Reply to “Ventricular remodelling following acute myocardial infarction: The role of altered collagen homeostasis"

Abstract

We agree with Turhan and colleagues that the results from our clinical observational study are consistent with other works on collagen metabolism following infarction [1]. They highlight the importance of matrix metalloproteinase (MMP) activity in collagen homeostasis. While we agree that MMPs strongly influence collagen and matrix activity, attempts to attenuate this process have yielded conflicting results. Indeed, Hudson et al. recently reported that selective MMP inhibition fails to reduce LV remodeling post infarction [2]. We believe that this illustrates the complexity of the relationship between the MMP/TIMP system and collagen homeostasis. Turhan and colleagues criticise the “heterogenous study groups”, but this was a “real world” study, examining patients presenting early with typical presentation of myocardial infarction and ECG criteria for thrombolysis. The fact that the findings remain robust despite this heterogeneity supports the utility of serological markers of collagen metabolism in identifying those at risk of remodeling. We chose wall motion index as a dichotomous variable due to the fact that this is a powerful predictor of subsequent remodeling and mortality [3], rather than dividing the patients by site of infarct. However, we agree that anterior infarction is likely to be associated with abnormal wall motion and increased CITP and indeed, our study supports this (there were more anterior infarcts in the abnormal wall motion group 39% vs. 18%). Turhan and colleagues also state that it is not possible to see normal wall motion index