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| Model Number AV00 |
| Device Problems
Calcified (1077); Degraded (1153); Occlusion Within Device (1423); Incomplete Coaptation (2507)
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| Patient Problems
Aortic Valve Stenosis (1717); Calcium Deposits/Calcification (1758); Stenosis (2263)
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| Event Date 11/07/2011 |
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Event Type
Injury
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Event Description
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According to the information received from the study, the patient was diagnosed on (b)(6)2011 with severe aortic stenosis and structural valve deterioration due to homograft calcification affecting homograft valve hemodynamic identified by transthoracic echocardiogram.Homograft calcification present in leaflets, aortic root, and ascending aorta.Echocardiogram report indicated e/e ratio of 34.63, severe concentric left ventricular hypertrophy (lvh) with ejection fraction (ef) 55-65%, left atrium (la) severely dilated, borderline to mild mitral leaflet thickening with normal leaflet mobility, no mitral stenosis, trace mitral regurgitation (mr), trace tricuspid regurgitation (tr), aortic homograft present, aortic valve (av) leaflets are heavily thickened and appear calcified, systolic excursion of valve leaflets appear significantly reduced, mean aortic gradient 30-40 mmhg, severe aortic stenosis (as) with calculated aortic valve area (ava)<1.0 and dimensionless index of <0.25, aortic root 2.3cm, ascending aorta 2.9cm.On (b)(6) 2011, patient was diagnosed with worsening aortic stenosis and homograft calcification of leaflets.Transesophageal echocardiogram (tee) report indicated severe concentric lvh, aortic homograft present, the pedicle of the homograft extends about 5.5-6cm above the aortic annulus, max diameter of the aortic homograft is 2.7cm and above this region the ascending aorta measures 3.9cm in diameter and is mildly dilated, mild mitral leaflet thickening and normal leaflet mobility, no mv stenosis, mild mr, motion of non coronary aortic cusp is best preserved, left coronary cusp appears fixed and immobile, aortic leaflet commissures appear calcified, ava 0.8-0.9cm2, the dimensionless index is about 0.3, no subaortic membrane, based on continuity equation the ava is about 1.0cm2, no aortic insufficiency (ai).The homograft was explanted on (b)(6) 2011 and aortic valve replacement (avr) with ascending aorta reconstruction with darcon graft was performed.Preoperative diagnosis was structural valve deterioration, calcification, and aortic stenosis.Aortic homograft root, annulus, and leaflets were found to be heavily and entirely calcified.Explanted pathology report found aorta with calcified atherosclerosis, suture granuloma, and wall up to 0.2cm thick and calcified, as well as aortic valve replacement with dystrophic calcification, no acute inflammation, and tan-yellow in color.
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Manufacturer Narrative
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This allograft was manufactured prior to may 25, 2005 and therefore is regulated as a medical device.This investigation is currently ongoing.Any additional information will be provided in the follow-up report.
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Manufacturer Narrative
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According to the report, the surgeon saw a (b)(6) hero graft patient because the dialysis clinic thought his graft was clotted.Upon x-ray he found that the outflow component was actually broken at the area where it made contact with the clavicle.The patient lifts heavy weights on a daily basis and the surgeon believes the repeated stress between the clavicle and the outflow component caused the breakage.He removed the device and implanted another graft and outflow component.He still has that portion of the outflow component and graft to return to us, so he will need an explant kit.He could not find the lot numbers for either the graft and outflow component.Initially there was no accusation of a deficiency with the hero 1002 component therefore a medwatch was not filed.Upon receipt of the additional information it was decided that the hero 1002 component would also be investigated.This medwatch is a combined initial and follow-up report for the hero 1002 component.Additional information was received from the surgeon on 12/16/2014 in the form of a clinical summary which included an x-ray picture.The hero was implanted on (b)(6) 2011.On (b)(6) 2012 the patient had a revision due to intermittent high venous pressure.Calcification was seen in graft near arteriovenous fistula (avf) connection, section of graft resected.On (b)(6) 2012 the patient had a thrombectomy and revision due to kinking of the outflow component to graft connection with adduction of shoulder.Between (b)(6) 2013 and (b)(6) 2013 the patient had a total of 6 thrombectomies/revisions.On (b)(6) 2013 was when the fractured outflow component was noted and the outflow was replaced.On (b)(6) 2014 there was bleeding from a pseudoaneurysm of the arterial graft component (agc), new segment of acuseal inserted.On (b)(6) 2014 and (b)(6) 2014 the patient underwent thrombectomies.Also on (b)(6) 2014 the patient underwent a revision due to calcification causing 90% narrowing of the graft/hero