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. Author manuscript; available in PMC: 2023 Jun 28.
Published in final edited form as: JACC Adv. 2023 Apr 26;2(3):100308. doi: 10.1016/j.jacadv.2023.100308

Table 2.

Pathologic Analysis by Mechanistic Hypothesis

Hypothesis Analysis (Stain) Hypothesis Findings
Mechanical Elastic fibers (Weigert Resorcin/Fuschin)
Collagen fibers (trichrome)
Leaflet thickness		 Chronic flow drag forces and friction on the valve cause strain, stretch, and fibrotic tissue deposition Compared with control valves, HCM residual leaflets showed:
1. An expanded spongiosa layer with increased, fragmented, and disorganized elastic fibers
2. An attenuated, disrupted, and disorganized collagenous fibrosa layer
3. An added layer of super-imposed collagenous tissue overlying both atrial and ventricular surfaces
4. Elongated, slack and curlicued chordae and a trend to decreased leaflet thickness
Developmental Epicardium derived cells (TBX-18)
Paracrine signaling from epicardium-derived cells (periostin)		 Dysregulated stem cell differentiation during valve development No difference in number of epicardium-derived cells
No significant difference in amount of paracrine signaling
Adaptive Endocardial-to-mesenchymal transition (CD31-αSMA)
Valvular interstitial cells (vimentin)
Inflammatory cells (CD45)		 Adaptive cell lines activate in response to chronic tethering forces No evidence of endocardial-to-mesenchymal transition in HCM or control valves
No difference in valvular interstitial or inflammatory cells
Genetic Cardiomyocytes (cardiac troponin I) Persistence of mutated cardiomyocytes in the valve No cardiomyocytes in HCM or control valves

HCM = hypertrophic cardiomyopathy; Tbx-18 = t-box transcription factor 18.