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Complaint conclusion: as noted in the literature publication, cardaioli et al complication with an embolic protection device during carotid angioplasty; catheter cardiovasc interv.2004 jun;62(2):234-6.; report a case of carotid artery stenting with an angioguard cerebral protection device is described in a patient with tight internal carotid stenosis.Deployment of angioguard induced sudden severe vasospasm, with subsequent minor stroke.A (b)(6)-year-old white female with a history of hypertension and dyslipidimia, affected by tight left ica stenosis (90% at continuous wave doppler evaluation), without symptomatic neurological episodes, was referred to our branch to be submitted to cas on informed consent, because she has already refused carotid endoarterectomy.A cerebral angiogram confirmed the presence of a subocclusive stenosis with severe calcification and a moderately tortuous course of the ica (fig.1).After selective cannulation of the common carotid artery with an 8 fr guide catheter, a 0.014_ guidewire was advanced through the stenosis and predilatation with a 2.5 mm diameter coronary balloon was performed (fig.2) in order to facilitate progression of the embolic protection device.The device used was an angioguard xp system (cordis, miami lakes, fl) with an extra support wire consisting of a polyurethane membrane filter (diameter 6mm).The filter was supported by a nitinol frame connected to a 0.014_ wire extra supportive shaft, which served as a guidewire for the interventional procedure.The device crossed the lesion with moderate difficulty, but immediately after the filter had been successfully opened distally to the stenosis, the patient developed severe hypotension and bradycardia, with loss of consciousness.An angiographic check revealed a diffuse flow-limiting spasm of the left ica, with multiple kinks of the vessel, particularly evident at the level of the carotid bulb (fig.3).Carotid bulb involvement may justify strong stimulation of baroreceptors and the hypotensive-bradycardiac reflex.Local administration of nitrates was not advisable in view of low pressure (systolic blood pressure _ 50 mm hg).The filter was rapidly removed in spite of difficult advance of the retrieval sheath, with immediate resolution of the vessel spasm (fig.4) and slow progressive normalization of hemodynamic parameters.Immediately after regaining consciousness, the patient showed neurological deficits consisting of right hemiparesis, which was more evident in the right leg.A brain ct scan performed in the acute phase (within 3 hr from the event) and repeated in the subacute phase (48 hr after the event) only revealed a small subcortical hypodense area in the left frontal region, probably consistent with previous asymptomatic embolic events, without any other new changes.Subsequently, mild reduction of right arm and leg strength (national institutes of health stroke scale (nihss) score 3) lasted a few days, and the patient recovered fully within 7 days.Based on the information available, it appears that the difficulty experienced by the customer may have been caused by device interaction and is not related to a product quality issue.The product was not returned for analysis.Additionally, as the sterile lot number was not available, device history record review could not be performed.An angioguard filter is indicated for use as a guidewire and embolic protection system to contain and remove embolic material (thrombus/debris) while performing carotid artery angioplasty and stenting procedures in carotid arteries for patients in which antiplatelet and/or anticoagulant therapy is contraindicated, the guide catheter is unable to be placed, have uncorrected bleeding disorders, known allergies to nitinol, and lesions in the ostium of the common carotid artery.Hypotension, vasospasm, and stroke do not represent a device malfunction.Hypotension, hypoperfusion and the resultant tia are well-known potential adverse events associated with this type of procedure.Tia symptoms are similar to those of stroke but do not last as long.Typically symptoms of a tia often last only a few minutes, most symptoms resolve within an hour but they may last up to 24 hours.Tia occurs when the blood supply to part of the brain is briefly interrupted.The hemodynamic instability that occurs is influenced by the baro-receptors, which are located at the carotid bifurcation.These baro-receptors are stimulated by the stretch of interventional balloons, sds (stent delivery system) and distal protection devices, initiating a reflex via the glossopharyngeal nerve.This results in a fall in blood pressure and bradycardia.These reactions are anticipated relatively short-term adverse events associated with