connector lumen.A sample review was held on 12/23/2014.The hero venous outflow component (voc) was returned in a cryolife provided specimen cup (10% buffered formalin) which is contained within the sample return kit.The hero voc was visually inspected in a biological safety cabinet.Damage could be seen on the voc approximately at the location of the clavicle and first rib, the voc appeared to have been damaged.The damage was through the braiding and holes could be seen in the silicone material.The damage visible appeared to have been caused by repeated crushing and stress between the clavicle and first rib.The marker band was also been damaged.No damage was noted on the silicone around the marker band and the marker band appeared fully intact.Damage noted during the review is consistent with damage caused by the voc be repeatedly crushed between the first rib and clavicle.The clinical summary provided by the surgeon indicates that the hero graft was implanted on (b)(6) 2011 to salvage a transposed vein arterio-venous fistula (avf).On (b)(6) 2012, the arterial graft component (agc) was revised to treat high venous pressures which were attributed to calcification in the agc near the avf connection.On (b)(6) 2012, the venous outflow component (voc) was revised to treat occlusion due to kinking of the voc which was attributed to repetitive arm movements.Subsequent to this revision the patient experienced multiple episodes of occlusion and underwent successful thrombectomies to restore patency.On (b)(6) 2013 the voc was replaced due to a fracture that was approximated to be at the location of the clavicle and first rib region as seen in the radiograph.The use of the hero graft to salvage an existing avf has been previously reported.Thrombosis is the most common cause of vascular access dysfunction and a potential complication listed in the hero graft instructions for use (ifu).Gibson, et.Al., report that a history of hemodialysis access thrombosis was associated with an 81% increase in risk of primary access failure and 2.56 times the risk of secondary failure.As such, it is not unexpected that this patient experienced multiple thrombotic episodes.Vascular calcification is a common complication in patients with chronic kidney disease and therefore the probable cause of the reported calcification and not related to the hero graft.Device kinking and/or fracture would impact the blood flow hemodynamics through the device; as such it is plausible that this event may have contributed to the thrombotic episodes.Given the anatomic placement of the device in the shoulder area, it is possible that repetitive arm movements and/or implant technique could contribute to the reported kinking and/or subsequent fracture of the voc.Per the operative summary supplied, an acuseal graft was used on (b)(6) 2014 to replace the avg portion that had a documented pseudoaneurysm.No additional information is available as to the potential cause of the pseudoaneurysm, although this too is a known complication, and is typically associated with a cannulation site.The described treatment for the pseudoaneurysm is a modification to the device, so cryolife cannot support this modification as it is not an approved indication/modification to the device.The ifu provides adequate instructions to implant the graft in the approved configuration but no allowance is made for off label use.Clinical outcomes with a modified device have not been evaluated by cryolife, so it is difficult to discuss the basis of any relationship of subsequent clinical events listed in the provided summary to the hero graft.The ifu lists vascular graft revision/replacement, partial stenosis or full occlusion, kinking, device migration, pseudoaneurysm, and device compression as potential complications with the use of the hero graft.The ifu also provides the following information: "when using the subclavian vein for venous access, a more lateral approach might mitigate the risk of clavicle crush or occlusion of the venous outflow component.Consideration should be made to follow these patients with clavicle imaging to monitor the potential of interaction of the clavicle and first rib with the venous outflow component." the root cause for the reported damage to the voc is most likely due to compression and movement related to the patient's activity.The hero graft was implanted via a right subclavian approach also increasing the risk of clavicle crush; precautions regarding this approach are included in the ifu.The root cause of the calcification is likely due the patient's hyperparathyroidism due to renal failure.The multiple thrombosis events are related to poor flow through the graft which is most likely due to kinking of the device or inadequate inflow.The ifu states that thrombosis is the most common cause of vascular access dysfunction.The pseudoaneurysm of the agc was likely related to repeated needle access.This is a known potential complication addressed in the ifu.There is no indication that an error or deficiency occurred at cryolife; therefore, a capa is not warranted at this time.This event represents known potential complications of the hero graft which are outlined in the device's ifu.These known potential complications are common among all arteriovenous grafts, and do not suggest that there is a deficiency in the hero or the hero ifu.There is no indication that an error or deficiency occurred at cryolife and the ifu adequately communicates risk.
