Biomechanical modeling of hemodynamic factors determining bulging of ventricular aneurysms

Ventricular aneurysm formation is a frequent complication of transmural myocardial infarction. The hemodynamic determinants of aneurysmal bulging remain unclear.

A rubber heart placed in a water tank served as an in vitro model. Rhythmic injections of specific volumes into the tank simulated heart beats. The heart rate was adjustable in increments. A section of the heart model's wall was shielded from compression to simulate an aneurysm. To quantitate the relation between hemodynamics and bulging, pressures, echocardiographic measurements of maximal expansion, and mean velocity were recorded. Bulging volume, stroke volume, aneurysmal wall stress, and systemic resistance were calculated.

The mean velocity was the echocardiographic factor most closely related to bulging volume (r = 0.92, p < 0.01). When bulging indices were compared with hemodynamics, bulging volume and mean velocity were found to directly depend on heart rate (r = 0.66, p < 0.01; r = 0.70, p < 0.01). Polynomial regression revealed bulging volume to reach minimal values near 80 beats/min. Maximal systolic aneurysmal wall stress was closely related to the peak positive rate of pressure change (r = 0.94, p < 0.01) and moderately to stroke volume (r = 0.75, p < 0.01). Filling pressures were unrelated to bulging. The greatest bulging volume reduction occurred below 790 dynes x s x cm(-5); bulging was practically eliminated at systemic resistance values less than 395 dynes x s x cm(-5).

Aneurysmal bulging and aneurysm formation depend mainly on heart rate, contractility, and afterload. This suggests that hemodynamic management may affect the extent of bulging in a clinical setting.