Infarction

‘Turning the right screw’: targeting the interleukin-6 receptor to reduce unfavourable tissue remodelling after myocardial infarction

Möllmann H et al. Cardiovasc Res (2010) 87(3): 395-396 first published online June 16, 2010 doi:10.1093/cvr/cvq186 - Click here to view the abstract

Partial overview of targets and mechanisms involved in LV remodelling after myocardial infarction (MI). Early inhibition of IL-6 signalling using an anti-IL-6 receptor antibody (M16-1) leads to decreased mortality after MI, mainly through reduction of inflammation and extracellular matrix remodelling of the healthy surrounding myocardial tissue. Infarct size and apoptosis were not altered by interference with IL-6 receptor signalling.

Vicious relationship between wall stress and ventricular remodelling to aggravate postinfarction heart failure

Takemura G et al. Cardiovasc Res (2009) 83(2): 269-276 first published online January 28, 2009 doi:10.1093/cvr/cvp032 - Click here to view the abstract

(A) Transverse ventricular sections taken from mouse hearts on Day 3, 7, or 28 postinfarction and stained with Masson's trichrome. Left ventricular remodelling progresses with time following myocardial infarction (MI). (B) Photomicrographs of infarct tissue collected from mouse hearts on Day 3, 7, or 28 post-MI, showing, respectively, acute inflammation, granulation, and scar. (C) With the passage of time after the onset of MI, the infarct length and left ventricular cavity become larger, whereas the infarct wall thickness decreases. Wall stress is proportional to the cavity diameter and intracavitary pressure and inversely proportional to the wall thickness (Laplace's law). Thus, wall stress and ventricular remodelling (dilatation and wall thinning) have a vicious relationship, aggravating one another and exacerbating post-infarction heart failure.