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Event Description
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Dr.(b)(6) saw this (b)(6) hero graft patient because the dialysis clinic thought his graft was clotted.Upon x-ray he found that the outflow component was actually broken at the area where it made contact with the clavicle.The patient lifts heavy weights on a daily basis and dr.(b)(6) believes the repeated stress between the clavicle and the outflow component caused the breakage.He removed the device and implanted another graft and outflow component.Initially there was no accusation of a deficiency with the hero 1002 component.Upon receipt of additional information however, it was decided that the hero 1002 component would be investigated.This medwatch represents an initial and a follow-up report for the hero 1002 component.
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Manufacturer Narrative
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*follow up 1 was incorrectly submitted under this report number but for a separate complaint.This is the first followup associated with this complaint.This allograft was manufactured prior to may 25, 2005 and therefore is regulated as a medical device.The allograft was not returned, so no direct observations could be made.The certificate of assurance for batch number 6696491 was reviewed.All attributes noted during inspection of the allograft was documented appropriately and the allograft met specifications.The patient underwent allograft implantation at age (b)(6) years and explantation at (b)(6) years.Therefore, the allograft was implanted for a total of 11.3 years.The use of aortic allografts for aortic valve replacement has often been reported as a good option for a younger patient populations due to a lack anticoagulation therapy required and excellent hemodynamic characteristics, which favor a more vigorous lifestyle and functional status (doty, 1998).However, a younger age (under 60 years of age) at implantation has also been associated with accelerated rates of valve failure and explant among biologic valves (dagenais, 2005; smedira, 2006).Koolbergen et al.Also noted that reoperations of the allograft wall and valve calcification may be encountered in 50% of allograft reoperations (koolbergen, 2002).Rates of reoperation and explant following aortic valve replacement with an aortic homograft have been described in the literature.Smedira et al.Reported 46 explants in a series of 744 patients who received aortic homografts for aortic valve replacement.Structural valve deterioration (svd) was cited as the most common mechanism of valve failure, occurring in 59% (n= 27/46) of the population.At 5, 10, and 12 years, risk-unadjusted freedom from homograft explant for svd was 98.0%, 91%, and 77%, respectively (smedira, 2006).Indications for valve explant were as follows: stenosis - 5.3% (n= 2), regurgitation - 79% (n= 30), mixed - 16% (n= 6), and unknown (n=8).It is important to note that the majority of patients included in this series were less than or equal to 60 years of age at time of implant [<30 (6.3%, n= 47); 30-40 (21%, n= 154); 40-50 (27%, n= 205); 50- 60 (27%, n= 203)].Increased risk of svd was associated with younger age at time of implantation (smedira, 2006).A study by doty et al.Reported that seven (6%) patients required valve explant, four of which for structural deterioration.At 10 years, freedom from reoperation for allograft-related causes was 92% (doty 1998).All explants due to svd occurred in younger patients (under the age of 50 years; mean age 33.8 years) at a mean of 6.9 years post-implant (doty, 1998).Similarly, o'brien et al.Reported that 39% of patients between ages 41 and 60 underwent reoperation by 15 years postoperatively (o'brien, 2001).Rates of freedom from svd in younger patients (less than or equal to 50 years of age at time of time of implant) vary in the literature.Rates from 4 large cohort studies of younger patients are reported below: · cryolife - 85% @ 10 years (<50 years; 348 patients), · o'brien - 95%@ 10 years; 81%@ 15 years (41-60 years; 332 patients).At 10 years, the results are comparable across all the patient age groupings with >90% freedom from svd.However, at 15 years the younger patients <60 start to show a slight increase in svd as is expected in the younger patient populations: · doty - 97%@ 10 years (mean age- 48 years; 117 patients), · dossche - 100% @ 8 years (mean age- 51years; 132 patients).Rates of freedom from reoperation due to svd in younger patients (less than or equal to 50 years of age at time of time of implant) vary in the literature.Rates of freedom from