Key result
Myocardial strain showed reduced longitudinal septal strain in patients with thickened septum versus controls (P<0.001), but could not differentiate between hypertrophic and infiltrative etiologies.
Why the study?
Can myocardial strain differentiate hypertrophic from infiltrative etiology in patients with a thickened septum?
Cross-Sectional (n=74)
Can myocardial strain differentiate hypertrophic from infiltrative etiology in patients with a thickened septum?
p-value: p=<0.001
Myocardial strain assessment demonstrated reduced longitudinal function in patients with thickened septums but failed to differentiate between hypertrophic and infiltrative etiologies.
Strain cannot differentiate hypertrophic from infiltrative septal thickening; leaves open its diagnostic role pending prospective studies.
OBJECTIVES: Radial systolic strain (ε) assessed by echocardiography has been shown to identify patterns of normal septal motion brought about by different layers, including left ventricular (LV) subendocardial (LV subendo) and mural (LV mural) layers. We aimed to use myocardial strain in assessing radial and longitudinal myocardial function in normal and thickened septum and to test if myocardial strain can differentiate hypertrophic from infiltrative cause of thickened septum. METHODS: Forty-five patients (age 61 ± 13 years, 22 males), 13 with hypertrophic cardiomyopathy, 15 with aortic stenosis, and 17 with familial amyloid polyneuropathy, were studied and compared with 29 controls (age 61 ± 12 years, 17 males) using 1D strain and conventional echocardiography. RESULTS: Patients had normal LV ejection fraction and stroke volume but heart rate was higher (P < 0.05) compared to controls. Septal ɛ was reduced (-7.6 ± 7.0% vs. -14.0 ± 5.5%, for LV mural and -7.9 ± 14.7% vs. -20.3 ±-7.9% for LV subendo, P < 0.001 for both layers) across LV longitudinal axis but not along its radial axis. No difference was found in any of ɛ measurements between patient groups. A decrease in strain length by 50% increased the septal strain by more than 60% in both radial and longitudinal axes. CONCLUSION: Septal systolic strain measurements showed reduced longitudinal function but its localized nature failed to demonstrate radial disturbances in patients with pathologically thickened septum. No difference was found in systolic strain between patients according to the etiology of septal thickness. This limitation might be either technical or is explained by the maintained radial function in all patient groups.
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Engvall et al. (2011) conducted a cross-sectional in Thickened septum (hypertrophic cardiomyopathy, aortic stenosis, familial amyloid polyneuropathy) (n=74). Myocardial strain assessment (1D strain and conventional echocardiography) vs. Healthy controls was evaluated on Septal systolic strain (radial and longitudinal) (p=<0.001). Myocardial strain showed reduced longitudinal septal strain in patients with thickened septum versus controls (P<0.001), but could not differentiate between hypertrophic and infiltrative etiologies.
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