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Forty-four cases of myocardial infarction with cardiac rupture, 88 cases of unruptured myocardial infarction, and 88 cases without myocardial infarction were studied retrospectively. The incidence of cardiac rupture in cases with acute myocardial infarction alone was 5.5% while in hearts having both healed and acute myocardial infarction the incidence was 2.3%. One instance of cardiac rupture was encountered in a heart having only a healed myocardial infarction with subsequent aneurysmal dilation of the healed infarct. Although females represented only 37% of the population having acute myocardial infarction in this institution, they accounted for 55% of the cases of cardiac rupture. On the average the hearts which ruptured following myocardial infarction were lighter and thinner than in the control group of patients having infarction without rupture. Among the clinical correlates possibly associated with postinfarction rupture the most significant finding in the present study is the presence of postinfarction hypertension. In the group of cases with cardiac rupture this was present in 40% while in the control group not having suffered cardiac rupture the comparable figure was 14%. A history of diabetes was found in 18% of the cases of myocardial infarction not having suffered cardiac rupture. A similar history was found in only 9% of the cases having a postinfarction cardiac rupture. This latter incidence is identical with the frequency of diabetes mellitus in the general autopsy population. There is a suggestion that early and severe atherosclerosis may cause earlier heart disease and when infarction occurs provide some protection against rupture. Of interest among the 44 cases of cardiac rupture, none of the patients had cirrhosis, in striking contrast to the 11% incidence of this condition in our general autopsy population.

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Sunitinib appears to target the cytosolic MEK/ERK and SAPK/JNK pathways in the RET/PTC1 cell lines, suggesting that blocking these pathways is at least part of the mechanism by which sunitinib inhibits cell proliferation and causes stimulation of NIS gene expression in RET/PTC1 cells.