Altered left ventricular geometry changes the border zone temporal distribution of stress in an experimental model of left ventricular aneurysm: a finite element model study.
BACKGROUND
Left ventricular aneurysm (LVA) is a significant complication of myocardial infarction that may lead to global left ventricular (LV) dysfunction. However, the exact mechanism underlying the abnormal function has not been elucidated. In this study we tested the hypothesis that changes in LV geometry cause both an increase in wall stress and a change in the temporal distribution of stress in the LVA border zone (BZ) during systole.


METHODS
Transmural anteroapical infarcts were created in adult Dorsett sheep (n=8) and were allowed to mature into LVAs for 10 weeks. Animals were imaged subsequently using MRI with simultaneous recording of intraventricular pressures. Cardiac models were constructed from the MRI images at end-diastole, isovolumic systole, peak-systole and end-systole. Two short-axis slices, 1 basal and 1 apical were analyzed. The apical slice included the septal and anterior component of the aneurysm as well as the corresponding BZs and normal myocardium. Regional wall stresses were calculated using finite element analysis and compared with stresses in corresponding regions from normal control sheep (n=7).


RESULTS
In the LVA group, stress was significantly increased in the BZ at the end-diastolic, isovolumic, peak-systolic, and end-systolic instants (P<0.001 for all). In addition the temporal distribution of stress was significantly altered with maximum stress occurring at peak instead of isovolumic systole.


CONCLUSIONS
Geometric changes in the LVA hearts increased wall stress and altered its temporal distribution in the BZ region. Correlation of this finding with the corresponding regional blood flow, oxygen consumption, and mechanical systolic performance may help elucidate the mechanism underlying the observed global LV dysfunction.
D000818:Animals; D020342:Finite Element Analysis; D006322:Heart Aneurysm / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D006439:Hemodynamics; D007700:Kinetics; D008279:Magnetic Resonance Imaging; D008962:Models, Theoretical; D009203:Myocardial Infarction / Q000150:complications; D012756:Sheep; D013314:Stress, Mechanical; D013599:Systole; D020257:Ventricular Remodeling