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Cardiac, Experimental and Miscellaneous

Measurement of coronary flow response to cold pressor stress in asymptomatic women with cardiovascular risk factors using spiral velocity-encoded cine MRI at 3 Tesla

, , , , &
Pages 420-426 | Accepted 18 Dec 2009, Published online: 19 Mar 2010
 

Abstract

Background: Coronary sinus (CS) flow in response to a provocative stress has been used as a surrogate measure of coronary flow reserve, and velocity-encoded cine (VEC) magnetic resonance imaging (MRI) is an established technique for measuring CS flow. In this study, the cold pressor test (CPT) was used to measure CS flow response because it elicits an endothelium-dependent coronary vasodilation that may afford greater sensitivity for detecting early changes in coronary endothelial function.

Purpose: To investigate the feasibility and reproducibility of CS flow reactivity (CSFR) to CPT using spiral VEC MRI at 3 Tesla in a sample of asymptomatic women with cardiovascular risk factors.

Material and Methods: Fourteen asymptomatic women (age 38 years ± 10) with cardiovascular risk factors were studied using 3D spiral VEC MRI of the CS at 3 T. The CPT was utilized as a provocative stress to measure changes in CS flow. CSFR to CPT was calculated from the ratio of CS flow during peak stress to baseline CS flow.

Results: CPT induced a significant hemodynamic response as measured by a 45% increase in rate-pressure product (P<0.01). A significant increase in CS volume flow was also observed (baseline, 116 ± 26 ml/min; peak stress, 152 ± 34 ml/min, P=0.01). CSFR to CPT was 1.31 ± 0.20. Test-retest variability of CS volume flow was 5% at baseline and 6% during peak stress.

Conclusion: Spiral CS VEC MRI at 3 T is a feasible and reproducible technique for measuring CS flow in asymptomatic women at risk for cardiovascular disease. Significant changes in CSFR to CPT are detectable, without demanding pharmacologic stress.

Acknowledgments

The authors would like to thank Tommy Tillery for his assistance with MR image acquisition and Debbie Travalini for her administrative and clinical support. This research was supported by grant no. UL1RR024982, titled, “North and Central Texas Clinical and Translational Science Initiative” (Milton Packer, MD) from the National Center for Research Resources (NCRR), a component of the National Institutes of Health, the American Heart Association, and the Reynolds Cardiovascular Research Center at the University of Texas Southwestern Medical Center.

Declaration of interest: C.M., A.C., A.K., and R.P. declare that they have no competing interests. M.K. and I.D. are employed by Philips Medical Systems. The authors alone are responsible for the content and writing of the paper.

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