An assessment of dobutamine echocardiography and end-diastolic wall thickness for predicting post-revascularization functional recovery in patients with chronic coronary artery disease

AIMS: This study investigated the functional outcome of wall-thinned,akinetic myocardium after revascularization and evaluated theaccuracy of dobutamine echocardiography in predicting post-revascularizationfunctional recovery with the assessment of end-diastolic wallthickness in chronic ischaemic patients. METHODS AND RESULTS: Fifty-three patients underwent dobutamine echocardiography beforecoronary revascularization. End-diastolic wall thickness wasalso evaluated before and after revascularization. The sensitivityand specificity of dobutamine echocardiography to predict post-revascularizationfunctional recovery were 69% and 100% in 58 akinetic/dyskineticsegments, and 86% and 57% in 96 hypokinetic segments. Of 19akinetic/dyskinetic segments with a preserved end-diastolicwall thickness, 17 (89%) showed functional recovery after revascularization,and dobutamine detected 14 (83%) of these 17 segments. Of 39akinetic/dyskinetic segments with a thinned end-diastolic wallthickness, 15 (38%) achieved functional recovery, whereas dobutamineechocardiography detected recovery in only eight (53%). Further,of these 15 viable, wall-thinned segments, 12 (80%) showed anincreased end-diastolic wall thickness after revascularization(mean±SD were from 5·6±0·7 mm atbaseline to 7·4±1·3 mm and 9·7±1mm after 1 week and after 3 months, respectively), and only5 (42%) of these responded to dobutamine. CONCLUSION: Dobutamine echocardiography showed a lessened sensitivity topredict post-revascularization functional recovery in akinetic/dyskineticsegments with a thinned end-diastolic wall thickness that subsequentlyincreased in size.     

多巴酚丁胺负荷201Tl心肌断层显像对冠状动脉病变的诊断

目的 :探讨多巴酚丁胺 (DOB)负荷 2 0 1Tl心肌单光子发射计算机断层显像对冠状动脉病变的诊断价值。方法 :对 70例临床确诊或疑诊冠心病的患者在冠状动脉造影前后 2周内进行 DOB负荷 2 0 1Tl心肌断层显像。结果 :DOB2 0 1Tl心肌断层显像诊断冠心病的敏感性为 93.3% ,特异性为80 .0 % ;单、双、三支冠状动脉受累时的敏感性为 90 .9%、93.7%、10 0 % ;心肌显像对左前降支、回旋支和右冠状动脉病变诊断的敏感性和特异性分别为 6 8.5%、75.0 % ,4 2 .9%、97.6 %和 81.6 % ,87.5%。负荷试验终点时双支、三支血管病变 DOB用量明显低于单支病变用量 (P <0 .0 1)。试验中未见严重不良反应。结论 :DOB2 0 1Tl心肌断层显像对冠状动脉病变有一定的诊断价值     

小剂量多巴酚丁胺负荷超声心动图试验对可逆性功能障碍心肌预测的新指标

目的：探讨小剂量多巴酚丁胺负荷超声心动图（DSE）试验中左心室功能EF值的变化,即ΔEF这一量化指标预测急性心肌梗死（AMI）后患者的功能障碍心肌是否可逆及其可恢复程度。方法：入选患者25例, 接受小剂量DSE检查,测定负荷试验各阶段的收缩功能EF值,25例患者亦接受冠脉造影,并择期行经皮经腔太动脉成形术（PTCA）治疗,根据病变血管的情况植入支架,在术后3．5－13个月之间复查小剂量DSE试验。结果：以小剂量DSE过程中EF增加值,即ΔEF大于等于15％作为衡量标准,预测可逆性功能障碍心肌的敏感性,特性和准确性分别为70．6％,75％和72％,此预测改善值与无改善值之间的差异有显著性意义（P＜0．05）,结论：ΔEF可以作为准确评价可逆性功能障碍心肌的指标,并且是一种定量测定方法。     

