Structural epicardial disease and microvascular function are determinants of an abnormal longitudinal myocardial blood flow difference in cardiovascular risk individuals as determined with PET/CT

Ines Valenta, Alessandra Quercioli, Gabriella Vincenti, René Nkoulou, Stephan Dewarrat, Olivier Rager, Habib Zaidi, Yann Seimbille, Francois MacH, Osman Ratib, Thomas H. Schindler*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

25 Citations (Scopus)

Abstract

Background. The aim of this study was to determine whether epicardial structural disease may affect the manifestation of a longitudinal decrease in myocardial blood flow (MBF) or MBF difference during hyperemia in cardiovascular risk individuals, and its dependency on the flow increase. Methods and Results. In 54 cardiovascular risk individuals (at risk) and in 26 healthy controls, MBF was measured with 13N-ammonia and PET/CT in mL/g/min at rest and during dipyridamole stimulation. Computed tomography coronary angiography (CTA) was performed using a 64-slice CT of a PET/CT system. Absolute MBFs during dipyridamole stimulation were mildly lower in the mid-distal than in the mid-LV myocardium in controls (2.20 ± .51 vs 2.29 ± .51, P < .0001), while it was more pronounced in at risk with normal and abnormal CTA (1.56 ± .42 vs 1.91 ± .46 and 1.18 ± .34 vs 1.51 ± .40 mL/g/min, respectively, P < .0001), resulting in a longitudinal MBF difference that was highest in at risk with normal CTA, intermediate in at risk abnormal CTA, and lowest in controls (.35 ± .16 and .22 ± .09 vs .09 ± .04 mL/g/min, respectively, P < .0001). On multivariate analysis, log-CCS and mid-LV hyperemic MBF increase, indicative of microvascular function, were independent predictors of the observed longitudinal MBF difference (P ≤ .004 by ANOVA). Conclusions. Epicardial structural disease and microvascular function are important determinants of an abnormal longitudinal MBF difference as determined with PET/CT.

Original languageEnglish
Pages (from-to)1023-1033
Number of pages11
JournalJournal of Nuclear Cardiology
Volume17
Issue number6
DOIs
Publication statusPublished - Dec 2010
Externally publishedYes

Bibliographical note

Funding Information: This study was supported by the Swiss National Science Foundation (SNF Grant: 3200B0-122237), the Department of Internal Medicine of the University Hospitals of Geneva (Switzerland) and Fellowship grants from the Novartis Foundation, and the European Society of Cardiology and the Italian Society of Cardiology

Copyright 2010 American Society of Nuclear Cardiology

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