Mechanisms of cardiac regeneration following a transmural myocardial infarction were analysed in rat hearts using immunohistochemistry for α-SMA, caspase-3, Ki-67, PGP 9.5, TH and nestin markers. Seven weeks after experimental myocardial infarction, two different types of healing processes were revealed: with and without aneurysmatic bulging of the left ventricular wall. Besides thinning of the ventricular wall, three distinct zones characterized both types of scars: the central scar zone, the peri-infarct zone and the border zone. The presence of a central necrotic zone was found inside the aneurysmatic wall, while connective tissue with myofibroblasts was found in the same zone within non-bulging wall. Apoptotic caspase-3 positive cells were found in the granulation tissue of the border zone in aneurysmatic scar, while in non-bulging scar they characterized all three zones. Proliferating Ki-67 positive cells displayed reverse expression pattern compared to apoptotic cells. Quantification of α-SMA positive cells revealed 60% α-SMA positive cells inside the central part of the non-bulging scar zone but only 30% in the peripheral part. The aneurysmatic scar had 39% of myofibroblasts distributed in invaginating areas of peri-infarct zone, versus 19% in non-invaginating areas. The difference in number or distribution of TH and PGP 9.5 positive cells in these two groups was not found. Nestin positive cells were detected in both types of scars, but with distinctly different distribution. These results suggest that even seven weeks after myocardial infarction, the healing processes in non-bulging scars are in chronic phase, while aneurysmatic scars are still in subacute phase. Histological differences in scar healing appear to be important for functional properties of the heart wall and have prognostic value in heart recovery prognosis.