Key result
Reduced thoracic dimensions can alter myocardial strain patterns, potentially mimicking subclinical heart disease.
Why the study?
Reduced myocardial strain is frequently interpreted as subclinical myocardial dysfunction, but myocardial deformation also reflects extrinsic mechanical factors such as thoracic geometry, which may affect strain measurements even without structural heart disease.
Does accounting for extrinsic mechanical determinants like thoracic geometry reduce the misclassification of extrinsically mediated strain abnormalities as subclinical myocardial disease?
Does accounting for extrinsic mechanical determinants like thoracic geometry reduce the misclassification of extrinsically mediated strain abnormalities as subclinical myocardial disease?
Extrinsic factors such as thoracic geometry can cause unexpectedly reduced myocardial strain, emphasizing the need to interpret strain data within a broader mechanistic and anatomical context to avoid misdiagnosing subclinical myocardial disease.
Thoracic geometry may confound strain-based subclinical dysfunction diagnosis; hypothesis-generating and challenges intrinsic-only interpretations pending prospective validation.
Myocardial strain imaging has become an established tool for detecting subtle abnormalities in cardiac mechanics, and reduced strain is frequently interpreted as evidence of subclinical myocardial dysfunction. However, myocardial deformation reflects not only intrinsic myocardial properties but also the mechanical environment in which the heart operates. Emerging evidence suggests that extracardiac factors, particularly thoracic geometry and reduced antero-posterior (A–P) thoracic dimensions, may be associated with variations in global and regional strain even in individuals without overt structural heart disease. This narrative review examines the evidence supporting an extrinsically mediated myocardial deformation phenotype across different anatomical and physiological models, including pectus excavatum, mitral valve prolapse, healthy pregnancy, and obesity. A recurring feature is the preferential impairment of basal and, to a lesser extent, mid-ventricular deformation with relative preservation of apical mechanics, potentially generating a mechanical phenocopy of relative apical sparing. These abnormalities may reflect true mechanical constraint, measurement-related effects, or their combination, while intrinsic and extrinsic mechanisms may coexist. Thoracic morphometry may therefore provide valuable context when unexpectedly reduced strain is encountered despite preserved conventional cardiac structure and function. The A–P thoracic diameter can be readily measured from the parasternal long-axis view, while the modified Haller index provides a more comprehensive, radiation-free characterization of thoracic conformation. However, the available evidence is predominantly observational, derives in part from selected single-center cohorts, and does not establish a causal relationship between thoracic geometry and myocardial strain abnormalities; accordingly, these morphometric parameters should currently be considered exploratory and not yet validated as diagnostic markers. Rather than equating abnormal strain with abnormal myocardium, myocardial deformation should be interpreted within a multiparametric and mechanistic framework integrating regional strain distribution, conventional cardiac findings, clinical probability, and the mechanical environment surrounding the heart. Accounting for these factors may improve diagnostic specificity and reduce the misclassification of extrinsically mediated strain abnormalities as subclinical myocardial disease, although independent multicenter and multi-vendor validation is required before this hypothesis-generating framework can be incorporated into routine clinical decision-making.
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Sonaglioni et al. (2026) reported a review. Thoracic geometry / Extracardiac factors was evaluated. Extracardiac factors, particularly reduced antero-posterior thoracic dimensions, may cause variations in myocardial strain that mimic subclinical disease without overt structural heart disease.
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