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Impact of Complications During Transfemoral Transcatheter Aortic Valve Replacement: How Can They Be Avoided and Managed?

Originally published of the American Heart Association. 2019;8:e013801

    Transcatheter aortic valve replacement (TAVR) has revolutionized the treatment of aortic stenosis and is the treatment of choice for patients at prohibitive and high surgical risk. Extension of indications into intermediate surgical risk has begun, and recently 2 large randomized trials demonstrated that TAVR may be superior to surgery in patients at low surgical risk and can potentially offer better results at initial follow‐up.1, 2, 3 TAVR practice has evolved continuously with concomitant simplification of the procedure. If one disregards the financial considerations, predictability of the procedural outcome and certainty regarding the durability of TAVR prostheses are 2 of the main remaining restrictions to universal implementation.

    Transfemoral access is the preferred approach, as it has a 20% relative reduction in mortality compared with surgical aortic valve replacement (SAVR) (hazard ratio HR, 0.80; 95% CI, 0.69–0.93; P=0.024).3 Understanding the mechanisms that underlie complications during transfemoral TAVR is essential, and familiarity with the techniques for their prevention and treatment is mandatory. In this review, we provide a state‐of‐the‐art overview on the avoidable procedural complications of contemporary transfemoral TAVR practice, with a specific focus on strategies for their prevention and management.

    Vascular Access Complications

    Prevention, early identification and effective management of vascular access complications remain an important aspect of managing patients undergoing TAVR. The incidence of vascular complications has varied according to the definition that has been applied. In patients receiving first‐generation valves, ≈12% of patients experienced a major vascular complication and 16% a life‐threatening bleed, as defined by the Valve Academic Research Consortium criteria.4 Over time, there has been a significant reduction in major vascular complications, with an incidence of 6% to 8% in recent TAVR trials.5, 6, 7 This reduction has been driven by a combination of smaller sheath sizes, flexible delivery systems, multidetector computed tomography (MDCT) assessment of the peripheral vasculature, and operator experience.8, 9 However, vascular complications and hemorrhage remain a significant challenge in contemporary practice and are associated with increased length of stay and higher mortality at 1 year (HR, 2.31; 95% CI, 1.20–4.43; P=0.012).6, 10, 11

    The contemporary Valve Academic Research Consortium‐2 criteria include aortic and peripheral access complications within the category of major vascular complications.12 This category comprises aortic/annular dissection or rupture, ventricular perforation, and pseudoaneurysm or aneurysm. Major access complications include vascular injury (dissection, stenosis, perforation, rupture, fistula, pseudoaneurysm, hematoma, irreversible nerve injury, compartment syndrome, closure device failure), or a requirement for unplanned surgical/endovascular intervention leading to death, life‐threatening or major bleeding, visceral ischemia, or neurological impairment. The Valve Academic Research Consortium‐2 also includes distal embolization resulting in amputation or irreversible end‐organ damage, and any significant ipsilateral lower extremity ischemia or access‐site nerve injury (Table S1).

    Vascular complications most commonly occur at the access site, and bleeding and/or hematoma formation occurs most frequently. Interestingly, studies consistently show that failure of a closure device (adopted to prevent vascular access complication) is the most common cause of a major vascular complication.13, 14

    A number of patient‐ and procedural‐related risk factors have been identified. Patient‐related factors include vascular calcification (especially when circumferential), preexisting peripheral vascular disease, and female sex.11, 13 Procedural‐related risk factors include larger sheath sizes, increased sheath:femoral artery ratio, and operator inexperience.14, 15

    Complications involving the femoral segment are more common than those involving the iliac segment, with dissection being more frequent than rupture.13 In larger series of patients undergoing TAVR, ileofemoral dissection has been reported in ≈6.5% of patients and rupture in ≈3% to 5%.16, 17 Pseudoaneurysm, embolization, occlusion, and access site infection are uncommon.

    How to Avoid

    Avoidance of vascular complications begins with meticulous MDCT assessment of the peripheral vessels (Figure 1). The role of MDCT is to assess the minimal luminal diameter and identify heavy (>270°) calcification or calcification at the site of probable puncture, the position of the femoral bifurcation relative to the femoral head, and any significant vascular pathology.18 In patients with significant anterior calcification or deep femoral arteries, surgical cutdown may be preferable to percutaneous access to avoid the increased risk of vascular closure device failure. When transfemoral access is not feasible, MDCT is the modality of choice to assess suitability for subclavian access or to determine the location of “calcium‐free windows” in the descending aortic wall if transcaval access is being considered.

    Figure 1.

    Figure 1. Checklist of avoidable procedural complications as part of the procedural planning for TAVR. AGU indicates angiographic, guidewire, and ultrasound; CEPD, cerebral embolic protection device; LMS, left main stem; LV, left ventricular; LVOT, left ventricular outflow tract; MDCT, multidetector computed tomography; PPM, permanent pacemaker; RBBB, right bundle branch block; TAVR, transcatheter aortic valve replacement; TPW, temporary pacing wire.

    Several intraprocedural techniques have emerged to reduce vascular access complications. The use of real‐time ultrasound guidance to puncture the common femoral artery has become commonplace. Ultrasound reduces the incidence of vascular complications during cardiac catheterization19 and was associated with reduced vascular complications in patients undergoing TAVR in a single‐center retrospective cohort.20 Fluoroscopy can be used to facilitate femoral puncture, using a radiopaque marker to “label” the position of the femoral head or digital subtraction angiography to puncture the vessel in real time. An alternative approach is to “road‐map” the common femoral artery after performing an angiogram from the contralateral access site. Use of a micropuncture kit (Cook Medical, Bloomington, IN) to confirm the position of the puncture prior to upsizing the sheath is an intuitive strategy to minimize trauma before passage of a large catheter at an unfavorable common femoral artery site.

