冠状动脉心肌桥的不同治疗方式的比较

2008年10月07日 · 来自专栏论文精选

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随着冠状动脉介入诊疗技术的不断普及，关于冠状动脉心肌桥(Coronary Myocardial Bridge CMB)的报道越来越多。但对其存在的意义、临床表现以及处理措施等尚无统一认识^{[1 2]}。本文研究冠状动脉造影检查发现的冠状动脉心肌桥不同处理措施结局的异同。

1 研究方法：

统计我院和上海市第六人民医院自2002年4月至2007年11月2475例冠状动脉造影检查资料。对在至少一个投照体位发现某一段冠状动脉在舒张期内径正常，而在收缩期突然狭窄，呈“挤奶效应”(milking effect)者，诊断该段冠状动脉外存在心肌桥。

按NOBEL法将心肌桥按狭窄程度分为3级^[3]：I级收缩期狭窄0-50%； II级收缩期狭窄50%-75%；III级收缩期狭窄75%-100%。.

结合患者的临床表现特征和心电图、心肌灌注显像资料，判定该心肌桥是否引起缺血相关改变。心肌桥相关的缺血临床表现是指与肌桥相关的稳定劳力性心绞痛、不稳定心绞痛、ST段抬高心肌梗塞和非ST段抬高心肌梗塞等。如临床表现和心肌桥无关，则认为该心肌桥无临床症状。心肌桥相关的缺血心电图和心肌灌注显像表现是指与壁冠状动脉供血区域一致的心电图（运动平板或HOLTER）或心肌灌注显像缺血改变。二者具备其一即认为该心肌桥引起相关缺血改变。

对引起缺血相关改变的心肌桥患者，或心肌桥压迫达NOBEL II级的患者，依据病情和患者的选择决定治疗方式，分为两组，即介入治疗组和药物治疗组。介入治疗组患者均置入药物支架治疗，药物治疗组给予抗血小板、β受体阻断剂和钙拮抗剂等药物治疗。两组患者均严格控制动脉粥样硬化的危险因素。所有患者签署知情同意书。

观察指标：随访半年，观察缺血性心脏事件的发生情况，心电图（运动平板或HOLTER）心肌灌注显像心肌缺血改善情况及3-6个月随访冠状动脉造影。如患者无缺血相关症状也无心电图或心肌灌注显像缺血表现,则认为临床治愈。

采用SPSS10.0软件进行统计学分析。计量资料采用t检验，计数资料采用FISHER精确检验。P<0.05有显著性差别。

2 结果

2.1基本情况

自2002年4月至2007年11月的2475例患者，共发现冠状动脉心肌桥72例，占2.91%（72/2475）。其中有缺血相关表现的心肌桥患者35例，占1.41%（35/2475），其中男性27例，女性8例。缺血相关心肌桥全部发生在左前降支，其中中段29例，远段4例，第一对角支2例。

2.2治疗情况

20例患者选择了药物治疗，15例患者选择介入治疗，共植入支架19枚，均为药物支架（雷帕霉素或紫杉醇）。其中左前降支17枚，第一对角支2枚，手术均顺利，未见冠脉穿孔、术后心绞痛加重、急性心肌梗塞等发生，术前两组患者基本情况无显著差别。（表1）

表1：术前两组患者基本情况比较

	药物治疗组	介入治疗组	P
例数	20	15
年龄	64.70±11.64	59.93±9.24	0.20
高胆固醇血症	8	6	0.64
高血压病	3	4	0.33
糖尿病	4	3	0.66
吸烟	6	3	0.36
稳定心绞痛	4	6	0.57
急性冠脉综合征	11	7	0.44
心电图或灌注显像缺血表现	5	2	0.66

2.2术后随访

随访发现，在药物治疗组20例中，临床治愈5例，8例仍存在与肌桥相关的稳定劳力性心绞痛，4例患者表现为劳力恶化性心绞痛，发生与肌桥相关的急性心肌梗塞3例。在介入治疗15例患者中，临床治愈10例，3例有稳定心绞痛发作，不稳定心绞痛2例，未见有急性心肌梗塞。（表2）

