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LV twisting and untwisting in HCM: ejection begets filling. Diastolic functional aspects of HCM
1School of Medicine, Duke University, Durham, NC 27710, USA. apasipou@duke.edu
Insights
Hypertrophic cardiomyopathy (HCM) mechanisms causing diastolic dysfunction are explored. New models focus on myofiber sheet dynamics and ultrastructural changes for better understanding of left ventricular (LV) filling in HCM.
Area of Science:
- Cardiology
- Biomedical Engineering
- Structural Biology
Background:
- Diastolic dysfunction is a key feature of hypertrophic cardiomyopathy (HCM).
- Current understanding of HCM's impact on diastolic function relies on traditional left ventricular (LV) approaches.
- Polymorphic phenotypes of HCM present complex challenges in understanding LV filling dynamics.
Purpose of the Study:
- To survey conventional and emerging concepts on how hypertrophic cardiomyopathy (HCM) causes diastolic dysfunction.
- To propose a shift towards advanced models for understanding LV diastolic function in HCM.
- To clarify intricate patterns of early diastolic rebound and suction in HCM phenotypes.
Main Methods:
- Review of conventional and emerging scientific literature on diastolic dysfunction in HCM.
- Conceptualization of large-scale (twist-untwist) and small-scale (titin unfolding-refolding) wall rebound models.
- Integration of myofiber sheet dynamics and ultrastructural constituent interactions.
Main Results:
- A paradigm shift is suggested from traditional LV diastolic function assessment to dynamic wall rebound models.
- Incorporation of myofiber sheet distortion and ultrastructural rearrangements offers a new perspective.
- These advanced models may elucidate complex diastolic filling patterns in HCM.
Conclusions:
- Emerging paradigms in diastolic dynamics, focusing on myofiber sheet and ultraconstituent distortion, are crucial for understanding HCM.
- The relationship between structural distortions and LV mechanics is key to explaining diastolic dysfunction in HCM.
- This new perspective may clarify early diastolic rebound and suction mechanisms essential for LV filling in diverse HCM phenotypes.
Abstract:
Conventional and emerging concepts on mechanisms by which hypertrophic cardiomyopathy (HCM) engenders diastolic dysfunction are surveyed. A shift from familiar left ventricular (LV) diastolic function approaches to large-scale (twist-untwist) and small-scale (titin unfolding-refolding, etc.) wall rebound models, incorporating interaction and dynamic distortions and rearrangements of myofiber sheets and ultrastructural constituents, is suggested. Such an emerging new paradigm of diastolic dynamics, emphasizing the relationship of myofiber sheet and ultraconstituent distortion to LV mechanics and end-systolic shape, might clarify intricate patterns of early diastolic rebound and suction, needed for LV filling in many of the polymorphic phenotypes of HCM.
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