    Recently, an integrated technique involving (1) angiographic assessment of the iliac‐femoral axis via secondary access, (2) a J‐tip 0.035‐inch guidewire placed as reference in the ideal femoral artery spot (above the bifurcation), and (3) ultrasound imaging to identify the J‐tip of the 0.035‐inch guidewire and guide the femoral puncture has been proposed21 (Figure 2). Another novel technique in heavily calcified iliofemoral vessels is the use of intravascular lithotripsy to facilitate transfemoral access by disrupting intimal and medial calcification and increasing vascular compliance via controlled microfractures and microdissections. This technology has been tested in patients with calcific femoropopliteal vascular lesions in the DISRUPT‐PAD (Shockwave Medical Peripheral Lithoplasty System Study for Peripheral Artery Disease) I and DISRUPT‐PAD II studies.22, 23 Interestingly, the incidence of vascular complications was low in these studies, with only 1 (1.7%) wire‐related dissection requiring stent placement. Notably, no embolic debris was present when distal embolic filters were used, suggesting a low risk of distal embolization.23

    Figure 2.

    Figure 2. The angiographic, guidewire, and ultrasound (AGU) technique for vascular management. The J tip of the 0.035‐inch guidewire is placed, under fluoroscopic guidance, in the ideal femoral artery spot (above the bifurcation) (A). The J tip of the 0.035‐inch is identified using ultrasound imaging (B). The femoral artery puncture is performed under ultrasound guidance. The asterisk indicates the needle penetrating the anterior wall of the femoral artery (C). Site of sheath insertion (D).

    Recently, in a registry of 42 patients with iliofemoral vascular disease considered prohibitive for transfemoral access undergoing TAVR, intravascular lithotripsy allowed femoral access and safe delivery system passage in >90% of the cases.24, 25 In this experience, no iliofemoral perforation or dissection requiring stent implantation was observed, and only 1 (2.4%) patient developed pseudoaneurysm and 1 (2.4%) required endarterectomy.25

    Novel vascular closure devices, such as the MANTA (Teleflex, Wayne, PA) collagen‐plug device, may reduce the rate of closure failure but await evaluation in head‐to‐head studies against current suture‐based closure devices (eg, ProStarXL and Perclose ProGlide; Abbott Vascular, Abbott Park, IL).26

    How to Manage

    Optimal management of vascular complications relies on early recognition. Routine crossover angiography to assess for aortic/iliofemoral dissection or perforation after sheath removal is current standard practice, and placement of a crossover wire from the contralateral femoral artery allows rapid vascular access if required. Transradial secondary access has recently been demonstrated to be suitable for the management of peripheral vascular complications during TAVR and may reduce the rate of secondary femoral access site complications.27, 28

    Limited dissection or perforation may be successfully managed by prolonged occlusive balloon inflation. Percutaneous deployment of a covered stent or surgical repair is indicated for more extensive dissection or bleeding (especially if there is associated cardiovascular instability or threatened/actual limb compromise) and is associated with good long‐term outcome.29 Stenting is usually preferred to surgical repair when the injury is above the inguinal ligament.

    Device Landing Zone Rupture

    Device landing zone rupture is a rare but feared complication of TAVR, with an overall mortality up to 48% and can be as high as 75% in cases of uncontained rupture.30 Overall, landing zone ruptures account for 7% of all the cases of emergent conversion to surgery during TAVR.31 The reported incidence of landing zone rupture is up to 0.5% to 1% of all TAVR procedures,5, 30, 32, 33, 34 although the real incidence might be higher when cases with delayed presentation are accounted for.35

    The most frequent anatomic site of rupture is the aortic annulus (involved in two thirds of cases), although left ventricular outflow tract (LVOT, 10%), sinus of Valsalva (16%), and sinotubular junction (6%) rupture have also been described.30 Self‐expanding systems have rarely been associated with aortic root rupture (unless valve balloon postdilatation is performed) and landing zone rupture is usually related to use of a balloon‐expandable device.36

    How to Avoid

    Meticulous procedural planning using preprocedural imaging with MDCT and 3‐dimensional reconstruction is essential to minimize the risk of landing zone rupture. Both anatomic and procedural variables are associated, but a high burden of LVOT/subannular calcification is recognized as the most important predictor. Notably, in a large multicenter TAVR cohort, the calcium score was significantly increased in patients who experienced landing zone rupture compared with other patients (181±211 versus 22±37; P<0.001).30

    Perhaps more important than the calcific burden is the distribution of calcium. In particular, a higher calcium volume in the upper LVOT (but not in the aortic valve region) has been associated with the risk of landing zone rupture.37 Notably, Barbanti et al30 reported no significant difference in annular size or degree of aortic cusp calcification between patients with landing zone rupture and those with uncomplicated TAVR. Advanced MDCT analysis may provide useful parameters to predict the risk of landing zone complications, including (1) quantitative measurement of annular calcification (>550 Hounsfield units), (2) leaflet asymmetry, defined as:

    and (3) annular cover index (calculated as prosthesis nominal area − annular area/prosthesis nominal area×100). Notably, the multivariate MDCT‐based risk model provides incremental predictive value compared with single anatomic features.

    Condado et al38 reported that focal calcification extending from the annular plane to at least 4 mm into the LVOT was present in 4 of 7 patients who experienced annular rupture. Similarly, Hayashida et al39 suggested that significant calcification located in a particular vulnerable area, as revealed by MDCT, might be the possible mechanism for some cases of annular rupture. The vulnerable area was identified as the spot in the pericardial fat area of the annulus—an area uncovered by any cardiac structure and therefore at risk of mechanical stress at the time of forceful deployment of a balloon‐expandable valve over a calcified nodule. Other authors reported the association between LVOT perforation and severe subannular calcification adjacent to the vulnerable muscular region of the LVOT (between the left fibrous trigone and the left/right aortic cusp commissure),40 suggesting the critical importance of careful anatomic MDCT assessment and procedural planning.

    The choice of valve prosthesis is also critical, and a self‐expandable valve is preferable in cases with a high‐risk LVOT calcification pattern and shallow sinuses of Valsalva (Figure 1). Additionally, it must always be noted when optimizing TAVR results that postdilatation significantly increases the risk of landing zone rupture, especially with >20% area oversizing (Figure 3).

    Figure 3.

    Figure 3. Procedural and anatomical risk factors for device landing zone rupture. Heavy calcification in the annular and left ventricular outflow tract region are important risk factors for device landing zone complications. Careful assessment of the baseline multidetector computed tomography provides important information on the presence of high‐risk calcium distribution (A). Among the procedural variables, >20% area oversizing (B) and postdilatation (C) increase the risk of device landing zone rupture.

