Abstract
Introduction: Computational modeling of cardiac mechanics and hemodynamics in ischemic heart disease (IHD) is important for a better understanding of the complex relations between ischemia-induced heterogeneity of myocardial tissue properties, regional tissue mechanics, and hemodynamic pump function. We validated and applied a lumped two-compartment modeling approach for IHD integrated into
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the CircAdapt model of the human heart and circulation. Methods: Ischemic contractile dysfunction was simulated by subdividing a left ventricular (LV) wall segment into a hypothetical contractile and noncontractile compartment, and dysfunction severity was determined by the noncontractile volume fraction ((Formula presented.)). Myocardial stiffness was determined by the zero-passive stress length ((Formula presented.) and nonlinearity ((Formula presented.)) of the passive stress-sarcomere length relation of the noncontractile compartment. Simulated end-systolic pressure volume relations (ESPVRs) for 20% acute ischemia were qualitatively compared between a two- and one-compartment simulation, and parameters of the two-compartment model were tuned to previously published canine data of regional myocardial deformation during acute and prolonged ischemia and reperfusion. In six patients with myocardial infarction (MI), the (Formula presented.) was automatically estimated using the echocardiographic LV strain and volume measurements obtained acutely and 6 months after MI. Estimated segmental (Formula presented.) values at the baseline and 6-month follow-up were compared with percentage late gadolinium enhancement (LGE) at 6-month follow-up. Results: Simulation of 20% of (Formula presented.) shifted the ESPVR rightward while moderately reducing the slope, while a one-compartment simulation caused a leftward shift with severe reduction in the slope. Through tuning of the (Formula presented.), (Formula presented.), and (Formula presented.), it was found that manipulation of the (Formula presented.) alone reproduced the deformation during acute ischemia and reperfusion, while additional manipulations of (Formula presented.) and (Formula presented.) were required to reproduce deformation during prolonged ischemia and reperfusion. Out of all segments with LGE>25% at the follow-up, the majority (68%) had higher estimated (Formula presented.) at the baseline than at the follow-up. Furthermore, the baseline (Formula presented.) correlated better with percentage LGE than (Formula presented.) did at the follow-up. Conclusion: We successfully used a two-compartment model for simulation of the ventricular pump and tissue mechanics in IHD. Patient-specific optimizations using regional myocardial deformation estimated the (Formula presented.) in a small cohort of MI patients in the acute and chronic phase after MI, while estimated (Formula presented.) values closely approximated the extent of the myocardial scar at the follow-up. In future studies, this approach can facilitate deformation imaging–based estimation of myocardial tissue properties in patients with cardiovascular diseases.
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