treated (CVF), and untreated control rats that had been subjected to either 2 or 21 days of coronary artery occlusion were studied. In the rats examined at 2 days (n=20 for MP, n=16 for CVF, and n=20 for controls), a semiquantitative inflammation score (1–4) was attributed to each infarct. Mononuclear (MN) cells were counted in 4 oil-immersion fields per section and polymorphonuclear (PMN) cells in 9 oil-immersion fields per section. In the rats examined at 21 days (n=22 for MP, n=22 for CVF, and n=26 for controls), the thickness of the LV scar was measured every 1.6 mm along its circumference. Inflammation scores at 2 days were 3.5±.6 for controls, 1.5±.5 for MP, and 2.9±.8 for CVF (p<.05 among groups). The MN cells counted were 73±7 for controls, 47±5 for MP, and 61±9 for CVF (p<.05 among groups). There was no difference in PMN infiltrate among groups. Scar thickness at 21 days were .9±.1 mm for controls, .7±.1 mm for MP, and .9±.1 mm for CVF (MP compared to CVF and controls, p<.01). Thus, a severe reduction in early MN cell infiltration was associated later with thinner LV scars, while a moderate reduction did not alter scar formation. Furthermore, though MN cell infiltration was suppressed by MP and CVF, PMN cell infiltration was unaffected.