不同小剂量多巴酚丁胺超声心动图与18F-脱氧葡萄糖心肌代谢显像对比检测冠心病左心室收缩功能严重受损患者存活心肌

目的 :与18F 脱氧葡萄糖单光子发射计算机断层摄影术 (SPECT)心肌代谢显像对比 ,评价不同小剂量多巴酚丁胺超声心动图 ,检测冠心病左心室收缩功能严重受损患者存活心肌的准确性和安全性。方法 :冠心病心肌梗死伴左心室收缩功能严重受损 (平均左心室射血分数 0 3 8± 0 0 5 )的患者 3 3例 ,1周内分别进行不同小剂量多巴酚丁胺 [3、5、10 μg/(kg·min) ]超声心动图和99m锝 甲氧基异丁基、18F 脱氧葡萄糖SPECT心肌灌注及代谢显像。图像分析均采用 16节段半定量法。以18F 脱氧葡萄糖SPECT检测结果为标准 ,评价不同小剂量多巴酚丁胺超声心动图检测存活心肌的敏感性、特异性、准确性和安全性。结果 :3 3例患者的 3 65个运动异常节段中存活心肌检出率 :18F 脱氧葡萄糖SPECT心肌代谢显像检出的存活心肌节段为 67 4% ,多巴酚丁胺 3、5和 10 μg/(kg·min)分别为 3 8 9%、61 4%和 70 4%。多巴酚丁胺 3 μg/(kg·min)检出的存活心肌节段显著低于18F 脱氧葡萄糖SPECT心肌代谢显像检出的存活心肌节段 (P <0 0 0 1)。多巴酚丁胺 3、5、10μg/(kg·min)超声心动图检出存活心肌的敏感性分别为 5 1 6%、82 9%和 91 8% ,准确性分别为 63 6%、81 6%和87 8% ,均显著递增 (P <0 0 5～ 0 0 0 1) ;副作用发生率分别     

多巴酚丁胺负荷试验QTcd对冠心病的诊断价值

目的探讨多巴酚丁胺负荷试验前、后冠心病与非冠心病患者QTc散离度(QTcd)的变化,评估多巴酚丁胺负荷试验QTcd对冠心病的诊断价值。方法测量选择性冠脉造影证实的30例冠心病与20例非冠心病患者试验前、后QTcd值,并比较分析。结果冠心病组多巴酚丁胺负荷试验终点QTcd明显高于试验前QTcd(P<0.01),非冠心病组无明显差异(P>0.05)。多巴酚丁胺负荷试验终点QTcd≥55ms诊断冠心病的敏感性、特异性、准确性分别为83.3%、85%、84%,QTcd≥10ms(86.7%、85%、86%)高于传统试验ST段压低诊断冠心病的价值(56.7%、50%、54%)(P<0.05)。结论多巴酚丁胺负荷试验QTcd、QTcd可提高冠心病的诊断价值,是一种安全、简便、有效的无创检查方法。     

多巴酚丁胺和多巴胺对低心排综合征患者血流动力学和氧代谢的影响

目的 :比较小剂量多巴胺及多巴酚丁胺对心脏手术后低心排综合征患者血流动力学和氧代谢的影响。方法 :12例心脏手术后低心排患者分别持续静脉泵入 5～ 10 μg·min- 1 ·kg- 1 多巴胺或多巴酚丁胺 ,观察血流动力学和氧代谢的改变。结果 :与给药前相比 ,10 μg·min- 1 ·kg- 1多巴胺和 5～ 10 μg·min- 1 ·kg- 1 多巴酚丁胺给药后均能显著提高心脏指数 (CI) ,但同样使CI增加5 0 %～ 70 % ,多巴酚丁胺只需 5 μg·min- 1 ·kg- 1 ,而多巴胺需要 10 μg·min- 1 ·kg- 1 。 5～ 10 μg·min- 1 ·kg- 1 多巴酚丁胺使体血管阻力指数 (SVRI)和肺动脉嵌顿压 (PAWP)显著降低 ,而多巴胺对SVRI和PAWP无显著影响 ,两者对肺动脉压 (PAP)和肺血管阻力指数 (PVRI)均无显著影响。5～ 10 μg·min- 1 ·kg- 1 多巴酚丁胺均导致氧输送指数 (DO2 )和氧耗指数 (VO2 )显著提高 ,但 5～10 μg·min- 1 ·kg- 1 多巴胺对DO2 和VO2 无明显影响。结论 :与多巴胺相比 ,多巴酚丁胺更为有效的提高CI和DO2 、降低心脏前后负荷 ,有助于改善组织缺氧。     

