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(Circulation. 1997;96:2969-2977.)
© 1997 American Heart Association, Inc.

Articles

Metabolic Response of Normal Human Myocardium to High-Dose Atropine-Dobutamine Stress Studied by ³¹P-MRS

Hildo J. Lamb, MSc; Hugo P. Beyerbacht, MD; Ronald Ouwerkerk, PhD; Joost Doornbos, PhD; Babette M. Pluim, MD; Ernst E. van der Wall, MD; Arnoud van der Laarse, PhD; ; Albert de Roos, MD

From the Department of Radiology (H.J.L., J.D., A. de R.) and the Department of Cardiology (H.P.B., B.M.P., E.E. van der W., A. van der L.), Leiden University Medical Center, and the Heart Lung Institute, Utrecht University Hospital (R.O.), The Netherlands.

Correspondence to Hildo J. Lamb, Department of Radiology, Building 1, C2-S, Leiden University Medical Center, Albinusdreef 2, 2300 RC Leiden/2333 ZA Leiden, The Netherlands. E-mail lamb{at}rullf2.medfac.leidenuniv.nl

Background ³¹P-MRS during cardiac stress may provide (patho)physiological insights into the high-energy phosphate metabolism of the myocardium. Accordingly, the purpose of the present study was to determine the metabolic response of normal human myocardium to severe atropine-dobutamine (A-D) stress. To corroborate the results from the present in vivo study, a ³¹P-MRS experiment was performed with a moving phantom to simulate respiratory motion.

Methods and Results The phantom experiment showed no relation (P=.371) between the intensity ratio of two separate phosphate peaks and amplitude of phantom excursions. The phosphocreatine (PCr) and ATP signal strength and the PCr/ATP ratio were determined from the left ventricular wall in 20 healthy subjects (posttest likelihood for coronary artery disease was <2.5%) with ³¹P-MRS at rest and during high-dose A-D stress (rate-pressure product increased threefold). Stress-induced changes were -21% for PCr (P<.001) and -9% for ATP (P<.05). The average PCr/ATP value at rest was 1.42±0.18 and decreased by 14% to 1.22±0.20 during stress (P<.001).

Conclusions The phantom experiment shows that the in vivo decrease of myocardial PCr/ATP due to high-dose A-D stress we observed is not a motion artifact. Consequently, this indicates that myocardial high-energy phosphate metabolism of the normal human heart is altered at high workloads.

Key Words: spectroscopy • phosphates • metabolism • stress • inotropic agents

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