FACTORS INFLUENCING REGIONAL MYOCARDIAL CONTRACTILE RESPONSE TO INOTROPIC STIMULATION ANALYSIS IN HUMANS WITH STABLE ISCHEMIC-HEART-DISEASE

Citation
Ha. Skopicki et al., FACTORS INFLUENCING REGIONAL MYOCARDIAL CONTRACTILE RESPONSE TO INOTROPIC STIMULATION ANALYSIS IN HUMANS WITH STABLE ISCHEMIC-HEART-DISEASE, Circulation, 94(4), 1996, pp. 643-650
Citations number
38
Categorie Soggetti
Cardiac & Cardiovascular System",Hematology
Journal title
ISSN journal
00097322
Volume
94
Issue
4
Year of publication
1996
Pages
643 - 650
Database
ISI
SICI code
0009-7322(1996)94:4<643:FIRMCR>2.0.ZU;2-A
Abstract
Background We hypothesized that the response of a myocardial segment t o maximal dobutamine reflects not only maximal blood flow but also tet hering, metabolic, and beta-blocker status. Methods and Results patien ts with stable ischemic heart disease (n=27) had positron emission tom ographic measurement of blood flow at rest and with adenosine, and ech ocardiography at rest and with dobutamine. Positron emission tomograph ic measurement of [F-18]fluorodeoxyglucose myocardial distribution als o was made. Adenosine blood flow in segments that contracted normally at peak dobutamine was similar to that of segments that became hypokin etic (1.06+/-0.72 versus 1.02+/-0.77 mL . g(-1). min(-1)). Segments th at 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 norma lly at peak dobutamine increased blood dow with adenosine (0.70+/-0.31 to 0.86+/-0.46 mL . g(-1). min(-1); P <.05), whereas those that becam e 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 a bnormal (0.74+/-0.34 to 1.06+/-0.82 mL . g(-1). min(-1); P=NS). Howeve r, segments adjacent to ones with abnormal wall motion at rest had hig her 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 maxi mal dobutamine depends not only on increased myocardial blood how but also on tethering, metabolic, and beta-blocker status. Furthermore, im paired flow reserve does not preclude a normal response to maximal dob utamine, since blood flow need not increase greatly to meet demand.