1. 文献回顾 颈动脉支架成型术后血流动力学 改变及防治措施 四川省资阳市第一人民医院 陈艳2008-10-06

2. Periprocedural hemodynamic instability with carotid angioplasty and stenting 颈动脉支架成型术后血流动力学 不稳定 文献一： Surgical Neurology

3. Background: Carotid angioplasty and stenting is used for treatment of carotid stenosis. Stent deployment may induce HDI and thereby cause systemic or neurologic deficits. This study defines characteristics and predictors of HDI with CAS. Methods: A total of 132 patients who had undergone CAS were evaluated for periprocedural and postprocedural HDI (hypertension, systolic blood pressure >160 mm Hg; hypotension, systolic blood pressure <90 mm Hg; or bradycardia, heart rate <60 beats per minute). Results: Frequencies of HDI were 6.8% for hypertension, 32.6% for hypotension, and 15.9% for bradycardia.

4. 文献二： Stroke October 1999 Frequency and Determinants of Postprocedural Hemodynamic Instability After Carotid Angioplasty and Stenting 颈动脉支架成形术后血流不稳定因素

5. Background and Purpose —Hemodynamic instability can occur acutely after carotid angioplasty and stent placement (CAS). We performed this study to determine the frequency of hemodynamic instability in a series of patients who underwent CAS and to analyze factors associated with development of postprocedural hemodynamic events.

6. Methods —We reviewed medical records and angiograms in a series of 51 patients (mean age 68.3+8.9 years) who underwent CAS for symptomatic (n=29) or asymptomatic (n=22) carotid artery stenosis. Any episodes of hypotension (systolic blood pressure 160 mm Hg), or bradycardia (heart rate<60 bpm) that occurred in the acute postprocedural period were recorded. The effect of demographic, clinical,intraprocedural, and angiographic factors on subsequent development of hemodynamic instability was analyzed by logistic regression.

7. Results —The frequency of postprocedural hemodynamic complications in our patient series was as follows: hypotension,22.4%; hypertension, 38.8%; and bradycardia, 27.5%. Intraprocedural hypotension (odds ratio [OR] 14.6, P50.024) and history of myocardial infarction (OR 14.1, P50.04) independently predicted postprocedural hypotension. Postprocedural hypertension was predicted by intraprocedural hypertension (OR 7.6, P50.01) and previous ipsilateral carotid endarterectomy (OR 7.6, P50.02). Postprocedural bradycardia was associated with intraprocedural hypotension (OR 74, P50.001) and intraprocedural bradycardia (OR 12, P50.008). All events had resolved at the conclusion of the intensive care unit monitoring period (mean 25.7 hours, range 18 to 43 hours).

8. Conclusions —Postprocedural hemodynamic instability is frequent after CAS and supports the need for monitoring in settings suited to expeditious management of cardiovascular emergencies. Patients who have evidence of hemodynamic instability during the procedure are at highest risk. (Stroke. 1999;30:2086- 2093.)

9. 文献三： Neurosurgery, October 2001 Prevention of Carotid Angioplasty- induced Bradycardia and Hypotension with Temporary Venous Pacemakers 使用临时起搏器预防颈动脉血管成形术后 心动过缓及血压下降 使用临时起搏器预防颈动脉血管成形术后 心动过缓及血压下降

10. OBJECTIVE: Carotid angioplasty with stent placement is becoming an established treatment modality for patients with high-risk carotid stenosis. Unlike carotid endarterectomy, angioplasty causes direct mechanical dilation of the stenotic carotid artery and bulb. Stimulation of the sinus baroreceptors （压力感受器） induces a reflexive response that consists of increased parasympathetic （副交感神经 ） discharge and inhibition of sympathetic tone （交感紧张）, which results in bradycardia （心动过缓） and subsequent cardiogenic hypotension （继发心源性低血压）.

11. METHODS: At a single institution, the experience with 43 patients treated from November 1994 to January 2000 with 47 angioplasty and stent procedures for occlusive carotid artery disease was retrospectively reviewed （回顾性 研究）.Prophy‘lactic （预防性） temporary venous pacemakers were used to prevent hypotension from possible angioplasty- induced bradycardia. Pacemakers were set to capture a heart rate decrease below 60 beats per minute. Variables analyzed included demographics （人口统计）, etiology （病因） of disease, side of the lesion, the presence of symptoms, history of coronary artery disease, percent stenosis, type of stent used, number of dilations, pressure of dilation, and angioplasty balloon diameter.

12. RESULTS: Ten patients were excluded because pacemakers were not used during their angioplasty procedures,and these included three emergencies and a lesion that was unrelated anatomically to the carotid sinus (petrous carotid). The remaining 37 procedures were performed in 33 patients with a mean age of 67 years,and consisted of 17 men, 16 women, 20 right and 17 left- sided lesions.

13. The pacemakers maintained a cardiac rhythm in 23 (62%) of the 37 procedures and in no case did the pacemaker fail to respond when activated.Recurrent (56%; 10 of 18), radiation-induced (78%; 7 of 9), and medically refractory carotid stenosis (67%;6 of 9) required intraprocedural pacing. Two patients with recurrent stenosis became hypotensive despite the aid of the pacing device but were not symptomatic. Seventy-nine percent (15 of 19) of symptomatic lesions and 57% (8 of 14) of nonsymptomatic lesions required pacing, which was statistically significant (P 0.049). No patient experienced an operative morbidity or mortality as a consequence of the temporary pacing devices.

14. CONCLUSION: Angioplasty-induced bradycardia is a common condition, and it is more prevalent in radiationinduced stenosis and with symptomatic lesions. Temporary venous demand pacing is a safe procedure and may prevent life-threatening, baroreceptor （压力感受器） -induced hypotension.