the compression of the baro-receptors during balloon inflation, stent implantation and filter device manipulation.Certain factors may influence the likelihood of anticipated baro-receptor reactions such as advanced age, ventricular dysfunction and gender.Vessel spasm is a known potential adverse event associated with any interventional procedure where devices are introduced into the vasculature and is listed in the ifu (instructions for use) as such.Local vasospasm can be caused by the outward radial force and axial friction of the filter¿s basket, or by the device manipulations inherent in any procedure causing endothelial irritation.A carotid vessel spasm is a brief temporary tightening of the muscles in the vessel wall.This can narrow and briefly decrease or even prevent blood flow to the brain.Stroke is a well-known potential adverse event associated with the carotid stent implantation procedure and is listed in the ifu as such.Stroke is often associated with a temporary stoppage or slowing of blood flow to the cerebral arteries.The physical manipulation of the carotid arteries produces the risk of dislodgement of debris that may collect in the embolic protection device or flow downstream potentially disrupting perfusion both during and after carotid stent implantation.Clinical factors that may have influenced the event include patient, pharmacological and lesion characteristics.Given the limited information available for review at this time, there is nothing to suggest that the reported event is related to the design and/or manufacturing process of the device; therefore, no corrective action will be taken.Should additional information become available, the file will be updated accordingly.
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As noted in the literature publication, cardaioli et al complication with an embolic protection device during carotid angioplasty; catheter cardiovasc interv.2004 jun;62(2):234-6.; report a case of carotid artery stenting with an angioguard cerebral protection device is described in a patient with tight internal carotid stenosis.Deployment of angioguard induced sudden severe vasospasm, with subsequent minor stroke.A (b)(6) year-old white female with a history of hypertension and dyslipidimia, affected by tight left ica stenosis (90% at continuous wave doppler evaluation), without symptomatic neurological episodes, was referred to our branch to be submitted to cas on informed consent, because she has already refused carotid endoarterectomy.A cerebral angiogram confirmed the presence of a subocclusive stenosis with severe calcification and a moderately tortuous course of the ica (fig.1).After selective cannulation of the common carotid artery with an 8 fr guide catheter, a 0.014_ guidewire was advanced through the stenosis and predilatation with a 2.5 mm diameter coronary balloon was performed (fig.2) in order to facilitate progression of the embolic protection device.The device used was an angioguard xp system (cordis, (b)(4)) with an extra support wire consisting of a polyurethane membrane filter (diameter 6mm).The filter was supported by a nitinol frame connected to a 0.014_ wire extra supportive shaft, which served as a guidewire for the interventional procedure.The device crossed the lesion with moderate difficulty, but immediately after the filter had been successfully opened distally to the stenosis, the patient developed severe hypotension and bradycardia, with loss of consciousness.An angiographic check revealed a diffuse flow-limiting spasm of the left ica, with multiple kinks of the vessel, particularly evident at the level of the carotid bulb (fig.3).Carotid bulb involvement may justify strong stimulation of baroreceptors and the hypotensive-bradycardiac reflex.Local administration of nitrates was not advisable in view of low pressure (systolic blood pressure _ 50 mm hg).The filter was rapidly removed in spite of difficult advance of the retrieval sheath, with immediate resolution of the vessel spasm (fig.4) and slow progressive normalization of hemodynamic parameters.Immediately after regaining consciousness, the patient showed neurological deficits consisting of right hemiparesis, which was more evident in the right leg.A brain ct scan performed in the acute phase (within 3 hr from the event) and repeated in the subacute phase (48 hr after the event) only revealed a small subcortical hypodense area in the left frontal region, probably consistent with previous asymptomatic embolic events, without any other new changes.Subsequently, mild reduction of right arm and leg strength (national institutes of health stroke scale (nihss) score 3) lasted a few days, and the patient recovered fully within 7 days.
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