Related Experiment Video
Updated: Oct 28, 2026

Fabrication of 3D Cardiac Microtissue Arrays using Human iPSC-Derived Cardiomyocytes, Cardiac Fibroblasts, and Endothelial Cells
Published on: March 14, 2021
From Echo to Tissue: A Combined In Vivo and In Vitro Approach to Atrial Biomechanical Function
Elisa C H van Doorn1, Manouk H C Linderhof2, Annemien E van den Bosch2
1Department of Cardiothoracic Surgery, Erasmus Medical Center, Rotterdam.
Abstract:
Conventional echocardiography often identifies atrial dysfunction only after significant remodeling, offering limited insight into intrinsic myocardial mechanics. Speckle tracking echocardiography (STE) allows in vivo quantification of atrial deformation, but strain measurements remain strongly influenced by hemodynamic loading. Living myocardial slices (LMS) provide a complementary in vitro platform that preserves patient-specific atrial tissue architecture and intrinsic contractile behavior under controlled conditions. By integrating in vivo STE with in vitro LMS contractility, we aimed to determine patient-specific markers of intrinsic atrial dysfunction beyond hemodynamic effects. Atrial tissue from 34 patients yielded 194 LMS. STE parameters, including reservoir (Sr) and contractile (Sct) strain magnitude, timing, slopes, and area under the curve, were matched to physiologically corresponding LMS indices such as force amplitude (Fmax), contraction duration, time to peak or relaxation, and maximal contraction (Pslope)/relaxation rates. Moderate-to-strong correlations were observed between Sct and Fmax, and between Sct slope and Pslope, indicating that strain magnitude and velocity reliably reflects intrinsic myocardial contractile properties. Timing- and integrative parameters showed weaker correspondence, consistent with modulation by hemodynamic conditions. Subgroup analyses demonstrated persistence of these relationships in atrial fibrillation, dilatation, and heart failure. Our results support LMS as a translational model for human atrial biomechanics and demonstrate that in vivo strain, particularly amplitude- and velocity-derived indices, captures intrinsic myocardial contractility. Integrating in vivo and in vitro measures provides a mechanistically grounded approach to assess atrial dysfunction, with potential applications in patient-specific risk stratification and monitoring of therapeutic interventions.
