Key result
In vivo contractile strain correlates moderately-to-strongly with in vitro myocardial slice contractility.
Why the study?
Conventional echocardiography offers limited insight into intrinsic atrial mechanics, and speckle tracking echocardiography strain measurements remain strongly influenced by hemodynamic loading. This study integrated in vivo speckle tracking echocardiography with in vitro living myocardial slices to identify patient-specific markers of intrinsic atrial dysfunction beyond hemodynamic effects.
Does in vivo speckle tracking echocardiography accurately reflect intrinsic atrial myocardial contractility as measured in vitro by living myocardial slices?
Observational (n=34)
Does in vivo speckle tracking echocardiography accurately reflect intrinsic atrial myocardial contractility as measured in vitro by living myocardial slices?
Answers are grounded in this paper and cite their sources.
Integrating in vivo speckle tracking echocardiography with in vitro living myocardial slices demonstrates that amplitude- and velocity-derived strain indices capture intrinsic human atrial myocardial contractility beyond hemodynamic loading effects.
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.
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Doorn et al. (2026) conducted an observational in Atrial biomechanical dysfunction (including subgroups with atrial fibrillation, dilatation, and heart failure) (n=34). In vivo speckle tracking echocardiography (STE) matched with in vitro living myocardial slices (LMS) contractility was evaluated on Correlation between in vivo STE parameters (reservoir and contractile strain magnitude, timing, slopes, AUC) and physiologically corresponding in vitro LMS indices (force amplitude, contraction duration, time to peak/relaxation, maximal contraction/relaxation rates). In vivo contractile strain magnitude and slope correlated moderately-to-strongly with in vitro force amplitude and maximal contraction rate across 194 slices from 34 patients.
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