表2：两组临床表现特征

分组病例数治愈 AP UAP AMI

药物治疗组 20 5 8 4 3

介入治疗组 15 10 3 2 0

P 0.001 0.28 0.68 0.24

冠脉造影随访结果：药物治疗组仍有缺血相关表现的15位患者，12位患者接受了冠脉造影随访，其中5例接受冠脉内支架治疗。介入治疗组5例有临床缺血表现的患者进行了冠脉造影复查，发现支架内再狭窄3例，占20%（3/15）。其中，2例无症状，1例表现为劳力性心绞痛。

3 讨论：

冠状动脉心肌桥(Coronary Myocardial Bridge CMB)简称心肌桥，是指部分心肌行走于某段冠状动脉之上，而此段冠状动脉则称为壁冠状动脉。随着冠状动脉介入检查的推广，其发现也越来越多。有报道心肌桥的尸检发现率为15-85.7%^[4]，选择性冠状动脉造影检出率为0.5-16%^[5]。本研究共2475例患者，检出72例，发现率为2.91%，与以往报道类似。其中68例位于前降支，第一对角支2例，回旋支2例。其中引起缺血相关改变的35例，占1.41%，均发生在前降支。

大多数研究均表明，发生于左前降支的心肌桥容易引起缺血改变。本研究中所有引起缺血改变的35例肌桥均位于左前降支，占51%（35/68）。这可能与胚胎期此段冠脉位于心肌内、左前降支走行易于发生变异有关，另外和左室前壁易于发生心肌肥厚、左前降支供血范围较大等有关。

心肌桥引起心肌缺血，可能和肌桥压迫引起冠脉狭窄、肌桥近端冠脉继发动脉粥样硬化^{[6 7]}等有关。但也有认为存在继发性壁冠状动脉或肌桥后冠状动脉动脉粥样硬化性狭窄的报道^{[8 9]}。在此基础上，有可能并发冠状动脉的痉挛，加重心肌缺血^[10]。

目前认为，对无症状的患者也非良性病变，由于局部特殊的血流动力学效应，易发生动脉粥样硬化性狭窄^[11]，因此对无症状者应加强随访。对NOBEL II级以上或有缺血表现者多选用药物治疗。主要药物包括β受体阻断剂、钙离子拮抗剂、抗凝及抗血小板药物等。β阻断剂通过抑制心肌收缩力缓解心肌桥对壁冠状动脉的压迫，通过减慢心率、延长舒张期增加冠脉供血等，改善心肌缺血，尤其适用于合并高血压、冠心病、心室率偏快的患者。对以冠脉痉挛为主的患者，钙离子拮抗剂可能为更理想的选择，它不但有利于解除冠脉痉挛，还具有负性肌力作用。硝酸酯类药物可能使“挤奶效应”更加明显，从而使缺血加重，因此应避免使用。部分患者通过药物治疗可获得良好的控制。然而，部分心肌桥患者的药物控制效果有限，可发生不稳定心绞痛、心肌梗死、致命性心律失常甚至猝死。而外科搭桥手术和心肌松解术由于创伤大，手术风险大，效果也不肯定，临床很少采用。

自1995年Stables等^[12]首次报道应用金属裸支架治疗药物治疗无效的症状性心肌桥以来，不断有使用冠状动脉内支架置入进行治疗^[13-16]的报道。但是目前对冠脉内支架治疗症状性心肌桥仍存在很大争议。