    How to Treat

    In cases of uncontained rupture, conversion to emergency surgery is the only possible solution. Maintenance of hemodynamic stability is essential in the acute setting, and circulatory support should be immediately considered alongside a rapid search for the cause of hemodynamic instability using angiography and/or transthoracic/transesophageal echocardiography. In some cases, the correct diagnosis is established only by direct surgical exploration.35

    Percutaneous coil embolization to seal the point of landing zone rupture has been described and may be a bailout option in cases of rapid deterioration.41

    Contained rupture producing a periaortic hematoma has a less dramatic presentation. Pericardial drainage and/or observation may be initially considered in cases with limited injury and noncatastrophic clinical presentation. Nevertheless, close surveillance and repeated MDCT assessment remain important because adverse evolution is possible up to several hours or days from the rupture event.35

    Device Embolization

    Valve embolization is an infrequent yet important TAVR complication (Table 1) and accounts for ≈45% of emergency cardiac surgery in patients treated with TAVR.42, 43, 44, 45, 46, 47 Its occurrence imparts a 9‐fold increase in mortality compared with uncomplicated cases.31 Embolization usually happens acutely and intraprocedurally, though late device migration (up to 1 year after TAVR) has also been described.48, 49, 50 Notably, the incidence of valve embolization has decreased over the years attributable to increasing institutional and operator experience and the availability of preplanning MDCT and newer‐generation valves.8, 44, 45, 51

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    Table 1. Incidence of Valve Embolization in TAVR

    Hamm et al20110.5%42
    Gaede et al2014–20160.2%43
    Ludman et al2008–20150.2%–1.7%44
    Ludman et al2016–20170.3%45
    Auffret et al2010–20151.2%46
    Holmes et al2012–20140.9%47

    TAVR indicates transcatheter aortic valve replacement.

    Valve dislocations are either cranial toward the aorta or caudal into the LVOT/left ventricle. Aortic embolization is commonly the result of deployment in a high position and/or poor coaxial alignment of the device to the valve plane during implantation. Rarely, delivery system failure can lead to misalignment of the balloon and stent frame of balloon expandable systems or failed valve release in self‐ and mechanically expanding systems.52

    Caudal migration toward the LVOT or left ventricle usually occurs because of low implantation depth, eccentric and asymmetric calcification, and more rarely because of device undersizing.53

    How to Avoid

    Avoidance of stored tension in the delivery system is important to prevent the risk of valve dislocation. During general anesthesia, a “breath hold” maneuver may be useful during valve deployment.

    TAVR device migration can also arise during equipment retrieval after valve deployment. Inaccurate maneuvering of the pigtail catheter can hook the stent frame and snare the device during withdrawal. Use of a conventional 0.035‐inch wire to straighten the pigtail facilitates safe removal.

    How to Treat

    Treatment options are strictly related to operator experience, clinical and anatomic factors, and the mechanics of device migration.

    Hemodynamics determine initial management in the case of acute valve embolization. Where necessary, general anesthesia and femoral‐femoral cardiopulmonary bypass can be considered before conventional cardiac surgery. Fortunately, hemodynamics are usually not catastrophic, and the dislocated valve can be snared and secured in a suitable position. Permanent fixation of the embolized valve may be achieved using an aortic stent (Figure 4), and a second valve can then be deployed in standard fashion. When caudal embolization occurs toward the LVOT/left ventricle, the choice is either to implant a second device to secure the embolized valve in a suitable subannular position or surgical removal of the embolized valve followed by transapical deployment of a second device or conventional surgical aortic valve replacement.52, 53, 54, 55, 56

    Figure 4.

    Figure 4. A case of aortic TAVR device embolization. In this case, a balloon‐expandable Sapien XT valve was deployed in a standard fashion under rapid pacing (A). However, the device was dislocated into the aortic root during delivery system retrieval (B). The Sapien XT was snared and secured in a suitable position in the descending aorta (C and D). A second Sapien XT was deployed in the standard position (E) and an aortic stent used to secure the embolized valve position (F).

    If surgery is not an option because of prohibitive risk, the embolized valve can be dragged into a subannular position using a partially inflated valvuloplasty balloon under rapid ventricular pacing. Maintaining coaxial wire positioning is essential during this maneuver. A partially overlapping second valve can then be implanted to anchor the dislocated valve and prevent distal migration. Tiroch et al55 described a successful case in which an Amplatz GooseNeck Snare (ev3; Endovascular Inc, Plymouth, MN) was used to retrieve a Sapien 3 valve from the left ventricle after unsuccessful attempts using standard valvuloplasty balloons.

    Coronary Occlusion

    Coronary artery obstruction by leaflet material during TAVR is a relatively infrequent complication but has potentially catastrophic clinical consequences, with an associated mortality of up to 50%. Coronary occlusion occurs in <1% of native valve interventions and tends to involve the left main stem more frequently than the right coronary artery.4

    Occlusion is typically caused by displacement of the calcified leaflets of the native aortic valve toward the coronary ostia valve implantation. Coronary flow obstruction can thus be related either to coverage of the coronary ostia or sealing of the sinus of Valsalva at the sinotubular junction. Identification of patients at high risk of coronary occlusion is therefore a key component of procedural planning. Anatomic features that predispose to coronary occlusion are low coronary height (<12 mm) and narrow sinus of Valsalva diameter (<30 mm).57

    Intraprocedural coronary occlusion is more common during valve‐in‐valve procedures (TAVR within a failed surgical bioprosthesis) as a consequence of reduced distance between the valve leaflets and coronary ostia (attributable to the supra‐annular design of surgical prostheses) and the narrower sinus of Valsalva (attributable to surgical bioprosthesis suturing). In particular, bioprosthetic valves with leaflets mounting outside an internal stent (eg, Mitraflow Sorin and Triflecta, St. Jude Medical Inc., St Paul, MN) or stentless bioprosthetic valves are at higher risk because the leaflets of these bioprostheses may extent outward beyond the surgical device implantation after TAVR.58

    Coronary occlusion causes rapidly worsening severe hypotension with dynamic ST‐segment changes in 50% and ventricular arrhythmias in 25% of cases.57 Immediate angiographic assessment of coronary patency is required in patients in whom coronary occlusion is suspected.

