(Circulation. 1996;94:643-650.)
© 1996 American Heart Association, Inc.
Articles |
Factors Influencing Regional Myocardial Contractile Response to Inotropic Stimulation
Analysis in Humans With Stable Ischemic Heart Disease
the Departments of Medicine (Cardiac Unit), Radiology, and Nuclear Medicine, Massachusetts General Hospital, Harvard Medical School, Boston.
Correspondence to Henry Gewirtz, MD, Cardiac Unit/Vincent Burnham 3, Massachusetts General Hospital, Boston, MA 02114. E-mail Gewirtz@PETW7.MGH.Harvard.Edu.
Background We hypothesized that the response of a myocardial segment to maximal dobutamine reflects not only maximal blood flow but also tethering, metabolic, and ß-blocker status.
Methods and Results Patients with stable ischemic heart disease (n=27) had positron emission tomographic measurement of blood flow at rest and with adenosine, and echocardiography at rest and with dobutamine. Positron emission tomographic measurement of [18F]fluorodeoxyglucose myocardial distribution also was made. Adenosine blood flow in segments that contracted normally at peak dobutamine was similar to that of segments that became hypokinetic (1.06±0.72 versus 1.02±0.77 mL·g-1·min-1). Segments that became akinetic failed to augment blood flow (0.68±0.30 mL·g-1·min-1). Fluorodeoxyglucose–blood flow mismatch was more common in segments with abnormal wall motion at peak dobutamine (24 of 59, 41%) versus those that contracted normally (63 of 269, 23%; 
2, 7.40; P<.01). In patients off ß-blockers, segments that contracted normally at peak dobutamine increased blood flow with adenosine (0.70±0.31 to 0.86±0.46 mL·g-1·min-1; P<.05), whereas those that became abnormal did not (0.63±0.24 to 0.65±0.19 mL·g-1·min-1; P=NS). Segments of patients on ß-blockers that contracted normally at peak dobutamine increased blood flow with adenosine (0.78±0.31 to 1.10±0.70 mL·g-1·min-1; P<.05), as did segments that became abnormal (0.74±0.34 to 1.06±0.82 mL·g-1·min-1; P=NS). However, segments adjacent to ones with abnormal wall motion at rest had higher frequency of abnormal response at peak dobutamine in groups on (48% versus 16%; 2, 14.1; P<.001) and off (51% versus 21%; 2, 10.9; P<.01) ß-blockers.
Conclusions Augmented contraction at maximal dobutamine depends not only on increased myocardial blood flow but also on tethering, metabolic, and ß-blocker status. Furthermore, impaired flow reserve does not preclude a normal response to maximal dobutamine, since blood flow need not increase greatly to meet demand.
Key Words: coronary disease • myocardial contraction • adenosine • regional blood flow • echocardiography
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