Role of infarct expansion in rupture of the ventricular septum after acute myocardial infarction: A two‐dimensional echocardiographic study

Abstract

Summary:To verify the role of infarct expansion (IE) in ventricular septal rupture (VSR) after transmural acute myocardial infarction (TAMI), topographic parameters were measured using tomographic imaging with twodimensional echocardiography (2-D echo) and computeraided analysis in four groups of patients: 8 patients with VSR (Group 1); 24 patients with TAMI but no mechanical complications (Group 2); 11 normal athletes (Group 3); 5 adults with congenital ventricular septal defect (Group 4). Measurements made on end-diastolic outlines of mid-left ventricular (LV) short-axis images included: LV asynergy (akinesis and/or dyskinesis), expansion index (asynergy/nonasynergy-containing endocardia1 segment length), thinning ratio (asynergichonasynergic wall thickness), and new indexes of regional shape distortion (RSD) by quantifying the deviation of the actual asynergic segment from the ideal asynergic arc constructed using the nearly circular nonasynergic contour. In Group 1, clinical IE (hypotension, congestive heart failure, no signs of new infarction) preceded detection of the VSR and portable 2-D echo showed the VSR associated with LV asynergy, marked IE, and RSD. Although Groups 1 and 2 had similar LV asynergy (28.7 vs. 26.9% LV) and ejection fraction (38.9 vs. 41.8%), Group 1 had higher expansion index (1 S O vs. 1.17, p <0.05), lower thinning ratio (0.54 vs. 0.67, p<0.005), and higher RSD parameters (e.g., peak distortion, Pk or maximum radial distance from the ideal arc, 19.3 vs. 3.9 mm, p<O.Ol; area of distortion, Ad, 7.4 vs. 1.1 cm2, pe0.05) than Group 2. Groups 3 and 4 had normal regional and global function and no evidence of expansion, thinning, or RSD. Thus, IE with marked diastolic RSD on an early 2-D echo after TAMI might identify patients at risk for VSR.

Myocardial Infarct Expansion and Matrix Metalloproteinase Inhibition

“…2,4 Moreover, similar MI size in patients was associated with post-MI LV dilation. 2,3 Therefore, in the present study, MI induction in pigs most likely recapitulated a commonly encountered clinical phenotype of post-MI remodeling.…”

“…[2][3][4][5][6] At the infarcted region, alterations in myocardial composition and structure occur after MI 6,7 and can lead to infarct thinning and expansion. 1,4 -7 Because the MMPs are enzymes that influence myocardial remodeling, 8 -16 the goal of the present study was to examine the relation between MMP activation and infarct expansion.…”

“…In the MI-only group, the wall thinning index 4,6 was 0.45Ϯ0.06 and was increased in the MIϩMMPi group (0.70Ϯ0.09, PϽ0.05).…”

“…[1][2][3][4][5][6] The summation of cellular and extracellular events that occur in the post-MI period results in changes in LV geometry and has been called "infarct expansion." [3][4][5][6] Past studies have demonstrated that a structural determinant of infarct expansion is extracellular remodeling. 1,5,6 A family of proteolytic enzymes that have been implicated in tissue remodeling are the matrix metalloproteinases (MMPs).…”

Relation of circulating interleukin‐6 to left ventricular remodeling in patients with reperfused anterior myocardial infarction

“…However, progressive remodeling of the myocardium leads to global LV enlargement, which results in congestive heart failure and subacute cardiac rupture. 3,4 There is a general consensus that large infarct size, wall stress, and overexpression of the renin-angiotensin-aldosteronesystem promote structural LV remodeling after MI, and thus, postinfarct remodeling is a complex process.…”