    How to Avoid

    Preprocedural cardiac MDCT is critical to identify patients at risk of coronary occlusion by measurement of the height of the coronary ostia in relation to the aortic annulus, the width and height of the sinus of Valsalva, and the width of the sinotubular junction.

    In patients who are deemed at high risk, coronary protection with a standard 0.014‐inch guidewire is advisable to help prevent and treat potential occlusion. In some cases, a preemptive coronary balloon or stent can be mounted on a guidewire and advanced in the left anterior descending artery and/or right coronary artery during valve deployment. If coronary occlusion occurs, the stent can be pulled back and deployed in a “chimney” fashion to maintain coronary patency59 (Figure 5).

    Figure 5.

    Figure 5. Preventive strategies to avoid coronary occlusion in a high risk valve‐in‐valve procedure. This case shows the wire and jailed stent protection technique in a patient with a degenerated Sorin Freedom stentless 23 mm valve (A through C). Baseline multidetector computed tomography and angiography showed the low bilateral coronary takeoff. An undeployed stent was prophylactically positioned in the left main stem (LMS) before advancing a Sapien XT 20‐mm valve (C and D). Immediately after valve deployment, the patient's hemodynamics crashed and the coronary stent was inflated at high pressure in the LMS at the ostial position (E). The final aortogram showed the Sapien‐XT valve in correct position and widely patent coronary arteries (F). Reprinted from Maggio et al59 with permission. Copyright ©2017, Oxford University Press.

    Although there are no prospective data, a repositionable TAVR valve is preferred in patients at high risk of coronary occlusion.

    How to Manage

    In patients in whom coronary occlusion occurs without a protective guidewire in situ, immediate cannulation of the affected coronary artery with a guiding catheter is required to allow balloon angioplasty. Coronary stent deployment with high‐pressure postdilatation is often needed to avoid ostial deformation.

    Engaging the coronary ostia with a TAVR device in situ may be difficult and requires dedicated strategies. Balloon‐expandable valves are deployed in the subcoronary position and interact with the coronary arteries in <10% of cases—even then, coronary access through the valve struts is generally straightforward.60 However, sudden coronary occlusion is more frequently observed with balloon expandable valves, especially following high implantation in an aortic root with shallow sinuses and low coronary ostia. The CoreValve Evolut self‐expandable valve (Medtronic, Minneapolis, MN) is deployed in the supra‐annular position, and coronary access can be difficult through the alternating diamond‐shaped valve cells. Conversely, the ACURATE neo valve (Boston Scientific, Natick, MA), despite its self‐expanding surpra‐annular design, allows easy access to the coronary ostia thanks to the high commissure posts and a low sealing skirt profile. Moreover, the ACURATE neo is designed to minimally protrude into the LVOT, minimizing the risk of coronary occlusion.

    The catheter of choice for the left coronary artery should be the Judkins left catheter with preference for a smaller size (3.5 instead of 4.0), or the Extra‐Back‐up catheter 3.5, maintaining the diagnostic 0.035‐inch J‐wire within the catheter to facilitate orientation of the catheter tip to engage the coronary ostia through the valve struts. The basic technique is to curl the J‐wire against the valve leaflet and slide the catheter over to open the primary curve. At this point, the tip of the catheter usually passes through the valve strut to engage the left main ostium. Further catheter manipulation may be required to obtain the best coaxial engagement. The Judkins right catheter is effective for the right coronary artery in most cases.60

    Coronary occlusion after self‐expandable device deployment can be resolved by snaring the TAVR valve frame and lifting the deployed valve above the sinotubular junction. This option is not available after deployment of a balloon‐expandable valve.

    Recently, the BASILICA (Bioprosthetic or Native Aortic Scallop Intentional Laceration to Prevent Iatrogenic Coronary Artery Obstruction) trial assessed the safety and feasibility of transcatheter electrosurgery to lacerate the native aortic valve leaflets in patients with a high risk of coronary occlusion.61 This is a modification of the LAMPOON procedure in which an electrified guidewire (Astato XS 20, Asahi Intecc USA, Santa Ana, CA) is used to lacerate the anterior mitral leaflet to prevent LVOT obstruction in patients undergoing transcatheter mitral valve replacement.62 In the first experience on 30 high‐risk patients, the procedure was successful in 95%, and there was 100% freedom from coronary occlusion during TAVR. This new transcatheter technique may thus prove useful in elective high‐risk patients and as a bailout option for coronary occlusion. However, the safety of the procedure needs to be confirmed in larger studies because adverse cardiovascular events were observed in 30% of the cases, including 1 (3%) disabling stroke and 2 (7%) nondisabling strokes.61


    Recent trials in low‐risk patients have demonstrated a low incidence of disabling stroke (0.6% and 0.5% at 30 days in the PARTNER 3 [Safety and Effectiveness of the SAPIEN 3 Transcatheter Heart Valve in Low‐Risk Patients With Aortic Stenosis] and Evolut Low Risk trials, respectively) and noninferiority of TAVR compared with surgery with respect to stroke‐free survival (HR, 0.25; 95% CI; 0.07–0.88; P=0.02 in PARTNER 3).1, 2 Nevertheless, stroke remains one of the most feared complications of TAVR, with a high risk of 30‐day mortality (odds ratio [OR], 6.45; 95% CI, 3.9–10.6).1, 2, 63 Contemporary data including different TAVR technologies in high‐ and intermediate‐risk patients show a 30‐day stroke rate ranging from 1.4% to 1.9%.64, 65, 66, 67 Subclinical new cerebral ischemic lesions are much more common and can be identified using diffusion‐weighted magnetic resonance imaging in up to 80% of patients undergoing TAVR.68

    The occurrence of TAVR‐related stroke demonstrates a bimodal pattern of distribution, with up to 50% of events occurring within the first 24 hours after TAVR (dependent on clinical and procedural factors) and a late phase >10 days after TAVR (dependent on clinical characteristics—specifically, the atherosclerotic and overall frailty profile).69 Among early (0–10 days) patient‐related predictors, those associated with stroke in multivariate models in the CoreValve trials were peripheral vascular disease (HR, 1.44; 95% CI, 1.03–2.00), prior transient ischemic attack (HR, 2.48; 95% CI, 1.67–3.67), angina (HR, 1.63; 95% CI, 1.15–2.33), body mass index <21 kg/m2 (HR, 2.14; 95% CI, 1.37–3.34) and a previous fall (HR, 1.72; 95% CI, 1.20–2.47), while the absence of previous coronary artery bypass grafts was protective (HR, 0.58; 95% CI, 0.39–0.86). Among the procedural variables, total time in the catheterization laboratory (HR, 1.003; 95% CI, 1.000–1.005), total time of delivery system in the body (HR, 1.01; 95% CI, 1.004–1.02), and rapid pacing during valvuloplasty (HR, 9.86; 95% CI, 1.37–70.7) were associated with early stroke.70

    Histopathology of debris collected by cerebral embolic protection devices (CEPDs) used during TAVR demonstrates that embolized tissue particles can originate from the aortic valve, the aorta, and the left ventricle and often involve a thrombus. The embolized material can cause cerebral ischemia itself or can trigger further thrombus development, thus explaining why the clinical manifestation (and consequent diagnosis) of early TAVR‐related stroke can be delayed for up to 10 days.