15. The blood pressure variability is related to postoperative changes in the mechanical property of the carotid sinus wall (1). Unlike carotid endarterectomy,the use of angioplasty involves direct mechanical dilation of the carotid artery and bulb, and this reflex cannot be inhibited with the use of local anesthesia. Stretching the sinus causes increased parasympathetic discharge and a reduction of systemic arterial smooth muscle tone, which results in hypotension. Therefore, patients at our institution received prophylactic temporary venous pacemakers to prevent angioplasty-induced bradycardia and subsequent hypotension.

16. Neuronal circuits regulate systemic blood pressure andparticipate in a feedback loop that controls heart rate, cardiac output, and sympathetic tone. In the carotid artery, these nerve fibers are located in the wall of the carotid sinus, classified as mechanoreceptors( 机械感受器） or baroreceptors （压力感受器）, and are principally affected by distention of the carotid sinus. The stretching of the carotid vessel stimulates and activates the afferent fibers （传入纤维） that project to the nucleus tractus solitarius （孤束核） via the glossopharyngeal nerve ( 舌咽神经） (Fig. 1). Second-order solitary nucleus neurons excite cells in the dorsal motor nucleus of the

17. Neuronal circuitry （神经传导通路） involved during carotid angioplasty that results in hypotension and bradycardia. The glossopharyngeal （窦房结） nerve transmits impulses from the carotid sinus baroreceptors （压力感受 器） to the nucleus solitarius （孤束核）. Collateral nerve fibers are sent to the nucleus ambiguous, dorsal motor nucleus of the vagus, and red nucleus. The vagus nervecarries parasympathetic signals to the heart, which produce bradycardia when activated. Collateral fibers from the reticulospinal （网状脊髓束） and solitariospinal tract synapse on the lateral horn of the thoracic spinal cord inhibit sympathetic fibers （交感神经纤 维）, producing vasodilation and decreased heart rate. These effects may be synergistic and result in symptomatic hypotension. Pathophysiology of carotid sinus-induced hypotension

18. CASE1: 患者，男性， 46 岁，因 “ 一过性晕厥 1 月，右侧肢体无力 半月 ” 第一次入院。 患者，男性， 46 岁，因 “ 一过性晕厥 1 月，右侧肢体无力 半月 ” 第一次入院。 DSA 提示双侧颈内动脉起始重度狭窄， MRI 提示双侧半 卵圆中心腔隙性梗塞。DSA 提示双侧颈内动脉起始重度狭窄， MRI 提示双侧半 卵圆中心腔隙性梗塞。 既往有 HT10 年， DM10 年，有高血脂病史及烟酒嗜好。 术前血压 150/90mmHg,HR72 次 / 分，行左侧颈动脉支 架置入术，术后病情稳定 BP120/80mmHg,HR62 次 / 分。 既往有 HT10 年， DM10 年，有高血脂病史及烟酒嗜好。 术前血压 150/90mmHg,HR72 次 / 分，行左侧颈动脉支 架置入术，术后病情稳定 BP120/80mmHg,HR62 次 / 分。 术后一月行右侧颈动脉支架成形术，术后 2 小时发生血 压下降， 80/40mmHg ，心率 35-45 次 / 分，患者诉心慌， 全身大汗，颦死感，经使用阿托品、多巴胺、扩容等症 状 1 小时缓解，心率 45-50 次 / 分，血压升至 100 - 110/50mmHg, 多巴胺持续泵入 48 小时停用，无自觉症 状。 术后一月行右侧颈动脉支架成形术，术后 2 小时发生血 压下降， 80/40mmHg ，心率 35-45 次 / 分，患者诉心慌， 全身大汗，颦死感，经使用阿托品、多巴胺、扩容等症 状 1 小时缓解，心率 45-50 次 / 分，血压升至 100 - 110/50mmHg, 多巴胺持续泵入 48 小时停用，无自觉症 状。 Holter 提示窦性心动过缓。Holter 提示窦性心动过缓。

19. 术前：双侧颈内动脉近段重度狭窄，右侧：残 余管径 / 原始管径 =1.0/5.5mm; 左侧 =1.2/4.3mm 术前：双侧颈内动脉近段重度狭窄，右侧：残 余管径 / 原始管径 =1.0/5.5mm; 左侧 =1.2/4.3mm

20. 第二次术后 DSA 片

21. CASE2: 患者，男性， 72 岁，因 “ 发作性意识丧失伴跌倒 10 月 ” 入院。 患者，男性， 72 岁，因 “ 发作性意识丧失伴跌倒 10 月 ” 入院。 DSA 发现 LV 开口重度狭窄， RICA 起始段重度 狭窄并行 LV 开及 RICA 起始段支架成形术，入 院时 ECG 提示房室传导延搁， PR 间期 0.27 秒。 术中（球囊扩张时）患者出现心率下降 32-43 次 / 分，无自觉症状，行临时起搏器安置，术后 5 天心率升至 45-52 次 / 分，拔出起搏器，无症状 出院， Holter 提示 2 度房室传导阻滞，偶发室早， 短阵室速。术后 1 月发生心悸，心率 35-45 次 / 分， 安置永久起搏器。DSA 发现 LV 开口重度狭窄， RICA 起始段重度 狭窄并行 LV 开及 RICA 起始段支架成形术，入 院时 ECG 提示房室传导延搁， PR 间期 0.27 秒。 术中（球囊扩张时）患者出现心率下降 32-43 次 / 分，无自觉症状，行临时起搏器安置，术后 5 天心率升至 45-52 次 / 分，拔出起搏器，无症状 出院， Holter 提示 2 度房室传导阻滞，偶发室早， 短阵室速。术后 1 月发生心悸，心率 35-45 次 / 分， 安置永久起搏器。