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This editorial refers to 'Plasma matrix metalloproteinase- 9 and left ventriclar remodelling after acute myocardial infarction in man: a prospective cohort study ' by Kelly et al., doi:10.1093/eurheartj/ehm003 In basic science research laboratories dedicated to heart failure, several substances have been studied as candidate markers of the disease's severity, as target of therapy and as indicators of therapheutical success. Many potential bio- logical markers have emerged and are now under research, among which, markers of myocyte injury (e.g. troponins), markers of inflammation (e.g. tumour necrosis factor a, IL-6), markers of oxidative stress (e.g. urinary byopyrrins), markers of sodium pump activity (e.g. caridiotonics steroids), and a separate group of peptides associated with heart failure.1 However, at present, only natriuretic pep- tides, in particular, B-type natriuretic peptide, has an estab- lished clinical impact. Several reasons account for the frequent failure for substances under research to reach clinical laboratories including the multifactorial causes of heart failure and its progression, the capability/willingness of the manufacturing companies to push, costs and cultural background. Matrix metalloproteinases (MMPs) have a strategic role in the regulation of extracellular collagen matrix turnover, a slow process (t1/2 around 25 days) which, in the heart, is crucial for keeping the most efficient shape of the ventri- cles. Cardiac repair after a myocardial infarction is a highly complex process that involves temporarily overlap- ping phases which comprehend inflammation, new tissue formation, and tissue remodelling.2 MMPs are present in the myocardium, are capable of degrading all the matrix components of the heart, and are the driving force behind myocardial matrix remodelling which is responsible for the progressive worsening of the pump function.3 Considering that the remodelling phenomenon represents an indepen- dent adverse prognostic factor affecting mortality and pro- gression of heart failure, it would make complete sense to correlate the degree of disruption of the extracellular matrix and its turnover with the circulating levels of MMPs. Accordingly, there is a strong rationale to use MMPs as the substances to follow and to foresee ventricular remo- delling, and possibly, to understand if a specific treatment is efficient in the single patient. For example, the efficacy of beta-blockers or ACE-inhibitors in the prevention of post- myocardial infarction ventricular remodelling. Furthermore, it has been proposed that antagonists of MMPs might be used to prevent ventricular remodelling. The real picture, however, is much more complicated and unlikely to provide us with the above reported hopes, at least in the near future. Indeed, left ventricle regional remodelling is a continuous process that lasts for months to years after the injury, and which will, eventually, lead to the development of heart failure.4 Moreover, post-

Matrix metalloproteinase and heart failure: is it time to move from research to clinical laboratories?