Identification of patients prone to infarct expansion by the degree of regional shape distortion on an early two–dimensional echocardiogram after myocardial infarction

Abstract

Summary:Early detection of potential expanders (patients who develop clinically significant infarct expansion with acute left ventricular (LV) dilatation and failure but no necrosis) after acute myocardial infarction (AMI) is necessary in order to apply preventive therapy. To determine whether the degree of regional shape distortion (RSD), or dilatation, on early two-dimensional echocardiogram (2-D echo) after AM1 can identify potential expanders, serial clinical and echocardiographic data were studied prospectively in 244 consecutive patients with a first Qwave AMI. Initial (mean 2 days) and final (mean 10 days) two-dimensional echocardiograms were compared for regional LV asynergy, RSD, and conventional indices of expansion measured on endocardial diastolic outlines of mid-LV short-axis sections. Analysis of clinical and 2-D echo data revealed 5 1 expanders and 193 nonexpanders. Expanders showed greater LV dysfunction and more inhospital deaths (27% vs. 8%. pcO.001) compared with nonexpanders; conventional indices of expansion showed more marked increase between initial and final twodimensional echo in expanders, but initial indices were not predictive. In contrast, the new RSD index Pk, a Supported in part by a grant from the Canadian Heart Foundation, Ottawa. measure of the outward bulge, was markedly greater in expanders than nonexpanders on both initial (16.5 vs. 2.4 mm, p c 0.001) and final echo. Furthermore, expanders with z 30% increase in P k (to 21 mm) developed rupture of the ventricular septum (n = 10) or free wall (n =2). Also, 50 of 5 1 expanders compared with 3 of 193 nonexpanders had a Pk 2 10 mm on the initial echo. A simpler index, the depth of RSD (rd), provided similar discrimination as Pk. Thus, the degree of diastolic RSD on an early 2-D echo after AM1 can identify potential expanders. Rtsented in part at

Ventricular Remodeling After Infarction and the Extracellular Collagen Matrix

“…7 Several studies suggested potentially harmful effects with some therapies after MI, 7,13,28,50 -52 supporting caveats against hypotension with vasodilators very early after MI, 50 or impairing healing with powerful anti-inflammatory drugs during early healing. 51 Other post-MI studies demonstrated progressive LV enlargement over 1 year 7,16 or 3 years 52 despite therapy, and morbidity and mortality remain high. 53 In addition, cardiac rupture remains a major cause of death after reperfused MI, 7,39 and the number of post-MI patients needing the LV assist device or awaiting transplantation is increasing, suggesting that protection against LV dilation, adverse ECCM remodeling, decreasing IZ collagen, and impairing healing is needed.…”

“…First, the LV remodeling process after MI is complex, dynamic, and time dependent, and progresses in parallel with healing over months. 1,2,7,16 Notably, it involves differential changes between the IZ and NIZ with respect to the following: (1) LV structure, shape, and topography 1,2 ( Figure 1); (2) cell type, such as myocytes and nonmyocytes (Table 1) 6,7,[17][18][19][20][21][22][23] ; (3) proteins, cytokines, and growth factors 7,24,25 ; and (4) the ECCM. 5-7,13-17,19 -23 Differential regional remodeling of the ECCM contributes significantly to global LV structural remodeling after MI ( Figure 2) 7,9,26 and plays a pivotal role in paradigm 1.…”

“…2 Sequential changes during LV remodeling after MI (Figure 1) span the phases of acute MI, healing, and repair over weeks to months (Figure 2) and beyond. 1,2,16 Because mechanical deformation forces and increased wall stress act on the IZ and NIZ throughout these phases, thereby promoting progressive LV dilation 1,2,7 and stimulating fibrosis, 6,7 early and prolonged antiremodeling therapy is favored.…”

Effect of prolonged nitrate therapy on left ventricular remodeling after canine acute myocardial infarction.

“…Seventy-five healthy mongrel dogs (weight, 16 to 29 kg) of either sex were instrumented through a left lateral thoracotomy under general anesthesia (sodium pentobarbital, 30 mg/kg IV), as described previously. 25 (11 control, 11 nitrate).…”

Infarct-Related Artery Patency and Long-Term Effects on Left Ventricular Remodelling

“…Nevertheless, a variety of potential tar gets for limiting postinfarct remodelling has been identi fied (table 1) [81], It is clear that a successful strategy is likely to involve a combination of interventions that pro vide additive, or even synergistic, benefits by altering one or more factors that influence infarct remodelling (ta ble 2) [81], For the primary prevention of cardiac remod elling, the optimal strategy based on current evidence should involve intervention that is instituted very early after the initial event, spans the entire healing process and continues well beyond [81]. A secondary prevention strat egy is also warranted for the early identification and treat ment of patients who already show evidence of cardiac remodelling after AML 32 Cardiology 1997:88(suppl 1 ):26-35 V isser…”