TITLE

'Hypersynchronisation' by tissue velocity imaging in patients with cardiac amyloidosis

AUTHOR(S)
D Bellavia
PUB. DATE
February 2009
SOURCE
Heart;Feb2009, Vol. 95 Issue 3, p234
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
OBJECTIVE: It is unknown if some patients with cardiac amyloidosis (CA) have mechanical dyssynchrony, as has been demonstrated in patients with ischaemic and dilated cardiomyopathies. The aim of this study was to assess mechanical dyssynchrony in patients with CA using tissue velocity imaging (TVI) and to define its usefulness for risk stratification. DESIGN AND PATIENTS: We included 121 patients with primary amyloidosis and 37 age-matched and sex-matched controls. Patients were divided into two groups: 60 with advanced-CA and 61 with no-advanced-CA, according to left ventricular (LV) wall thickness and diastolic dysfunction. Dyssynchrony assessment included: (1) atrioventricular dyssynchrony (dys), (2) interventricular dys, (3) intraventricular dys assessed longitudinally, using the standard deviation of time to systolic peak velocity (Ts-SD) of the 12 basal and mid level LV segments, and (4) intraventricular dys assessed radially, using the difference in radial Ts between mid anteroseptal and mid posterior segments. OUTCOME: Primary end-point was all-cause death. During a median follow-up of 13 months there were 35 events among patients. RESULTS: Contrary to the hypothesis, the intraventricular dys indices in advanced-CA patients were reduced compared to either the no-advanced-CA group or to controls (Ts-SD: 12.1 (9.0); 35.1 (18.6); 24.5 (14.1), respectively, p<0.001). This reduction was primarily the result of decreased ejection time (ET). Moreover, ET was the most significant predictor of survival (HR = 0.98, p<0.001). CONCLUSIONS: The regional timing of systolic motion measured by TVI was abnormally synchronised in the patients with advanced-CA. ET reduction plays a prominent part in this process and should be considered an essential parameter for assessment of patients with cardiac amyloidosis.
ACCESSION #
36355825

 

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