reoperation due to svd from 9 large cohort studies of younger patients are reported below: · cryolife: 85%@ 10years; n= 348, mean age 38.1 years (18- 50 years), · dagenais: 91%@ 7 years; n= 54, mean age 53.5 years (45-65 years), · doty: 97% @ 10years; n= 118, mean age 45.6 years (15- 83 years), · smedira: 91% @ 10 years; mean age 49.0 years (18- 84 years), · dossche: 100%@ 8 years; mean age 50.8 years (17- 77 years), · kaya: 86% @ 10 years; mean age 51.3 years (14- 79 years), · kilian: 87%@ 10 years; mean age 50.0 years (19- 70 years).According to the literature, reoperation of an aortic valve allograft due to svd after 11.3 years in a (b)(6) year old patient is not unexpected.According to the report, an aortic valve allograft was explanted approximately 11 years after implant due to calcification and stenosis.The pathologic findings are typical of svd, which is a known potential long-term complication of human heart valve transplantation.The surgical wound infection is likely related to the replacement procedure post-explant.Considering the duration of implantation of approximately 11 years, the findings of calcification and structural valve deterioration are not unanticipated and the sternal wound infection cannot be related to the explanted allograft.All attributes noted during inspection of the allograft were documented appropriately and the allograft met specifications per qs3001, cardiac allograft attributes.According to clinical literature, reoperation and explant of an aortic valve allograft due to svd after 11.3 years in a (b)(6) year old patient is not unexpected.Also, the pathologic findings are typical of svd, which is a known potential long-term complication of human heart valve transplantation.The ifu lists the following adverse events reported with the use of cardiac allografts: calcification, degeneration, valvular and perivalvular insufficiency, and valvular and conduit stenosis.At this time, there is no indication that errors or deficiencies occurred at cryolife and the ifu communicates precautions and warnings appropriately.
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Event Description
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According to the information received from the study, the patient was diagnosed on (b)(6) 2011 with severe aortic stenosis and structural valve deterioration due to homograft calcification affecting homograft valve hemodynamic identified by transthoracic echocardiogram.Homograft calcification present in leaflets, aortic root, and ascending aorta.Echocardiogram report indicated e/e ratio of 34.63, severe concentric left ventricular hypertrophy (lvh) with ejection fraction (ef) 55-65%, left atrium (la) severely dilated, borderline to mild mitral leaflet thickening with normal leaflet mobility, no mitral stenosis, trace mitral regurgitation (mr), trace tricuspid regurgitation (tr), aortic homograft present, aortic valve (av) leaflets are heavily thickened and appear calcified, systolic excursion of valve leaflets appear significantly reduced, mean aortic gradient 30-40 mmhg, severe aortic stenosis (as) with calculated aortic valve area (ava)<1.0 and dimensionless index of <0.25, aortic root 2.3cm, ascending aorta 2.9cm.On (b)(6) 2011 patient was diagnosed with worsening aortic stenosis and homograft calcification of leaflets.Transesophogeal echocardiogram (tee) report indicated severe concentric lvh, aortic homograft present, the pedicle of the homograft extends about 5.5-6cm above the aortic annulus, max diameter of the aortic homograft is 2.7cm and above this region the ascending aorta measures 3.9cm in diameter and is mildly dilated, mild mitral leaflet thickening and normal leaflet mobility, no mv stenosis, mild mr, motion of non coronary aortic cusp is best preserved, left coronary cusp appears fixed and immobile, aortic leaflet commissures appear calcified, ava 0.8-0.9cm2, the dimensionless index is about 0.3, no subaortic membrane, based on continuity equation the ava is about 1.0cm2, no aortic insufficiency (ai).The homograft was explanted on (b)(6) 2011 and aortic valve replacement (avr) with ascending aorta reconstruction with darcon graft was performed.Preoperative diagnosis was structural valve deterioration, calcification, and aortic stenosis.Aortic homograft root, annulus, and leaflets were found to be heavily and entirely calcified.Explanted pathology report found aorta with calcified atherosclerosis, suture granuloma, and wall up to 0.2cm thick and calcified, as well as aortic valve replacement with dystrophic calcification, no acute inflammation, and tan-yellow in color.
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