    How to Avoid

    Optimal anticoagulation throughout the procedure is essential to minimize thrombus formation. The BRAVO (Effect of Bivalirudin on Aortic Valve Intervention Outcome) trial has shown that bivalirudin and heparin yield similar rates of major bleeding and ischemic cardiovascular events 30 days after TAVR.71 Unfractionated heparin therefore remains the standard during TAVR, with a parenteral bolus followed by additional doses until an activated clotting time of 250 to 300 seconds is achieved.

    CEPDs positioned across the origins of the supra‐aortic vessels capture or deflect embolic debris away from the cerebral vasculature and potentially reduce the burden of ischemic strokes during TAVR. However, their use in current clinical practice remains limited, with <2% of CEPD‐assisted TAVR in the Evolut Low Risk trial and even less in routine clinical practice.2

    Use of CEPD has been associated with a smaller volume of silent ischemic lesions, although a recent meta‐analysis failed to demonstrate a reduction in the number of single or multiple ischemic lesions.72, 73 Despite a significant reduction in 30‐day stroke rate (OR, 0.55; 95% CI, 0.31–0.98), CEPDs have no impact on 30‐day mortality (OR, 0.43; 95% CI, 0.18–1.05).72

    A significant number of thromboembolic cerebral insults relate to territories supplied by the vertebral arteries (a segment of the cerebral circulation unprotected by most currently available CEPDs; Figure 6) and extended coverage across all the supra‐aortic vessels (including the left subclavian artery) is preferable. However, most currently available devices (including the Sentinel CPS [Claret Medical Inc, Santa Rosa, CA] and Embrella [Edwards Lifesciences, Irvine, CA]) protect only the brachiocephalic and left common carotid arteries, which supply only 9 of 28 brain regions as a consequence of the dual posterior circulation blood supply.

    Figure 6.

    Figure 6. Cerebral embolic protection device. The upper panel shows the degree of cerebral protection provided by currently available embolic protection devices. Devices that cover the brachiocephalic trunk and left common carotid arteries protect only 9 of 28 brain regions, considering the dual blood supply of the posterior cerebral circulation. TAVR indicates transcatheter aortic valve replacement.

    The TriGuard device (Keystone Heart Ltd., Herzliya, Israel) is the only commercially available CEPD that allows complete coverage of the supra‐aortic vessels. In the DEFLECT III (Prospective, Randomized Evaluation of the TriGuard HDH Embolic Deflection Device During Transcatheter Aortic Valve Implantation) trial, this device was successfully positioned in 89% of cases and appeared to mitigate new neurological deficits and cognitive impairment after transcatheter aortic valve implantation yielding a numeric greater freedom from new cerebral ischemic lesions (26.9% versus 11.5%) and smaller lesion volume (19.6 mm3 versus 34.8 mm3; P=0.07) and improved cognitive function compared with the control arm (P=0.028).74

    Several new CEPDs that provide full coverage of the aortic arch are under evaluation for clinical use,75 including the Emblock Embolic Protection System (Innovative Cardiovascular Solutions, LLC, Grand Rapids, MI) and the Emboliner Embolic Protection Catheter (Emboline Inc, Santa Cruz, CA). The Emblock device incorporates a 4F pigtail catheter to facilitate TAVR device positioning, while the Emboliner captures both cerebral and noncerebral emboli to provide full‐body embolic protection.

    The optimal combination (single versus double) and duration of antiplatelet therapy to mitigate the risk of thrombosis after TAVR has not been established,76 and dual antiplatelet therapy (aspirin and clopidogrel) for 3 to 6 months is the most commonly used regime.

    How to Manage

    Diagnosis of periprocedural stroke is often delayed because patients are often under general anesthesia or conscious sedation. When stroke is considered, prompt access to computed tomography of the brain, computed tomography cerebral angiography, and specialist care by a dedicated stroke team are essential. Anectodal experiences suggest that mechanical thrombectomy may have a role in acute and late‐presenting stroke following TAVR.77

    Periprocedural Conduction Abnormalities

    Conduction abnormalities requiring permanent pacemaker (PPM) implantation and development of new left bundle branch block (LBBB) remain the most common TAVR complications.78 Many patients with aortic stenosis have some conduction disease already, but the close proximity of the atrioventricular conduction system to the aortic valve apparatus makes it especially susceptible to injury during TAVR.79

    Perioperative conduction abnormalities result from mechanical compression of the conduction tissue as a result of pre‐ or postdilatation, deep implant depth, or the use of self‐expanding devices and those with longer stent frames.80

    High‐Grade Atrioventricular Block and PPM

    The development of high grade atrioventricular block usually occurs within 24 hours of the procedure independent of the valve used.81 However, 2% to 7% of patients can develop high‐grade atrioventricular block beyond 48 hours and 85% to 90% of PPM implants are required within 7 days of the procedure (median 3 days).81, 82 Late‐onset high‐degree atrioventricular block is uncommon, and in one recent study no patients with a normal ECG 2 days after TAVR developed delayed high‐degree atrioventricular block.81 Similarly, 99.6% of patients without LBBB remained PPM free after 1 year.83

    New LBBB

    New‐onset LBBB after SAVR is a predictor of syncope, atrioventricular block, and sudden cardiac death.80

