Key result
In vivo STE strain and velocity correlate 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 slice contractility to identify patient-specific markers of intrinsic atrial dysfunction beyond hemodynamic effects.
Does in vivo speckle tracking echocardiography correlate with in vitro living myocardial slice contractility to reflect intrinsic atrial biomechanical function in patients?
Observational (n=34)
Does in vivo speckle tracking echocardiography correlate with in vitro living myocardial slice contractility to reflect intrinsic atrial biomechanical function in patients?
In vivo speckle tracking echocardiography strain amplitude and velocity indices reliably reflect intrinsic human atrial myocardial contractility as validated by in vitro living myocardial slices, even in the presence of atrial fibrillation, dilatation, and heart failure.
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.
No takes yet. Share an insight, caveat, or question.
Doorn et al. (2026) conducted an observational in Atrial dysfunction (including subgroups with atrial fibrillation, atrial dilatation, and heart failure) (n=34). Speckle tracking echocardiography (STE) integrated with in vitro living myocardial slices (LMS) was evaluated on Correlation between in vivo STE parameters (reservoir and contractile strain magnitude, timing, slopes, AUC) and in vitro LMS contractility indices (Fmax, contraction duration, time to peak/relaxation, Pslope/relaxation rates). In vivo speckle tracking echocardiography strain amplitude and velocity correlated moderately-to-strongly with in vitro contractility across 194 myocardial slices from 34 patients.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: