Prevention of ventricular remodelling post myocardial infarction: timing and duration of therapy.
OBJECTIVE
To review the evidence for the temporal pathophysiological evolution of structural, topographic and functional changes during remodelling post infarction, and how the timing and duration of therapeutic interventions for limiting remodelling might influence outcome.


METHODS
Published English language literature.


METHODS
The focus was on experimental and clinical studies relating to modification of post infarct remodelling as well as pertinent clinical trials with clinical outcome and mortality end-points.


METHODS
An objective determination of the timing and duration of therapy from the indexed infarction, and the rationale for the approach and its possible relation to measured outcome parameters.


RESULTS
Several strategies targeted to salvage ischemic myocardium and unload the left ventricle have proven effective in limiting remodelling. Because remodelling begins very early and is a staged and progressive pathophysiological process, timing and duration of therapy are likely to have a profound effect on outcome. Different outcomes can be expected depending on whether therapy is begun very early (during the infarction process), early (after completion of the infarction process but before significant deposition of infarct collagen has occurred), late (after infarct collagen has peaked and infarct healing is completed) or very late (after healing is completed). Different outcomes can also be expected with therapy that spans one or more of these stages. Maximum benefit might be expected from therapy that is begun very early, spans the entire healing process and extends beyond. Two-dimensional echocardiograms can be used to assess the impact of therapies on remodelling and function. Very early thrombolysis and low dose intravenous nitroglycerin followed by prolonged angiotensin-converting enzyme inhibition and/or nitrate appear to be a very promising algorithm.


CONCLUSIONS
The optimal therapeutic strategy for limiting post infarct remodelling should recognize the pathophysiological staging of the process and be targeted at preventing infarction, early expansion and progressive dilation.
Jugdutt
B I
BI
Department of Medicine, University of Alberta, Edmonton.
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D002216:Captopril / Q000627:therapeutic use; D006801:Humans; D009203:Myocardial Infarction / Q000188:drug therapy / Q000503:physiopathology*; D015425:Myocardial Reperfusion; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control; D009206:Myocardium / Q000473:pathology*; D005996:Nitroglycerin / Q000627:therapeutic use; D013997:Time Factors; D016277:Ventricular Function, Left / Q000502:physiology*
D000806:Angiotensin-Converting Enzyme Inhibitors; D002216:Captopril; D005996:Nitroglycerin