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Ventricular synchrony is not determined by myocardial perfusion in heart failure: A 13N-ammonia PET study

Session Poster session 6

Speaker Luis Eduardo Juarez-Orozco

Event : ESC Congress 2017

  • Topic : imaging
  • Sub-topic : Nuclear Imaging
  • Session type : Poster Session

Authors : L E Juarez-Orozco (Turku,FI), FM Van Der Zant (Alkmaar,NL), J Knuuti (Turku,FI), N Hoogvorst (Alkmaar,NL), RJJ Knol (Alkmaar,NL)

Authors:
L.E. Juarez-Orozco1 , F.M. Van Der Zant2 , J. Knuuti1 , N. Hoogvorst2 , R.J.J. Knol2 , 1Turku University Hospital, PET Center - Turku - Finland , 2Cardiac Imaging Division Alkmaar, Northwest Clinics, Department of Nuclear Medicine - Alkmaar - Netherlands ,

Citation:
European Heart Journal ( 2017 ) 38 ( Supplement ), 1098-1099

Background: An inverse relationship between myocardial perfusion and PET ventricular synchrony has been proposed. Ventricular synchrony has been suggested as a useful marker for the detection of multivessel coronary artery disease. However, the potentially confounding influence of fixed perfusion defects (indicating previous infarction and scar) over the perfusion-synchrony relationship, has not been investigated. In heart failure, ventricular remodelling possibly affects perfusion and synchrony, adding a layer of complexity to this interrelation. The present study aimed to evaluate the relationship between quantitative PET regional myocardial perfusion and ventricular synchrony when accounting for the extent and severity of pre-existing fixed perfusion defects in patients with heart failure.

Methods: 98 patients with chronic heart failure underwent PET perfusion scanning with 13N-ammonia. Gender, age, and modifiable cardiovascular risk factors data was retrieved. Quantitative perfusion was analysed regionally per vessel territory (LAD, LCx and RCA) and a myocardial perfusion reserve (MPR) <2.0 was considered abnormal. The summed rest score (SRS) was retrieved as a proxy for the extent and severity of fixed perfusion defects in patients with previous infarction. Rest and stress synchrony was analysed through the histogram bandwidth (BW), standard deviation (SD) and Entropy. Prior comparison of synchrony parameters between patients with 0,1,2 and 3-vessels with abnormal MPR, we performed a stepwise multivariate analysis with stress synchrony (BW, SD and Entropy) as the dependent variable. Clinical data, number of vessel territories with abnormal MPR, history of a previous MI and SRS were input as the independent variables.

Results: An MPR (<2.0) was found in 0- (28 patients), 1- (10 patients), 2- (14 patients) and 3-vessels (37 patients). There were no significant differences in synchrony between rest and stress. Between groups, there was a significantly worse stress BW in patients with abnormal MPR in 3 vessels (Diff=28.8°, p=0.015) and only a trend in stress Entropy (Diff=7.23%, p=0.08). Multivariate analysis showed in the first step that the number of vessels with abnormal MPR (p=0.024), dyslipidemia (p=0.036), and sex (p=0.025) were significant predictors of stress synchrony. However, when adding the presence of a previous MI and SRS to the model, only SRS remained as a strong independent predictor of stress synchrony (p<0.001).

Conclusion: In patients with heart failure, the extent and severity of fixed perfusion defects constitute the strongest independent determinant of ventricular synchrony during stress. The previously reported relationship between ventricular synchrony and both myocardial perfusion and angiographic disease severity may not apply and should be reconsidered in patients with chronic heart failure. Further research in the relevance of myocardial scar and myocardial perfusion for mechanical synchrony is warranted.

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