A whole heart model with finite growth for hypertension-induced pathologies
Résumé
Heart failure (HF) is a leading cause of morbidity and has a 5-year mortality rate of 50%. Up to 70% of all HF conditions are of ischemic origin and all systolic HF conditions involve some degree of myocardial ischemia, in which there is a mismatch between coronary blood supply and myocardial demand. The incidence of advanced HF continues to increase despite considerable progress in medical management and the more recent development of devices for treating HF. For end-stage HF, heart transplantation or mechanical assist devices are the only viable options. Although current devices and therapies are useful, early diagnosis is most effective for long-term outcome. Clearly, early diagnosis and prediction of propensity to HF can stratify susceptible patients for preventative medical therapy, including treatment of co-morbidities, to combat this health care epidemic [1]. In this work, we investigate the role of multiple growth mechanisms in disease progression and ventricular mechanics. More precisely, we study longitudinal and transverse growth in systemic and pulmonary hypertension-induced hypertrophy. For this, we use the finite growth theory [2], [3], and the Living Heart Project's whole heart model [4].
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