首先，有作者^[17]认为多数冠状动脉心肌桥预后良好。Juilliere等^[18]对61例患者中的28例存在收缩期压迫的心肌桥患者（包括50%以上狭窄）(45.9%)进行了长达11年的随访，未发现一例心肌梗塞或心脏相关性死亡。本研究的72位患者中有28例存在心肌缺血相关的症状，占39.9%，其中18例表现为急性冠脉综合症，占51%。而只有7例接受了支架治疗，占38.9%。因此，心肌桥相关缺血表现并不少见，此类患者存在急性心肌梗塞甚至猝死的危险，而接受支架治疗的比率偏低。

其次，病理学研究发现，心肌桥外膜肌层较薄，容易破裂，因此，对其进行支架治疗的安全性尚不肯定，支架变形和冠状动脉破裂是其严重的并发症^{[19 20]}。我们的15例患者手术均顺利，表明对心肌桥患者植入支架是安全的。血管内超声研究^[21]发现心肌桥节段冠状动脉的血管面积及舒张期直径小于其参照血管，因此选择比参照血管小的支架，采用合适的扩张压力等可能会增加操作的安全性。

第三，对心肌桥血管行支架置入再狭窄发生率是否偏高。Haager^[14]等报道了11例症状性心肌桥置入金属裸支架后7周再狭窄率达46%（5/11）；Kursaklioglu^[15]报道了12例症状性心肌桥置入金属裸支架后6个月造影再狭窄发生率达67%（8/12），该研究认为除支架变形、挤压外，与一般冠脉支架类似的置入过程引起的血管损伤、支架对血管壁的持续刺激、局部血管活性物质的释放等可能是导致支架内再狭窄的原因。因此使用药物支架可能是理想的选择。我们在治疗过程中均选用了雷帕霉素和紫杉醇药物支架，随访6个月，造影显示3例发生支架内再狭窄，占20%。因此我们的研究结果支持上述假说。Sigh等^[16]也有类似发现。

临床观察发现^{[14-16 22]}，大部分症状性心肌桥患者在置入冠脉内支架后临床症状都能得到缓解。我们的研究发现，与使用药物治疗比较，选择介入治疗后更多的患者缺血得到临床治愈。发生稳定心绞痛、不稳定心绞痛的患者均有减少趋势（未达统计学显著性），未出现急性心肌梗塞患者。

因此，我们认为，对有缺血表现的心肌桥患者，选择合适的支架大小、选择药物支架，必要时参照血管内超声结果，介入治疗是安全的，并且能够达到满意的临床效果。

参考文献

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2 Diaz Widmann J, Cox SL, Roongsritong C. Myocardial bridge causing anterior myocardial infarction and postinfarction angina. South Med J, 2003,96:400-402.

3 Noble J, Bourassa MG, Pettclerdc R,et a1.Myocardial bridge and milk effect of the left anterior descending artery:normal variant or obstruction AI.Am J Cardiol, 1979,37:993-999

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7 贾新未，魏盟，陆志刚等，冠状动脉心肌桥的预后因素分析。上海医学，2006年，第29卷，第9期，618-620。

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13 Klues HG, Schwarz ER, VomDahl J, et al. Disturbed intracoronary hemodynamics in myocardial bridging: early normalization by intracoronary stent placement. Circulation,1997,96:2905-2913.

14 Haager PK, Schwarz ER, VomDahl J, et al. Long term angiographic and clinical follow up in patient with stent implantation for symptomatic myocardial bridging. Heart, 2000,84:403-408.

15 Kursaklioglu H, Barcin C, Iyisoy A, et al. Angiographic restenosis after myocardial bridge: Stenting: A comparative study with direct stenting of De-Novo atherosclerostic lesions. Jpn Heart J, 2004,45:581-589.

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17 Lozano I, Baz JA, Lo pez-palop, et al. Long-term prognosis of patients with myocardial bridge and angiographic milking of the left anterior descending coronary artery. Rev Esp Cardiol.2002,55:359-364.

18 Juilliere Y, Berder V, Suty Sclton C, et al. Isolated myocardial bridges with angiographic milking of the left anterior descending coronary artery: a long term follow-up study. Am Heart J, 1995, 129:663-665.