    After TAVR, the incidence of new periprocedural LBBB varies widely and is higher with self‐expanding (18%–65%, Medtronic CoreValve) compared with balloon‐expandable valves (4%–30%, Edwards Sapien/Sapien XT).79, 84 Studies of LBBB with new‐generation valves are limited: 12% to 22% for Sapien 3 valve,85, 86 34% for Evolut R,87 and 55% to 77% for Boston Lotus valve.1, 2, 88, 89

    In PARTNER 3, the incidence of new LBBB at 1 year was 23.7% in the TAVR cohort compared with 8.0% in the SAVR cohort (HR, 3.43; 95% CI, 2.32–5.08).1 LBBB usually develops within 24 hours of TAVR (85%–94%) and may resolve within 30 days, but 55% of patients have persistent LBBB.78 The main predictors are use of a self‐expandable valve (OR, 2.5–8.5),90, 91, 92 depth of prosthesis within the LVOT (OR, 1.15–1.4/1 mm),93, 94, 95 overexpansion of the native aortic annulus (OR, 5.3 if >15%),93, 96 and larger valve size.83, 84

    There are limited studies evaluating the association of new LBBB and need for PPM implantation, but 2 recent meta‐analyses97, 98 suggested a 2‐fold higher risk of PPM implant in patients with new LBBB after TAVR. Approximately 8% to 19% of patients with new LBBB require a PPM, the most frequent indication being progression to atrioventricular nodal block.83, 99, 100, 101 New LBBB is also associated with higher cardiovascular mortality (OR, 1.39; CI, 1.04–1.86),97 especially in patients with QRS >160 ms (HR, 4.78; CI, 1.56–14.53).102

    How to Prevent

    Conduction disturbances in patients undergoing TAVR are largely dependent on unmodifiable patient‐related risk factors, including electrical and anatomic variables. Baseline right bundle branch block is the strongest and most consistent risk factor for PPM regardless of valve type (OR, 2.8–46.7).78, 79, 96 First‐degree atrioventricular block is also strongly associated (OR, 4.0–11.4).103, 104, 105 Among anatomic predictors, the presence of calcification below the aortic annulus and in the LVOT increases the risk for PPM (OR, 1.03–4.7).103, 106

    Procedural variables are also important. In a recent systematic review,107 the rate of PPM varied considerably depending on the type of valve deployed—self‐ and mechanically expanding valves (CoreValve/Evolut/Lotus) have a consistently higher risk of PPM107 (Medtronic CoreValve versus Edwards Sapien/Sapien XT; OR, 2.6–25.7)79 (Table 2). In PARTNER 3 (using the Sapien 3 valve) there was no difference in PPM rate between TAVR and surgery (6.6% versus 4.1%; HR, 1.65; 95% CI, 0.92–2.95), while the Evolut Low Risk study showed a higher rate of PPM in the TAVR group (17.4% versus 6.1%).

    John Wiley & Sons, Ltd

    Table 2. Rate of Permanent Pacemaker Implantation

    ValvePermanent Pacemaker Implantation Rate (%)
    Sapien/Sapien XT2.3–28.2
    Sapien 34–24
    Evolut R14.7–26.7
    Direct flow medical17
    Accurate Neo2.3–10.2

    Reprinted from van Rosendael et al107 with permission. Copyright ©2018, Oxford University Press.

    Depth of implantation is also strongly associated with increased risk of PPM regardless of the type of prosthesis (OR, 1.1–1.5/1 mm of LVOT).84, 89, 106, 108, 109, 110 (Table 3). Another factor is oversizing/stretching of aortic annulus by 10% to 15%, which increases the risk of PPM with first‐generation devices.84

    John Wiley & Sons, Ltd

    Table 3. Risk of Conduction Disturbances According to the Depth of Implantation

    Valve ProsthesisProposed Cutoff ValuesReferences
    Edwards Sapien XT6.3 mm108
    Edwards Sapien 37 mm or 25% of stent frame106, 108
    Medtronic CoreValve6–7.8 mm109, 110
    Lotus5–6.7 mm89, 108

    The baseline risk of developing conduction abnormalities may also influence the strategy of pacing support during the TAVR procedure. Rapid ventricular pacing is indeed often required during balloon aortic valvuloplasty or valve deployment and use of pacing via the left ventricular guidewire is an established technique to simplify the procedure and reduce the risk of vascular complications and pericardial effusion.111 However, left ventricular guidewire pacing could expose the patient to a period of hemodynamic instability if the left ventricular guidewire was removed prematurely. Thus, a right ventricular temporary pacing wire may be preferable in patients at high risk of periprocedural conduction disturbances. Prophylactic PPM implantation may also be considered in patients with preexisting high‐grade conduction abnormalities (Figure 1).

    How to Manage

    The prognostic implications of PPM after TAVR are currently unclear, with conflicting data. Registry data from the United States99 showed increased mortality in patients requiring PPM (HR, 1.31; CI, 1.09–1.58), whereas other studies observed mortality reduction (HR, 0.31; CI, 0.11–0.85).108 Furthermore, a recent systematic review107 and meta‐analysis112 have shown no association between PPM and all‐cause mortality.

    The European Society of Cardiology guidelines113 suggest 7 days of observation for stable high‐degree atrioventricular block before PPM implant, in contrast with current routine clinical practice, where 50% of patients receive a PPM within 3 days of TAVR.97 Recovery of intrinsic rhythm has been observed in up to 50% of paced patients at the time of TAVR follow‐up.114, 115

    Clear indications are crucial, as PPM implantation exposes patients to prolonged hospital stay, risk of infection, thromboembolism, and suboptimal functional recovery. While immediate PPM implant can be considered in stable patients with preexisting conduction disease (right bundle branch block and first‐degree atrioventricular block) who develop high‐grade atrioventricular block during valve deployment, spontaneous recovery of atrioventricular node function might occur within 24 hours of observation in cases without preexisting conduction disorder.

    Management of new LBBB following TAVR remains controversial. The general consensus is for a period (48–72 hours) of inpatient monitoring to detect possible progression to atrioventricular nodal block and need for PPM implant. Persistent LBBB with QRS >160 ms and associated first‐degree heart block may require prophylactic PPM. An implantable loop recorder may be an option when LBBB persists and further studies are required to define optimal management.

