Factors influencing regional myocardial contractile response to inotropic stimulation analysis in humans with stable ischemic heart disease

被引:36
|
作者
Skopicki, HA
Abraham, SA
Weissman, NJ
Mukerjee, AK
Alpert, NM
Fischman, AJ
Picard, MH
Gewirtz, H
机构
[1] HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,CARDIAC UNIT,BOSTON,MA 02114
[2] HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02114
[3] HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NUCL MED,BOSTON,MA 02114
关键词
coronary disease; myocardial contraction; adenosine; regional blood flow; echocardiography;
D O I
10.1161/01.CIR.94.4.643
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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. 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 [F-18]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 dow 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 how 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.
引用
收藏
页码:643 / 650
页数:8
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