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20 程中伟，张抒扬。心肌桥内经皮冠状动脉介入术致冠状动脉破裂引起缩窄性心包炎一例。中国介入心脏病学杂志，2007，第15卷第1期，46。

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中文摘要

目的：比较对缺血性冠状动脉心肌桥给予药物治疗和支架治疗结局的异同。

方法：将35例缺血性心肌桥患者分为介入治疗组（15例）和药物治疗组（20例）。介入治疗组患者均置入药物支架治疗，药物治疗组给予抗血小板、β受体阻断剂和钙拮抗剂等药物治疗。两组患者均严格控制动脉粥样硬化的危险因素。随访半年，观察缺血性心脏事件的发生情况，心电图（运动平板或HOLTER）心肌灌注显像心肌缺血改善情况，3-6个月随访冠状动脉造影。

结果：介入治疗组患者共植入药物支架19枚，手术均顺利，未见冠脉穿孔、术后心绞痛加重、急性心肌梗塞等发生。随访发现，在药物治疗组20例中，临床治愈5例，8例仍存在与肌桥相关的稳定劳力性心绞痛，4例患者表现为劳力恶化性心绞痛，发生与肌桥相关的急性心肌梗塞3例。在介入治疗15例患者中，临床治愈10例，3例有稳定心绞痛发作，不稳定心绞痛2例，未见有急性心肌梗塞。冠脉造影随访发现，药物治疗组仍有缺血相关表现的15位患者，12位患者接受了冠脉造影随访，其中5例接受冠脉内支架治疗。介入治疗组5例有临床缺血表现的患者进行了冠脉造影复查，发现支架内再狭窄3例，占20%（3/15）。

结论：对有缺血表现的心肌桥患者，选择合适的支架大小、选择药物支架，必要时参照血管内超声结果，介入治疗是安全的，并且能够达到满意的临床效果。

关键词：心肌桥；药物支架；药物

Treatment of Coronary myocardial bridge: A comparison of drugs versus drug eluted stent

Xinwei JIA^a, Xianghua Fu^a*, Xinshun GU^a, Meng Wei^b

a: Cadre cardiovascular department, the second hospital of Hebei medical university

b: Cardiovascular department, Shanghai sixth people’s hospital

*: Conrresponding author

With the spreading of coronary interventional technologies, more and more coronary myocardial bridges are diagnosed, but their clinical features and management are unsolved^{[1 2]}. Sometimes they are regarded as benign conditions and need not special treatment^[3], however, sometimes they are considered culprit which might result in angina pectoris, myocardial infarction and even sudden cardiac death, and further intervention with either drugs or stent is needed. This study discusses the different outcomes of coronary myocardial bridge using different clinical strategis such as drugs therapy and drug eluting stent implantation.

Material and methods

Patients who underwent coronary angiography in our hospital and Shanghai sixth people’s hospital from April 2002 to November 2007 were enrolled into our study. If any coronary artery segments show normal diastolic diameter and abrupt systolic narrowing angiographically, which is known as milking effect, a coronary myocardial bridge is diagnosed.

According to the method described before ^[3], Coronary myocardial bridges were divided into 3 grades, that is, systolic stenosis 0-50% (grade I), 50-75% (grade II) and 75-100% (grade III).

The clinical, electrocardiographical and myocardial emission tomograpical materials of every patient were taken into accounts in order to decide if the CMB caused myocardial ischemia. The CMB related clinical ischemic events means CMB related stable angina pectoris, unstable angina pectoris, ST elevated myocardial infarction and non-ST elevated myocardial infarction. The CMB related ischemia electrocardiographical and ECT changes means regional myocardial ischemic changes consistent with the region of coronary artery blood supplying. CMB is thought to be ischemic if it causes at least one of the two ischemic changes.