    General Considerations and Conclusion

    The PARTNER 3 trial has shown superiority of TAVR for the composite end point of mortality, stroke, and hospital readmission at 1 year (HR, 0.38; 95% CI, 0.15–1.00) compared with SAVR. Similarly, the Evolut Low Risk trial demonstrated the noninferiority of TAVR versus SAVR regarding the composite primary end point of death and stroke (5.3% versus 6.7%) with a longer follow‐up of 2 years.1, 2 If confirmed at long‐term follow up, these favorable results in low‐risk patients will drive expanded indications for TAVR. Focus on the prevention and treatment of procedural complications is therefore essential.

    Before any TAVR procedure, it is essential for the heart team to discuss bailout options, including whether conversion to open heart surgery is appropriate. Procedural planning is key to prevent potentially catastrophic complications, including landing zone rupture, device embolization, or coronary occlusion. Preprocedural imaging is essential to plan vascular access, and intravascular lithotripsy may have a role in high‐risk cases. Further studies are warranted to define the place of CEPDs in reducing the risk of stroke during TAVR and the indications for their use. Ultimately, all members of the heart team need to understand strategies for the prevention and management of procedural complications during TAVR. This will produce a more predictable procedure with better long‐term outcomes for more of our patients with aortic stenosis.


    Dr Scarsini received an education and training grant from European Association of Percutaneous Cardiovascular Interventions and served on the advisory board for Abbott. Dr Prendergast received unrestricted education and research grants from Edwards Lifesciences and speaker fees from Edwards Lifesciences. Dr Ribichini received an institutional research grant from Philips‐Volcano and Edwards Lifesciences. Dr Banning received institutional funding for an interventional fellowship from Boston Scientific. The remaining authors have no disclosures to report.


    *Correspondence to: Adrian P. Banning, MD, FRCP, Oxford Heart Centre, Oxford University Hospitals, Headley Way, Oxford OX3 9DU, United Kingdom. E‐mail:


