BACKGROUND: This investigation examines the effects of inotropic stimulation on myocardial blood flow (MBF) and glucose metabolism (MRGlc) in dysfunctional myocardium through the use of positron emission tomography (PET). METHODS AND RESULTS: Nineteen patients with chronic coronary artery disease and 12 normal volunteers were studied with 13N-ammonia, 18F-deoxyglucose, and PET and with two-dimensional echocardiography at baseline and during intravenous dobutamine (5 to 10 micrograms/kg per minute). At rest, MBF in mismatch regions (n = 10) averaged 0.53 +/- 0.19 mL/g per minute and increased by 41.4 +/- 46.6% (P = .01) during dobutamine, whereas in match regions (n = 16) MBF was 0.28 +/- 0.09 mL/g per minute at rest without an increase during dobutamine (26.4 +/- 47.3%; NS). Myocardium with normal rest MBF was classified as normal remote (normal wall motion, n = 8) or abnormal remote (abnormal wall motion, n = 11). Dobutamine raised MBF similarly in normal subjects and in normal remote regions (by 82 +/- 85% and 84 +/- 42%, P < .01) but by only 33 +/- 34% in abnormal remote regions. MRGlc declined by 49 +/- 28% (P < .005) with dobutamine in the normal subjects, remained unchanged in normal and abnormal remote regions of the patients, but increased in mismatch and match regions (by 49 +/- 74% and 46 +/- 77%; P < .05). Wall motion improved with dobutamine only in mismatch and abnormal remote regions but not in match regions. CONCLUSIONS: Blood flow-metabolism mismatch patterns are not consistently associated with a fixed downregulation of MBF; the increased contractile work in response to dobutamine stimulation is associated with an increase in MBF and a greater reliance on glucose utilization, possibly reflecting acute ischemia or alterations in substrate selection by chronically dysfunctional myocardium. Importantly, functionally impaired though normally perfused myocardium frequently exists in chronic coronary artery disease patients and may represent repetitively stunned or, more likely, remodeled left ventricular myocardium.
BACKGROUND: This investigation examines the effects of inotropic stimulation on myocardial blood flow (MBF) and glucose metabolism (MRGlc) in dysfunctional myocardium through the use of positron emission tomography (PET). METHODS AND RESULTS: Nineteen patients with chronic coronary artery disease and 12 normal volunteers were studied with 13N-ammonia, 18F-deoxyglucose, and PET and with two-dimensional echocardiography at baseline and during intravenous dobutamine (5 to 10 micrograms/kg per minute). At rest, MBF in mismatch regions (n = 10) averaged 0.53 +/- 0.19 mL/g per minute and increased by 41.4 +/- 46.6% (P = .01) during dobutamine, whereas in match regions (n = 16) MBF was 0.28 +/- 0.09 mL/g per minute at rest without an increase during dobutamine (26.4 +/- 47.3%; NS). Myocardium with normal rest MBF was classified as normal remote (normal wall motion, n = 8) or abnormal remote (abnormal wall motion, n = 11). Dobutamine raised MBF similarly in normal subjects and in normal remote regions (by 82 +/- 85% and 84 +/- 42%, P < .01) but by only 33 +/- 34% in abnormal remote regions. MRGlc declined by 49 +/- 28% (P < .005) with dobutamine in the normal subjects, remained unchanged in normal and abnormal remote regions of the patients, but increased in mismatch and match regions (by 49 +/- 74% and 46 +/- 77%; P < .05). Wall motion improved with dobutamine only in mismatch and abnormal remote regions but not in match regions. CONCLUSIONS: Blood flow-metabolism mismatch patterns are not consistently associated with a fixed downregulation of MBF; the increased contractile work in response to dobutamine stimulation is associated with an increase in MBF and a greater reliance on glucose utilization, possibly reflecting acute ischemia or alterations in substrate selection by chronically dysfunctional myocardium. Importantly, functionally impaired though normally perfused myocardium frequently exists in chronic coronary artery diseasepatients and may represent repetitively stunned or, more likely, remodeled left ventricular myocardium.
Authors: F Piscione; P Perrone-Filardi; G De Luca; M Prastaro; C Indolfi; P Golino; S Dellegrottaglie; M Chiariello Journal: Heart Date: 2001-12 Impact factor: 5.994