Patients with ischemic CMB or Noble II-III CMB were divided into two groups ,that is, stent intervention group and drug intervention group, according to patient’ choice. Drug eluting stent were imlpanted in all patients in stent intervention group. Patients in drug intervention group were treated by antiplatelet, βblockers and calcium channel blockers. The risk factors of atherosclerosis were controlled strictly in both groups. The study protocol was approved by the Ethical Committee of the hospital. Informed written consent was obtained from all patients.

The clinical cardiac ischemic events, ECG (treadmill and holter) and ECT ischemic changes were followed up for six months. Coronary angiography was performed in parts of the patients who showed above ischemic changes. If patient showed no above ischemic changes, he was considered clinically cured.

Statistical analysis: Continuous parameters are described as mean±standard deviation. The t-test was performed between two groups. Categorical variables were compared by Fisher’s exact test. A probability value of <0.05 was considered statistically significant.

Results

Totally 2475 patients during April 2002 to November 2007 were enrolled into this study, with 72 cases of CMB found (2.91%).Of all the CMB patients, 35 patients showed CMB related cardiac ischemia(1.41%), including 27 male and 8 female. The ischemic related CMB were all found in left anterior descending (LAD) artery, 29 in the middle segments, 4 in the distal segments and 2 in the first diagonal.

Demographics

Twenty patients were enrolled into drug intervention group and fifteen patients into stent intervention group. Totally 19 stents were implanted, 17 in LAD and 2 in diagonal without coronary artery perforation and postoperative cardiac ischemic events. Clinical characteristics of the two groups are presented in Table 1. There was no significant difference between the groups in cardiovascular risk factors and ischemic events.

Table 1: Clinical characteristics of the study population

	Drug intervention group	Stent intervention group	P
Cases	20	15
Age	64.70±11.64	59.93±9.24	0.20
Hypercholesterol	8	6	0.64
Hypertension	3	4	0.33
Diabetic mellitus	4	3	0.66
Cigar-Smoking	6	3	0.36
Stable angina pectoris	4	6	0.57
Acute coronary syndrom	11	7	0.44
ECG or ECT ischemic changes	5	2	0.66

Following up

In drug intervention group, five patients were clinically cured, eight patients had CMB related stable angina pectoris, four patients showed exaggerated exerted angina pectoris and three patients underwent CMB related acute myocardial infarction. In stent intervention group,ten patients were clinicaly cured, three patients had stable angina pectoris and 2 patients showed unstable angina pectoris, without acute myocardial infarction attack.(Table 2)

Table 2: Following up clinical characteristics of the study population

Groups cases cured AP UAP AMI

Drug intervention group 20 5 8 4 3

Stent intervention group 15 10 3 2 0

P 0.001 0.28 0.68 0.24

Coronary angiographical following up

In drug intervention group, of the 15 patients who showed ischemic changes, 12 patients received coronary angiographical reexamination and five patients had stent implanted. In stent intervention group, the five patients who showed ischemic changes underwent coronary angiographical reexamination and intrastent restenosis were found in three patients (20%, 3/15).

Discussion

Coronary myocardial bridge means that a bundle of myocardial muscle run over a coronary artery segment and thus results in functional systolic coronary artery stenosis. This coronary artery segment is called mural coronary artery. It has been reported that its occurrence rate is about 15-85.7% in corpse autopsy studies^[4] and 0.5-16% in selective coronary angiographical studies^[5]. In our study, its occurrence rate is 2.91% (72/2475), similar to those results. Of all the 72 CBMs, 68 located at LAD, 2 at the first diagona and 2 at left circumflex (LCX) artery. Thirty-five CMBs, which all located at LAD, caused ischemia related changes (1.41%, 35/2475).

It has been found that CBMs located at LAD often lead to cardiac ischemia. In this study, the 35 CMBs which caused ischemic changes are all at LAD (51%, 35/68). The reasons might lies in the following: This coronary artery segments run in myocardium during embro period and aberrance are easily to occur. Hypertrophy ofen occur at anterior wall of left ventricle. The LAD often supply blood to larger myicardial region.

