Increased afterload aggravates infarct expansion after acute myocardial infarction

Arter acute transmural myocardial infarction, the heart may undergo major remodeling characterized by thinning and dilation of the infarct zone and overall enlargement of the heart. The effect of increased left ventricular pressure on infarct expansion and the extent to which it alters postinfarction remodeling were studied in a rat model. Rats with either aortic banding or a sham operation and a survival period of 3 weeks were further randomized to sham thoracotomy or left coronary ligafion. Surviving rats were killed 7 days later and the hearts were fixed in diastole for morphologic analysis. Hearts with aortic banding had a mean peak to peak gradient of 20.7 ± 4.9 mm Hg across the aortic band at death and a significantly thicker heart than that of the comparison group without an aortic band. Infarct size, as a percent of total left ventricular mass, at the time of death was less in the group with aortic banding, yet infarct expansion was more marked. However, when original infarct size was estimated taking into account the effects of aortic banding, scar formation, infarct expansion and infarct-induced hypertrophy, it was found to be similar in both infarct groups (45.50 ± 4.2 versus 47.90 ± 3.1%). Infarct expansion, as measured by cavity dilation and infarct thinning, occurred in both infarct groups but was greater in the group with aortic banding. Cavity volume was 121.35 ± 17.3 mm³ in the infarct group and 150.72 ± 18.6 mm³ in the aortic band/infarct group (p = 0.05) compared with 64.33 ± 8.89 mm³ in the sham rats and 65.24 ± 5.54 mm³ in the rats with aortic banding alone. Infarcts were also thinner in the rats with an aortic band compared with those without a band (1.09 ± 0.03 versus 1.37 ± 0.09 mm, p = 0.02) and these wall dimensions were significantly thinner than comparable regions in either control group (2.25 ± 0.10 and 2.61 ± 0.12 mm). Thus, chronic increases in afterload caused by aortic banding, sufficient to produce left ventricular hypertrophy, were associated with increased infarct expansion, suggesting that intraventricular cavity pressure is an important determinant of the detrimental shape change that may occur after transmural infarction.