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  • Title: [Value of assessing left ventricular longitudinal systolic peak strain in differential diagnosis of primary cardiac amyloidosis from hypertrophic cardiomyopathy].
    Author: Zhang L, Wang Y, Cheng L, Wang J, Zhou X, Liu M, Zhang W, Zhang M, Zhang B, Zhi G.
    Journal: Nan Fang Yi Ke Da Xue Xue Bao; 2014 May; 34(5):609-16. PubMed ID: 24849421.
    Abstract:
    OBJECTIVE: To analyze the endocardial, myocardial, and epicardial longitudinal systolic strain (LSsys) in the left ventricle (LV) segments and walls in patients with cardiac involvement due to primary amyloidosis (AL-CA) and hypertrophic cardiomyopathy (HCM). METHODS: Twenty patients with biopsy-proven AL-CA, 20 with asymmetric HCM, and 20 age-matched healthy volunteers were analyzed for their clinical characteristics and underwent conventional echocardiography for evaluating LV wall thickness, left atrial and ventricle size, systolic and diastolic function and 2-dimensional velocity vector imaging for evaluating the endocardial, myocardial and epicardial LSsys of the LV segments and walls. AL-CA and HCM patients also underwent cardiac magnetic resonance to evaluate the late gadolinium enhancement (LGE) features. RESULTS: Compared with the control group, AL-CA and HCM groups, with similar clinical symptoms and physical signs, both showed increased LV wall thickness, left atrial diameter, E/A ratio, septal E/e' ratio and the prevalence of granular sparkling. LV segments and walls endocardial LSsys were significantly lower in AL-CA patients than in HCM patients and the control subjects. The endocardial-epicardial LSsys difference in all the left ventricle walls were significantly smaller in AL-CA group than in the control group, but this difference appeared variable in HCM group. The LGE also presented with different features in AL-CA and HCM: AL-CA group showed subendocardial LGE in almost all the LV walls, but HCM group showed patchy LGE with a regional, multifocal distribution. CONCLUSION: AL-CA is characterized by a significantly reduced endocardial LSsys in the LV segments and an uniform decrease of the endocardial-epicardial LSsys difference in all the LV walls, but the changes in HCM appear variable, and 2-dimensional velocity vector imaging is therefore a useful modality to differentiate AL-CA from HCM.
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