Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis · 2022
Alterations in multi-layer strain in AL amyloidosis.
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Sivapathan Shanthosh, Geenty Paul, Deshmukh Tejas, Boyd Anita, Richards David, Stewart Graeme, Taylor Mark S, Kwok Fiona, Thomas Liza
Аннотация
BACKGROUND: Cardiac involvement in AL amyloidosis portends a poor prognosis. 2D-speckle tracking echocardiography (2D-STE) strain can identify subclinical cardiac involvement. This study performed multilayer and multiplanar 2D-STE myocardial strain analysis.
METHODS: We compared 75 AL amyloidosis patients to 49 hypertensive patients and 49 healthy controls. Longitudinal strain was obtained from epicardial, mid-myocardial and endocardial layers; segmental strain was measured from mid-myocardial basal, mid and apical segments.
RESULTS: Global longitudinal strain was reduced in epicardial (-14.3 ± -4.0% vs. -17.4 ± 2.2% vs. -17.5 ± -2.0%, p < .001), mid-myocardial (-16.3 ± -4.5% vs. -19.7 ± 2.5% vs. -19.7 ± -2.2%, p < .001) and endocardial layers (-18.7 ± -4.9% vs. -22.2 ± 3.0% vs. -22.3 ± -2.6%, p < .001) in amyloid patients compared to hypertensive and healthy controls. Segmental strain confirmed significant reduction in basal (-11.2 ± -3.9% vs. -17.6 ± 2.7% vs. -20.9 ± -3.4%, p < .001) and mid (-14.8 ± -4.3% vs. -19.2 ± 2.5% vs. -19.6 ± -2.2%, p < .001) LV segments in the AL amyloid group. Receiver operating curve analysis demonstrated that an optimal cut-off of -16% for basal segmental strain better differentiated AL amyloid from hypertensive group (sensitivity 96%, specificity 70%, AUC 0.93), compared to relative apical sparing (AUC of 0.85).
CONCLUSION: Strain demonstrated myocardial involvement in all layers in AL amyloidosis, with reduced basal segmental longitudinal strain a likely marker of early disease.
METHODS: We compared 75 AL amyloidosis patients to 49 hypertensive patients and 49 healthy controls. Longitudinal strain was obtained from epicardial, mid-myocardial and endocardial layers; segmental strain was measured from mid-myocardial basal, mid and apical segments.
RESULTS: Global longitudinal strain was reduced in epicardial (-14.3 ± -4.0% vs. -17.4 ± 2.2% vs. -17.5 ± -2.0%, p < .001), mid-myocardial (-16.3 ± -4.5% vs. -19.7 ± 2.5% vs. -19.7 ± -2.2%, p < .001) and endocardial layers (-18.7 ± -4.9% vs. -22.2 ± 3.0% vs. -22.3 ± -2.6%, p < .001) in amyloid patients compared to hypertensive and healthy controls. Segmental strain confirmed significant reduction in basal (-11.2 ± -3.9% vs. -17.6 ± 2.7% vs. -20.9 ± -3.4%, p < .001) and mid (-14.8 ± -4.3% vs. -19.2 ± 2.5% vs. -19.6 ± -2.2%, p < .001) LV segments in the AL amyloid group. Receiver operating curve analysis demonstrated that an optimal cut-off of -16% for basal segmental strain better differentiated AL amyloid from hypertensive group (sensitivity 96%, specificity 70%, AUC 0.93), compared to relative apical sparing (AUC of 0.85).
CONCLUSION: Strain demonstrated myocardial involvement in all layers in AL amyloidosis, with reduced basal segmental longitudinal strain a likely marker of early disease.