Factors influencing regional myocardial contractile response to inotropic stimulation. Analysis in humans with stable ischemic heart disease.
BACKGROUND
We hypothesized that the response of a myocardial segment to maximal dobutamine reflects not only maximal blood flow but also tethering, metabolic, and beta-blocker status.


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%; chi 2, 7.40; P < .01). In patients off beta-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 beta-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%; chi 2, 14.1; P < .001) and off (51% versus 21%; chi 2, 10.9; P < .01) beta-blockers.


CONCLUSIONS
Augmented contraction at maximal dobutamine depends not only on increased myocardial blood flow but also on tethering, metabolic, and beta-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.
Skopicki
H A
HA
Department of Medicine (Cardiac Unit), Massachusetts General Hospital, Harvard Medical School, Boston, USA.
Abraham
S A
SA
Weissman
N J
NJ
Mukerjee
A K
AK
Alpert
N M
NM
Fischman
A J
AJ
Picard
M H
MH
Gewirtz
H
H
D000241:Adenosine; D000318:Adrenergic beta-Agonists; D000368:Aged; D000641:Ammonia; D002247:Carbon Isotopes; D001026:Coronary Artery Bypass; D003326:Coronary Circulation / Q000187:drug effects*; D003327:Coronary Disease / Q000503:physiopathology; D003847:Deoxyglucose / Q000031:analogs & derivatives; D004280:Dobutamine; D004452:Echocardiography; D005188:False Negative Reactions; D005260:Female; D005462:Fluorine Radioisotopes; D019788:Fluorodeoxyglucose F18; D006801:Humans; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000187:drug effects; D009203:Myocardial Infarction / Q000503:physiopathology; D017202:Myocardial Ischemia / Q000000981:diagnostic imaging / Q000503:physiopathology*; D012680:Sensitivity and Specificity; D014055:Tomography, Emission-Computed
D000318:Adrenergic beta-Agonists; D002247:Carbon Isotopes; D005462:Fluorine Radioisotopes; D019788:Fluorodeoxyglucose F18; D004280:Dobutamine; D000641:Ammonia; D003847:Deoxyglucose; D000241:Adenosine