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.
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.
Authors: Lucy E Hudsmith; Damian J Tyler; Yaso Emmanuel; Steffen E Petersen; Jane M Francis; Hugh Watkins; Kieran Clarke; Matthew D Robson; Stefan Neubauer Journal: Int J Cardiovasc Imaging Date: 2009-08-21 Impact factor: 2.357
Authors: H J Lamb; A van der Laarse; B M Pluim; H P Beyerbacht; J Doornbos; E E van der Wall; A de Roos Journal: MAGMA Date: 1998-09 Impact factor: 2.310
Authors: Mohammad Haris; Anup Singh; Kejia Cai; Feliks Kogan; Jeremy McGarvey; Catherine Debrosse; Gerald A Zsido; Walter R T Witschey; Kevin Koomalsingh; James J Pilla; Julio A Chirinos; Victor A Ferrari; Joseph H Gorman; Hari Hariharan; Robert C Gorman; Ravinder Reddy Journal: Nat Med Date: 2014-01-12 Impact factor: 53.440
Authors: Ashish Gupta; Ashwin Akki; Yibin Wang; Michelle K Leppo; V P Chacko; D Brian Foster; Viviane Caceres; Sa Shi; Jonathan A Kirk; Jason Su; Shenghan Lai; Nazareno Paolocci; Charles Steenbergen; Gary Gerstenblith; Robert G Weiss Journal: J Clin Invest Date: 2011-12-27 Impact factor: 14.808