左室-右房通道的彩色多普勒超声诊断

目的;分析左室－右房通道的声像图特征。方法：９例左室－右房通道的患者进行彩色多普勒超声心动图检查。结果：９例均显示穿隔血流信号,８例显示左室流出道的血流汇聚区。结论：左室至右房的穿隔血流信号、左室流出道的血流汇聚区、可作为本病的诊断依据。同时对该病的鉴别诊断进行了初步分析。     

Interactions of the enantiomers of 3-O-methyldobutamine with α- and β-adrenoceptors in vitro

Summary The enantiomers of 3-O-methyldobutamine, a metabolite of dobutamine, were evaluated for their - and -adrenoceptor mediated effects in vitro in a variety of isolated organs and in radioligand binding studies. Neither enantiomer of 3-O-methyldobutamine possessed ₁-adrenoceptor agonist activity in isolated guinea pig aorta. However, both enantiomers of 3-O-methyldobutamine were competitive ₁-adrenoceptor antagonists, with the (+)-enantiomer being approximately 10-fold more potent than the (-)-enantiomer as assessed either in guinea pig aorta or by displacement of ³H-prazosin binding from ₁-adrenoceptors in rat cerebral cortex. The ₁-adrenoceptor blocking activity of (+)-3-O-methyldobutamine was relatively potent and corresponded to a pA₂ of 7.33 in guinea pig aorta and a-log K _i of 7.72 in radioligand binding studies. Neither enantiomer of 3-O-methyldobutamine possessed ₂-adrenoceptor agonist activity in field-stimulated guinea pig ileum. Although (+)-3-O-methyldobutamine weakly inhibited the twitch response in field-stimulated guinea pig ileum, the response was not blocked by the selective ₂-adrenoceptor antagonist, yohimbine, and was found to result from weak anticholinergic activity (pA₂=5.06). Neither enantiomer of 3-O-methyldobutamine possessed ₁-adrenoceptor agonist activity in guinea pig atria, however the (+)-enantiomer was a weak noncompetitive antagonist at ₁-adrenoceptors. In contrast, both enantiomers of 3-O-methyldobutamine were weak ₂-adrenoceptor agonists in rat uterus, however these weak effects were not highly stereoselective, which was also confirmed in radioligand binding studies. The results of the present study indicate that 3-O-methyldobutamine is a potent and highly selective ₁-adrenoceptor antagonist, with minimal activity at ₂-, ₁- and ₂-adrenoceptors. It is hypothesized that the potent ₁-adrenoceptor antagonist activity of 3-O-methyldobutamine, which resides predominantly in the (+)-enantiomer, may play a role in the hemodynamic effects of dobutamine, by contributing, in part, to the decrease in total peripheral vascular resistance observed following administration of dobutamine.     

Comparative haemodynamic effects of dobutamine and isoproterenol in man

Dobutamine was infused at a rate of 8 mcg/kg/min in 17 patients with or without congestive heart failure. Cardiac output increased from an average 2.92 to 4.45 1/min/m2 (p<0.001) with no change in mean aortic pressure (93.4 to 97.8 mmHg) and only a slight increase in heart rate (78 to 87 beats/min). Left ventricular end-diastolic pressure decreased from an average 19 to 13.7 mmHg (p<0.01). Peak left ventricular dp/dt was doubled (1147 to 2370 mmHg/sec, p<0.001) and Vmax increased from 1.08 to 2.18 circ/sec (p<0.001). In 10 patients given equi-inotropic doses (100 per cent increase in peak dp/dt) Isoproterenol produced a greater increase in cardiac output (71 percent) than Dobutamine (51 percent). isoproterenol caused mean aortic pressure to fall significantly (8 percent) while no change was noted with Dobutamine. Accordingly, peripheral vascular resistances were reduced to a greater extent with Isoproterenol than with Dobutamine (p<0.05). Mean pulmonary arterial pressure decreased significantly (25±5.9 to 22±5.7 mmHg, p<0.05) with Isoproterenol infusion and remained unchanged with Dobutamine infusion. Dobutamine increased both stroke work (57 percent) and minute work (83 percent). With Isoproterenol however, only minute work was significantly increased (90 percent). Dobutamine therefore is a potent inotropic drug, with mild chronotropic and peripheral vascular effects and may be valuable in the management of severe heart failure not associated with hypotension.