ASSESSMENT OF REGIONAL LEFT-VENTRICULAR WALL STRESS AFTER MYOCARDIAL-INFARCTION BY ECHOCARDIOGRAPHY-BASED STRUCTURAL-ANALYSIS

Citation
Sd. Solomon et al., ASSESSMENT OF REGIONAL LEFT-VENTRICULAR WALL STRESS AFTER MYOCARDIAL-INFARCTION BY ECHOCARDIOGRAPHY-BASED STRUCTURAL-ANALYSIS, Journal of the American Society of Echocardiography, 11(10), 1998, pp. 938-947
Citations number
55
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
08947317
Volume
11
Issue
10
Year of publication
1998
Pages
938 - 947
Database
ISI
SICI code
0894-7317(1998)11:10<938:AORLWS>2.0.ZU;2-R
Abstract
Objectives: The objective of this study was to determine the distribut ion of regional left ventricular (LV) wall stress after myocardial inf arction (MI). Background: After a large MI, structural changes occur i n the heart that ultimately may lead to alterations in LV size and sha pe, a process generally referred to as ventricular remodeling. Regiona l variation in myocardial wall stress may be responsible for initiatio n of physiologic and cellular changes that result in myocardial hypert rophy, dilatation, and remodeling after MI. Simplified geometric analy tic methods of estimating global LV wall stress cannot determine regio nal variation such as that occurring after MI. Methods and Results: To assess regional LV wall stress after MI, me applied the finite elemen t method to patient-specific end-systolic LV models generated from ech ocardiographic imaging. After validation by comparison with analytic s olutions of LV wall stress in idealized ventricles, LV models were con structed from rotated orthogonal apical images from 13 normal voluntee rs, 16 patients with recent (<4 days) anterior MI, and 7 patients with recent infero-posterior MT. The mean Von Mises stress was calculated for the entire LV and for 5 separate regions of the LV. Von Mises LV w all stress was increased globally in patients with anterior MI(211 +/- 46 kdyne/cm(2); P < .002) or infero-posterior MI (175 +/- 23 kdyne/cm (2); P = .04) compared with normal patients (144 +/- 57 kdyne/cm2). Gl obal wall stress correlated directly with ejection fraction (P < .0001 ) and inversely with wall motion index (P < .004) in patients with ant erior MI. Wall stress in the apical regions was increased by a factor of 2.3 in patients with anterior MI (P < .0001), whereas other regions did not differ from normal patients. There were no individual regions that were significantly different from normal in patients with infero -posterior MI. Conclusions: Anterior MX is associated with an increase in apical end-systolic wall stress compared with normal and infero-po sterior MI. This may be an important stimulus for LY remodeling after anterior MI.