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Year : 2012  |  Volume : 6  |  Issue : 1  |  Page : 92-93

Myocardial ischemia during carotid artery stenting in neuroradiologic suite

Department of Neuroanesthesiology, Neurosciences Center, All India Institute of Medical Sciences, New Delhi, India

Correspondence Address:
Tumul Chowdhury
Department of Neuroanesthesiology, Neurosciences Center, 7th?Floor, All India Institute of Medical Sciences, New Delhi - 110 029
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1658-354X.93084

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Date of Web Publication21-Feb-2012

How to cite this article:
Bharati SJ, Chowdhury T, Goyal K, Sokhal N. Myocardial ischemia during carotid artery stenting in neuroradiologic suite. Saudi J Anaesth 2012;6:92-3

How to cite this URL:
Bharati SJ, Chowdhury T, Goyal K, Sokhal N. Myocardial ischemia during carotid artery stenting in neuroradiologic suite. Saudi J Anaesth [serial online] 2012 [cited 2020 Oct 25];6:92-3. Available from:


In the era of endovascular intervention, carotid artery stenting (CAS) is the preferred treatment for atherosclerotic extracranial carotid artery diseases and has now become a safe alternative to carotid end arterectomy (CEA) in high-risk patients. Thromboembolic events, such as stroke and myocardial ischemia (MI), may occur during such procedures and use of distal protective devices is recommended as prophylaxis against such phenomena. [1] However, no case has been reported to note MI during carotid stenting. Here we have reported a case of myocardial ischemia during carotid stenting for bilateral carotid artery stenosis.

A 79-year-old male patient weighing 70 kg presented to neurology outpatient department with symptoms suggestive of transient ischemic attack over a period of 1 month. His cardiac evaluation was normal. 2-D Echocardiography was suggestive of left ventricular ejection fraction >60% with no regional wall motion abnormality. Carotid Doppler sonography showed >85% stenosis in bilateral internal carotid artery (ICA) further confirmed by angiography. In view of bilateral ICA stenosis and advanced age of the patient, carotid stenting was planned. The patient was put on antiplatelet agents (aspirin and clopidogrel) 7 days before the procedure. Stenting of the stenosed right ICA was done successfully under monitored anesthesia care. The procedure was uneventful and the total duration was 90 min. Stenting of left ICA was scheduled for third day after the first procedure. The stenting of left ICA was initially started in awake state, but was later converted into general anesthesia due to interference of patient movement with the procedure. His baseline BP was 122/87 mmHg and HR was 67/min. The patient was induced with fentanyl 150 μg, propofol 100 mg; and endotracheal intubation was facilitated with rocuronium 70 mg. The patient remained hemodynamically stable during induction and intubation without experiencing any significant hemodynamic fluctuations. Along with the routine standard monitoring, right radial artery was cannulated for intra-arterial BP monitoring and a blood sample was sent for baseline blood gases and electrolytes. Anesthesia was maintained with oxygen/nitrous oxide (50:50) and isoflurane to maintain MAC of 1. The right femoral artery was punctured with 7 Fr sheath. Since ACT machine was not functional, 3000 IU of unfractionated heparin was administered empirically for anticoagulation. After 10 min of femoral puncture, the patient developed bradycardia with hypotension (heart rate of 36/min and BP of 60/40 mmHg), and ECG revealed ST segment elevation of >2 mm. Inj. atropine was administered in titrated doses (each bolus of 0.2 mg) immediately; but bradycardia persisted and hypotension did not respond to vasopressor (boluses of mepenteramine). Hence, dopamine infusion was started at 8 μg/kg/min. ST- elevation still persisted, and at the same time interventional neuroradiologist noticed blood clots on aspiration from femoral artery. Suspecting inadequate anticoagulation, 2000 IU of unfractionated heparin was repeated and cardiologist was called to perform coronary angiography to exclude any significant cardiac event. By the time the coronary angiography was performed, the hemodynamic parameters (heart rate and BP) started stabilizing and ST-elevation started resolving by gradually coming to baseline. The coronary angiography was normal. The procedure was abandoned, and the patient was shifted intubated on inotropic support to the ICU. Serial Trop-T in ICU remained negative and 12 lead ECG showed no ST changes. Further cardiac evaluation was normal and no fresh ECG changes were observed. Dopamine infusion was tapered off over a period of 3 h, and the patient was extubated after 2 h of weaning from inotropic support. The patient was neurologically intact and stable in the ICU.

Carotid artery stenting is preferred over CEA for high risk symptomatic patients as it avoids the need for general anaesthesia, incision in neck, nerve injury associated with surgery and wound complication. DFD have been shown to reduce the incidence of stroke and there is consensus for routine use of protective devices. [2] Procedure related myocardial ischaemia during stenting is not yet reported. Myocardial ischaemia in our case is most probably due to thrombo-embolic phenomenon from the femoral puncture site. Since we were not able to measure ACT, empirically administered heparin probably did not produce adequate anti-coagulation; and this might have resulted in thrombus formation at the puncture site. Propogation of microemboli from puncture site to coronaries may have induced transient coronary vasospasm as manifested by bradycardia with hypotension and ST segment elevation; with subsequent normal coronary angiography. Once the transient coronary vasospasm got relieved, hemodynamic parameters returned to normal with subsequent successful weaning of the patient from inotropic and ventilator support; without causing permanent myocardial injury as evidenced by normal 12 lead ECG and negative serial Trop-T test. To conclude, Carotid artery stenting with distal protective device per se is a low risk procedure but carries antecedent risk of stroke. Therapeutic anti-coagulation is of paramount importance in avoiding thromboembolic phenomenon and associated complications. But achieving the same becomes very difficult without ACT monitoring. ACT should be measured hourly and maintained more than 2 times normal value as an effective monitor of anti-coagulation.

  References Top

1.Mas JL, Trinquart L, Leys D, Albucher JF, Rousseau H, Viguier A, et al. Endarterectomy versus angioplasty in patients with symptomatic severe carotid stenosis (EVA-3S) trial: Results up to 4 years from a randomised, multicentre trial. Lancet Neurol 2008;7:885-92.  Back to cited text no. 1
2.Cremonesi A, Manetti R, Setacci F, Setacci C, Castriota F. Protected carotid stenting: Clinical advantages and complications of embolic protection devices in 442 consecutive patients. Stroke 2003;34:1936-41.  Back to cited text no. 2


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