Key result
Midventricular obstruction increased maximum myofiber stress on the apical wall by 75.0% compared to subaortic obstruction (654.5 kPa vs. 373.9 kPa), suggesting a mechanical mechanism for apical aneurysm formation.
Why the study?
Apical aneurysm is associated with midventricular obstruction in hypertrophic cardiomyopathy, but the biomechanical mechanisms behind its genesis remained unclear.
Does midventricular obstruction increase apical myofiber stress compared to subaortic obstruction or healthy models in hypertrophic cardiomyopathy?
Does midventricular obstruction increase apical myofiber stress compared to subaortic obstruction or healthy models in hypertrophic cardiomyopathy?
Effect estimate: 75.0% increase
Absolute Event Rate: 654.5% vs 373.9%
p-value: p=0.014
Numerical simulations suggest that high myofiber stress on the apical wall caused by midventricular obstruction may initiate the formation of apical aneurysms in hypertrophic cardiomyopathy.
Hypothesis-generating for mechanical stress triggering apical aneurysms in midventricular HCM; prospective validation required before clinical consideration.
Apical aneurysm was observed to be associated with midventricular obstruction (MVO) in hypertrophic cardiomyopathy (HCM). To investigate the genesis of the apical aneurysm, the idealized numerical left ventricular models (finite-element left ventricle models) of the healthy left ventricle, subaortic obstruction, and midventricular obstruction in HCM of left ventricle were created. The mechanical effects in the formation of apical aneurysm were determined by comparing the myofiber stress on the apical wall between these three models (healthy, subaortic obstruction, and midventricular obstruction models). In comparing the subaortic obstruction model and MVO model with HCM, it was found that, at the time of maximum pressure, the maximum value of myofiber stress in MVO model was 75.0% higher than that in the subaortic obstruction model (654.5 kPa vs. 373.9 kPa). The maximum stress on the apex of LV increased 79.9, 69.3, 117.8% than that on the myocardium around the apex in healthy model, subaortic obstruction model, and MVO model, respectively. Our results indicated that high myofiber stress on the apical wall might initiate the formation process of the apical aneurysm.
No takes yet. Share an insight, caveat, or question.
Deng et al. (2021) studied Hypertrophic cardiomyopathy (n=3). Midventricular obstruction vs. Subaortic obstruction was evaluated on Maximum myofiber stress on the apical wall (75.0% increase, p=0.014). Midventricular obstruction increased maximum myofiber stress on the apical wall by 75.0% compared to subaortic obstruction (654.5 kPa vs. 373.9 kPa), suggesting a mechanical mechanism for apical aneurysm formation.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: