AIMS: To establish the response of cardiac flow and function to adenosine stress using phase-contrast magnetic resonance (pcMR) and cine steady-state free precession (SSFP) cardiac magnetic resonance (CMR). METHODS: Healthy volunteers (n = 10) were scanned on 1.5T at rest and under adenosine stress utilizing short-axis SSFP sequences and pcMR of the aorta and pulmonary trunk. RESULTS: Adenosine-induced increase in heart rate was 62.7% (P < 0.001). Left and right-ventricular stroke volumes (SVs) increased by 12.2% (P = 0.048) and 11.9% (P = 0.044), left-ventricular ejection fraction by 11.8% (P = 0.002), and left-ventricular and right-ventricular cardiac output (CO) by 81.0% (P < 0.001) and 81.8% (P = 0.005). Average flow velocities in the ascending aorta and pulmonary trunk increased by 77.3% (P < 0.001) and 73.6% (P < 0.001), and peak flow velocities in the ascending aorta and pulmonary trunk by 27.2% (P < 0.001) and 22.4% (P = 0.003). End-systolic volumes in the left ventricle (LV) and right ventricle (RV) decreased by 16.4% (P = 0.020) and 19.2% (P = 0.028). Planimetric cine SSFP and pcMR-derived SV showed an excellent correlation. CONCLUSION: In healthy volunteers, response to adenosine stress is characterized by an increase in heart rate, CO and SV of both ventricles. Excellent correlation is demonstrated between these increases and the increased blood flow velocities in the aorta and the pulmonary trunk. Thus, results support the use of flow measurements as an internal control of planimetric measurements of ventricular SV and CO.
AIMS: To establish the response of cardiac flow and function to adenosine stress using phase-contrast magnetic resonance (pcMR) and cine steady-state free precession (SSFP) cardiac magnetic resonance (CMR). METHODS: Healthy volunteers (n = 10) were scanned on 1.5T at rest and under adenosine stress utilizing short-axis SSFP sequences and pcMR of the aorta and pulmonary trunk. RESULTS:Adenosine-induced increase in heart rate was 62.7% (P < 0.001). Left and right-ventricular stroke volumes (SVs) increased by 12.2% (P = 0.048) and 11.9% (P = 0.044), left-ventricular ejection fraction by 11.8% (P = 0.002), and left-ventricular and right-ventricular cardiac output (CO) by 81.0% (P < 0.001) and 81.8% (P = 0.005). Average flow velocities in the ascending aorta and pulmonary trunk increased by 77.3% (P < 0.001) and 73.6% (P < 0.001), and peak flow velocities in the ascending aorta and pulmonary trunk by 27.2% (P < 0.001) and 22.4% (P = 0.003). End-systolic volumes in the left ventricle (LV) and right ventricle (RV) decreased by 16.4% (P = 0.020) and 19.2% (P = 0.028). Planimetric cine SSFP and pcMR-derived SV showed an excellent correlation. CONCLUSION: In healthy volunteers, response to adenosine stress is characterized by an increase in heart rate, CO and SV of both ventricles. Excellent correlation is demonstrated between these increases and the increased blood flow velocities in the aorta and the pulmonary trunk. Thus, results support the use of flow measurements as an internal control of planimetric measurements of ventricular SV and CO.