CMB results in myocardial ischemia via compressing coronary artery, inducing athrosclerosis lesions at proximal of CMB ^[6.7]. But there are reports that atherosclerosis lesions occurred at mural coronary artery, even at post CMB coronary artery ^{[8 9]}. Coronary spasm might occur on this basis and exacerbate myocardial ischemia ^[10].

CMB is not considered benign nowdays because it tends to induce atherosclertic stenosis later due to its special hemodynamical effect, even though it isn’t the ischemic culprit now. So carefull following up is necessary. For CMBs over Nobel grade II or with ischemic changes, drug therapy is of first choice. The most widely used drugs are βblockers, calcium channel blocker, antiplatelets and anticoagulants. Nitrate esters can not be used because it may aggravate “milking effects” and exacerbate ischemia. Most patients could be cured this way. However, sometimes drugs effect was limited in some patients, who might suffer unstable angina pectoris, myocardial infarction, fatal arrythmias and even sudden death.CABG and myocardial loosening operations is seldomly used because of severe trauma and higher risks.

In 1995, Stables^[12]first reported the successful treatment of intracoronary stent on drug effectiveless sympotomatic CMB. A large cohort of studies was published during the following years ^[13-16]. But there are still much quarrelling about this topic up to now.

Firstly, some authors ^[17] considered CMB as benign variation and its progniosis is optimistic. Juilliere ^[18] reported a 11 years following up study of 61 CMB patients, for the 28 patients with systolic compression (45.9%) (including stenosis over 50%), there was no myocardial infarction or cardiac related death occured. Our study also found that of the 72 CMB patients, 35 patients had ischemia related changes (48.6%), But on the other hand. of the 35 patients,18 patients had acute coronary syndrom (51% 18/28),only 7 patients had stent implanted(7/18 38.9%).So, CMB related ischemia is not rare and need positive stent treatment because it may lead to acute myocardial infarction or sudden cardiac death.

Secondly, the safty of stent implantation is uncertain, because the adventitia of CMB artery is thin and easy to perforate. Stent deformation and artery perforation is the severe complications of stent implatation. Our sucessful operations indicate that stent implantation for those people is safe. Intravascular ultrasound(IVUS) study^[21] has found that the vascular area and the diastolic diametre of CMB artery segment is smaller than its contrast artery, so to select a relatvely smaller stent diametre and adopt appropriate dilation pressure may improves the safty of the operation.

Thirdly, is the restenosis rate high if stent is implanted into CMB mural artery? Haager^[14]implanted metal bare stent in 11 sympotomatic CMB patients, 5 patients developed restenosis (46% 5/11) at the seventh week. Kursakliogu ^[15] reported a 67% restenosis rate during 6 months angiographical following up in 12 patients who received bare metal stent implantation. Besides the stent deformation and extrusion, the author thought that the vascular injury similar to common coronary stent implantation, the stimuli bare metal stent exerted on vascular wall and release of local vascular active substances are also the reasons of higher restenosis rate. So drug eluting stent may be the optimal choice for CMB patients. We choose rapamycin eluted stent and TAXUS stent in our study, and there were only 3 patients of the 15 patients developed restenosis (20%, 3/15) at 6 months follow up. So, our results support Kursakliogu’s study. Results from Sigh’s^[16]investigation does the same.

Clinical investigations ^{[14-16 22]} indicated that ischemic symptoms in most patients were alleviated after stent implantation in symptomatic CMB patients. In our study, compared with drug intervention group, stent implantation clinically cured much more patients (p<0.05). Patients of stable angina pectoris and unstable angina pectoris tend to decrease (didn’t reach statistical significance), no acute myocardial patients occurred.

In conclusion, our study indicated that for patients with ischemic CMB, if drug eluting stent of appropriate stent size was choosed, with the assistant of IVUS if necessary, stent implantation is safe and effective.

References