Post myocardial infarction left ventricular dysfunction – Assessment and follow up of patients undergoing surgical ventricular restoration by the endoventricular patchplasty

Authors of this important article by D'Mello et al, have nicely presented a prospective study of clinical and echocardiographic follow up of Left Ventricular (LV) geometry of 59 consecutive patients with previous transmural anterior myocardial infarction, who underwent LV restoration, analyzed between June 2007 and May 2008.1 The authors are to be complemented for this important series which showed excellent immediate and short-term results following LV restoration surgery. The results show a progressive remodeling after ventricular reconstruction mainly by excluding the scar area. Volume reduction is more important than the post surgical shape of the ventricle. The study was done before the MRI era; and hence the images of the scar are not demonstrated in the study.2,3 Analysis of the precise mechanism of remodeling is perhaps not possible without MRI. Distinction between dyskinetic and akinetic forms of the scar are not clearly brought out; it is usually transmural with dyskinesia and subendocardial with akinesia. The size of a synergy and its extension determine the extent of remodeling.4,5 It is surprising that these 59 patients were not severe cases of ischemic failing ventricle, as the mean ejection fraction was 33.5 ± 5%, preoperative end diastolic volume index 89.7 ± 6 and end systolic volume index 48.8 ± 11.3 which are below the threshold of very severe cardiac failure. White et al have given a figure of >60 ml of end systolic volume index as the major determinant of survival after recovery from myocardial infarction.6 This work is indeed of great interest and I hope the authors with their experience will present more severe cases showing a positive interest in LV reconstruction and thereby demonstrating that the S.T.I.C.H trial was a miss organized trial.7 The global approach of heart failure by Buckberg cannot be accepted; it is apparent that Buckberg is a prisoner of his “flying fancies” trying to establish something without any serious base.7 The myocardial systolic contraction is a “twist up” like a “snake” ascension. The crux of the problem of systolic heart failure is the ventricular spherical dilatation whatever be the anatomic substrate. The surgical ventricular restoration (S.V.R) or surgical anterior ventricular restoration (S.A.V.R) are acronyms in place of left ventricular reconstruction (L.V.R.) because this technique is applied most of time only for anterior LV wall, with the objective of “volume reduction” and to get an elliptical shape of LV. Finally, I would like to emphasize the following points: Ventricular wall has a systolic concentric (centripetal contraction) confirmed by MRI video examination of left ventricular wall in 4 projections.8 Heart failure is not an entity but a syndrome with various causes; in post myocardial infarction failure, the cause is an extension of the necrotic, then fibrous and finally calcified transmural or subendocardial scar, when it reaches = or <30% of LV perimeter. The dilatation is not the cause, but the consequence; dilatation is more ovoid than spherical. LVR as proposed by as in 1984, have these main goals: to suppress or exclude the scarred asynergic wall, to abolish the mechanism of progressive dilatation i.e. the eccentric systolic motion, restoring the curvature of non-infarcted myocardium and maintain the physiological diastolic volume of the rebuilt cavity by balloon sizing before “clothing” of the cavity by a patch anchored on contractile edge of normal myocardium.9 In conclusion, this article by D'Mello et al demonstrates and emphasizes the modern approach toward post myocardial infarction heart failure which is a very prevalent disease encountered in day to day clinical practice.