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This letter raises concerns that the relationship between global longitudinal strain by 2D-STE and myocardial infarct size may be confounded by unreported comorbidities and incomplete radial motion analysis.
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This letter raises methodological concerns regarding a prior study on 2D-STE and infarct size, highlighting the potential confounding effects of comorbidities and the need to evaluate radial and rotational mechanics.
I read with great interest the study by Gjesdal et al. [1], which confirmed that, in chronic infarction, peak systolic longitudinal strain by 2D-STE (two-dimensional speckle tracking echocardiography) correlates with the infarct mass assessed by CE MRI (contrast-enhanced magnetic resonance imaging) at a global level, and separates infarcted from non-infarcted tissue, and that global strain is an excellent predictor of myocardial infarct size in chronic ischaemic heart disease. The methods and interpretation of the results, however, raise several concerns. It is well-known that hypertension, hypercholesterolaemia, diabetes, Graves' disease and paroxysmal atrial fibrillation etc. could affect left ventricular myocardial segments and global function to some extent [2]. In the study by Gjesdahl et al. [1] the relevant history of the above-mentioned diseases was not described in the normal control group, although the disease history was described in the patient group. Is there a relationship between the decreased systolic strain and strain rate parameters with increasing relative hyperenhancement as defined by CE MRI to the relevant history of the above-mentioned diseases? On the other hand, could the relevant history of the above-mentioned diseases affect the precise discrimination between different transmurality states of myocardial infarction by 2D-STE for the analysis of myocardial deformation?It is well-known that normal myocardial motion is complex, with three separate components: radial contraction, longitudinal shortening and rotation. Myocardium has a transmural heterogeneity of contraction in normal conditions, contractility decreases from subendocardium to subepicardium, and that, during a reduction in myocardial perfusion capable of inducing myocardial ischaemia, the subendocardial layer undergoes contractility impairment even in the absence of functional impairment of the subepicardial layer [2,3]. The difference in myocardial longitudinal motion between subendocardial and subepicardial myocardium could also allow discrimination between different transmurality states of myocardial infarction [2]. In addition, Becker et al. [4] confirmed that radial strain allowed distinction of non-transmural infarction from transmural infarction with a sensitivity of 70.0% and a specificity of 71.2%, suggesting that frame-to-frame tracking of acoustic markers in two-dimensional echocardiographic images for the analysis of myocardial deformation allows discrimination between different transmurality states of myocardial infarction. In the study by Gjesdal et al. [1] however, myocardial radial motion characteristics of the patients were not well-described. Therefore the respective and complementary value of myocardium radial contraction, longitudinal shortening and rotation in discrimination between different transmurality states of myocardial infarction need to be studied further [2].
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Ze–Zhou Song (2007) conducted a letter in chronic ischaemic heart disease. Global longitudinal strain by two-dimensional speckle tracking echocardiography was evaluated. This letter raises concerns that the relationship between global longitudinal strain by 2D-STE and myocardial infarct size may be confounded by unreported comorbidities and incomplete radial motion analysis.
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