Abstract
ness during the healing phase of AM1 remains undefined. Recently, infarct expansion has been postulated as an important mechanism underlying acute cardiac failure after infarction.4 Such thinning and dilatation of infarcted myocardium, if it were to occur early in the course of ibuprofen therapy before collagen deposition, could result in a scar that is mechanically weakened.’ Although we observed a recent increase in the incidence of postinfarction VSD, we have no conclusive proof that a causal relationship exists between ibuprofen therapy and impaired scar formation in the 3 of 4 patients who were receiving this nonsteroidal antiinflammatory agent after AMI. The dose of ibuprofen administered to our patients is similar to the high-dose regimen used in the experimental study by Brown et a1.l In summary, we suggest the possibility that ibuprofen may have played a role in the pathogenesis of post-AM1 ventricular septal rupture in the cases we report. Because no data indicate that salicylates impair scar formation after AMI, salicylates probably should remain the preferred antiinflammatory agent for treatment of postinfarction pericarditis if symptoms are sufficient to warrant such therapy.
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