Skopicki H A, Abraham S A, Weissman N J, Mukerjee A K, Alpert N M, Fischman A J, Picard M H, Gewirtz H
Department of Medicine (Cardiac Unit), Massachusetts General Hospital, Harvard Medical School, Boston, USA.
Circulation. 1996 Aug 15;94(4):643-50. doi: 10.1161/01.cir.94.4.643.
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.
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.
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.
我们推测心肌节段对最大剂量多巴酚丁胺的反应不仅反映最大血流量，还反映牵拉、代谢和β受体阻滞剂状态。
27例稳定型缺血性心脏病患者接受了静息及腺苷激发下的正电子发射断层扫描血流测定，以及静息及多巴酚丁胺激发下的超声心动图检查。还进行了[18F]氟脱氧葡萄糖心肌分布的正电子发射断层扫描测定。多巴酚丁胺峰值时收缩正常节段的腺苷血流与运动减弱节段相似（分别为1.06±0.72与1.02±0.77 mL·g-1·min-1）。运动不能节段未能增加血流（0.68±0.30 mL·g-1·min-1）。多巴酚丁胺峰值时壁运动异常节段的氟脱氧葡萄糖-血流不匹配比收缩正常节段更常见（59个节段中的24个，41% 对269个节段中的63个，23%；χ2 = 7.40；P <.01）。在停用β受体阻滞剂的患者中，多巴酚丁胺峰值时收缩正常节段的腺苷血流增加（从0.70±0.31增至0.86±0.46 mL·g-1·min-1；P <.05），而异常节段则未增加（从0.63±0.24增至0.65±0.19 mL·g-1·min-1；P =无显著性差异）。服用β受体阻滞剂患者中，多巴酚丁胺峰值时收缩正常节段的腺苷血流增加（从0.78±0.31增至1.10±0.70 mL·g-1·min-1；P <.05），异常节段也是如此（从0.74±0.34增至1.06±0.82 mL·g-1·min-1；P =无显著性差异）。然而，静息时壁运动异常节段相邻的节段，在服用（48% 对16%；χ2 = 14.1；P <.001）和未服用（51% 对21%；χ2 = 10.9；P <.01）β受体阻滞剂的组中，多巴酚丁胺峰值时异常反应的频率更高。
最大剂量多巴酚丁胺时的增强收缩不仅取决于心肌血流量增加，还取决于牵拉、代谢和β受体阻滞剂状态。此外，血流储备受损并不排除对最大剂量多巴酚丁胺的正常反应，因为血流量无需大幅增加即可满足需求。
