Key result
Decreased ejection time, which contributed to abnormal hypersynchronisation in advanced cardiac amyloidosis, was a significant predictor of survival (HR 0.98, p<0.001).
Why the study?
Does mechanical dyssynchrony assessed by tissue velocity imaging predict survival in patients with cardiac amyloidosis?
Cohort (n=158)
Does mechanical dyssynchrony assessed by tissue velocity imaging predict survival in patients with cardiac amyloidosis?
Effect estimate: HR 0.98
p-value: p=<0.001
Patients with advanced cardiac amyloidosis exhibit abnormal 'hypersynchronisation' driven by reduced ejection time, which serves as a significant predictor of mortality.
Ejection time may aid prognostication in cardiac amyloidosis; leaves open whether hypersynchronisation is modifiable.
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.
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Bellavia et al. (2008) conducted a cohort in Cardiac amyloidosis (n=158). Advanced cardiac amyloidosis vs. No-advanced cardiac amyloidosis and controls was evaluated on All-cause death (HR 0.98, p=<0.001). Decreased ejection time, which contributed to abnormal hypersynchronisation in advanced cardiac amyloidosis, was a significant predictor of survival (HR 0.98, p<0.001).
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