    • 1 Mack MJ, Leon MB, Thourani VH, Makkar R, Kodali SK, Russo M, Kapadia SR, Malaisrie SC, Cohen DJ, Pibarot P, Leipsic J, Hahn RT, Blanke P, Williams MR, McCabe JM, Brown DL, Babaliaros V, Goldman S, Szeto WY, Genereux P, Pershad A, Pocock SJ, Alu MC, Webb JG, Smith CR; PARTNER 3 Investigators . Transcatheter aortic‐valve replacement with a balloon‐expandable valve in low‐risk patients. N Engl J Med. 2019; 380:1695–1705.CrossrefMedlineGoogle Scholar
    • 2 Popma JJ, Deeb GM, Yakubov SJ, Mumtaz M, Gada H, O'Hair D, Bajwa T, Heiser JC, Merhi W, Kleiman NS, Askew J, Sorajja P, Rovin J, Chetcuti SJ, Adams DH, Teirstein PS, Zorn GL, Forrest JK, Tchetche D, Resar J, Walton A, Piazza N, Ramlawi B, Robinson N, Petrossian G, Gleason TG, Oh JK, Boulware MJ, Qiao H, Mugglin AS, Reardon MJ; Evolut Low Risk Trial Investigators . Transcatheter aortic‐valve replacement with a self‐expanding valve in low‐risk patients. N Engl J Med. 2019; 380:1706–1715.CrossrefMedlineGoogle Scholar
    • 3 Siontis GCM, Overtchouk P, Cahill TJ, Modine T, Prendergast B, Praz F, Pilgrim T, Petrinic T, Nikolakopoulou A, Salanti G, Søndergaard L, Verma S, Jüni P, Windecker S. Transcatheter aortic valve implantation vs. surgical aortic valve replacement for treatment of symptomatic severe aortic stenosis: an updated meta‐analysis. Eur Heart J. 2019;ehz275. DOI: 10.1093/eurheartj/ehz275. [Epub ahead of print].CrossrefMedlineGoogle Scholar
    • 4 Généreux P, Head SJ, Van Mieghem NM, Kodali S, Kirtane AJ, Xu K, Smith C, Serruys PW, Kappetein AP, Leon MB. Clinical outcomes after transcatheter aortic valve replacement using Valve Academic Research Consortium definitions: a weighted meta‐analysis of 3,519 patients from 16 studies. J Am Coll Cardiol. 2012; 59:2317–2326.CrossrefMedlineGoogle Scholar
    • 5 Walther T, Hamm CW, Schuler G, Berkowitsch A, Kötting J, Mangner N, Mudra H, Beckmann A, Cremer J, Welz A, Lange R, Kuck K‐H, Mohr FW, Möllmann H; GARY Executive Board . Perioperative results and complications in 15,964 transcatheter aortic valve replacements: prospective data from the GARY registry. J Am Coll Cardiol. 2015; 65:2173–2180.CrossrefMedlineGoogle Scholar
    • 6 Leon MB, Smith CR, Mack MJ, Makkar RR, Svensson LG, Kodali SK, Thourani VH, Tuzcu EM, Miller DC, Herrmann HC, Doshi D, Cohen DJ, Pichard AD, Kapadia S, Dewey T, Babaliaros V, Szeto WY, Williams MR, Kereiakes D, Zajarias A, Greason KL, Whisenant BK, Hodson RW, Moses JW, Trento A, Brown DL, Fearon WF, Pibarot P, Hahn RT, Jaber WA, Anderson WN, Alu MC, Webb JG. Transcatheter or surgical aortic‐valve replacement in intermediate‐risk patients. N Engl J Med. 2016; 374:1609–1620.CrossrefMedlineGoogle Scholar
    • 7 Reardon MJ, Van Mieghem NM, Popma JJ, Kleiman NS, Søndergaard L, Mumtaz M, Adams DH, Deeb GM, Maini B, Gada H, Chetcuti S, Gleason T, Heiser J, Lange R, Merhi W, Oh JK, Olsen PS, Piazza N, Williams M, Windecker S, Yakubov SJ, Grube E, Makkar R, Lee JS, Conte J, Vang E, Nguyen H, Chang Y, Mugglin AS, Serruys PWJC, Kappetein AP. Surgical or transcatheter aortic‐valve replacement in intermediate‐risk patients. N Engl J Med. 2017; 376:1321–1331.CrossrefMedlineGoogle Scholar
    • 8 Cahill TJ, Chen M, Hayashida K, Latib A, Modine T, Piazza N, Redwood S, Søndergaard L, Prendergast BD. Transcatheter aortic valve implantation: current status and future perspectives. Eur Heart J. 2018; 39:2625–2634.CrossrefMedlineGoogle Scholar
    • 9 Carroll JD, Vemulapalli S, Dai D, Matsouaka R, Blackstone E, Edwards F, Masoudi FA, Mack M, Peterson ED, Holmes D, Rumsfeld JS, Tuzcu EM, Grover F. Procedural experience for transcatheter aortic valve replacement and relation to outcomes. J Am Coll Cardiol. 2017; 70:29.CrossrefMedlineGoogle Scholar
    • 10 Tchetche D, Van der Boon RMA, Dumonteil N, Chieffo A, Van Mieghem NM, Farah B, Buchanan GL, Saady R, Marcheix B, Serruys PW, Colombo A, Carrie D, De Jaegere PPT, Fajadet J. Adverse impact of bleeding and transfusion on the outcome post‐transcatheter aortic valve implantation: insights from the Pooled‐RotterdAm‐Milano‐Toulouse In Collaboration Plus (PRAGMATIC Plus) initiative. Am Heart J. 2012; 164:402–409.CrossrefMedlineGoogle Scholar
    • 11 Généreux P, Webb JG, Svensson LG, Kodali SK, Satler LF, Fearon WF, Davidson CJ, Eisenhauer AC, Makkar RR, Bergman GW, Babaliaros V, Bavaria JE, Velazquez OC, Williams MR, Hueter I, Xu K, Leon MB. Vascular complications after transcatheter aortic valve replacement: insights from the PARTNER (Placement of AoRTic TraNscathetER Valve) trial. J Am Coll Cardiol. 2012; 60:1043–1052.CrossrefMedlineGoogle Scholar
    • 12 Kappetein AP, Head SJ, Généreux P, Piazza N, van Mieghem NM, Blackstone EH, Brott TG, Cohen DJ, Cutlip DE, van Es G‐A, Hahn RT, Kirtane AJ, Krucoff MW, Kodali S, Mack MJ, Mehran R, Rodés‐Cabau J, Vranckx P, Webb JG, Windecker S, Serruys PW, Leon MB. Updated standardized endpoint definitions for transcatheter aortic valve implantation: the Valve Academic Research Consortium‐2 consensus document (VARC‐2). Eur J Cardiothorac Surg. 2012; 42:S45–S60.CrossrefMedlineGoogle Scholar
    • 13 Hayashida K, Lefèvre T, Chevalier B, Hovasse T, Romano M, Garot P, Mylotte D, Uribe J, Farge A, Donzeau‐Gouge P, Bouvier E, Cormier B, Morice M‐C. Transfemoral aortic valve implantation: new criteria to predict vascular complications. JACC Cardiovasc Interv. 2011; 4:851–858.CrossrefMedlineGoogle Scholar
    • 14 van Kesteren F, van Mourik MS, Vendrik J, Wiegerinck EMA, Henriques JPS, Koch KT, Wykrzykowska JJ, de Winter RJ, Piek JJ, van Lienden KP, Reekers JA, Vis MM, Planken RN, Baan J. Incidence, predictors, and impact of vascular complications after transfemoral transcatheter aortic valve implantation with the SAPIEN 3 prosthesis. Am J Cardiol. 2018; 121:1231–1238.CrossrefMedlineGoogle Scholar
    • 15 Van Mieghem NM, Tchetche D, Chieffo A, Dumonteil N, Messika‐Zeitoun D, van der Boon RMA, Vahdat O, Buchanan GL, Marcheix B, Himbert D, Serruys PW, Fajadet J, Colombo A, Carrié D, Vahanian A, de Jaegere PPT. Incidence, predictors, and implications of access site complications with transfemoral transcatheter aortic valve implantation. Am J Cardiol. 2012; 110:1361–1367.CrossrefMedlineGoogle Scholar
    • 16 Toggweiler S, Leipsic J, Binder RK, Freeman M, Barbanti M, Heijmen RH, Wood DA, Webb JG. Management of vascular access in transcatheter aortic valve replacement: part 2: vascular complications. JACC Cardiovasc Interv. 2013; 6:767–776.CrossrefMedlineGoogle Scholar
    • 17 Mangla A, Gupta S. Vascular complications post‐transcatheter aortic valve procedures. Indian Heart J. 2016; 68:724–731.CrossrefMedlineGoogle Scholar
    • 18 Blanke P, Weir‐McCall JR, Achenbach S, Delgado V, Hausleiter J, Jilaihawi H, Marwan M, Nørgaard BL, Piazza N, Schoenhagen P, Leipsic JA. Computed tomography imaging in the context of transcatheter aortic valve implantation (TAVI)/transcatheter aortic valve replacement (TAVR). JACC Cardiovasc Imaging. 2019; 12:1–24.CrossrefMedlineGoogle Scholar
    • 19 Sobolev M, Slovut DP, Chang AL, Shiloh AL, Eisen LA. Ultrasound‐guided catheterization of the femoral artery: a systematic review and meta‐analysis of randomized controlled trials. J Invasive Cardiol. 2015; 27:318–323.MedlineGoogle Scholar
    • 20 Elbaz‐Greener G, Zivkovic N, Arbel Y, Radhakrishnan S, Fremes SE, Wijeysundera HC. Use of two‐dimensional ultrasonographically guided access to reduce access‐related complications for transcatheter aortic valve replacement. Can J Cardiol. 2017; 33:918–924.CrossrefMedlineGoogle Scholar
    • 21 Burzotta F, Shoeib O, Aurigemma C, Trani C. Angio‐guidewire‐ultrasound (AGU) guidance for femoral access in procedures requiring large sheaths. J Invasive Cardiol. 2019; 31:E37–E39.MedlineGoogle Scholar
    • 22 Brodmann M, Werner M, Brinton TJ, Illindala U, Lansky A, Jaff MR, Holden A. Safety and performance of lithoplasty for treatment of calcified peripheral artery lesions. J Am Coll Cardiol. 2017; 70:908–910.CrossrefMedlineGoogle Scholar
    • 23 Brodmann M, Werner M, Holden A, Tepe G, Scheinert D, Schwindt A, Wolf F, Jaff M, Lansky A, Zeller T. Primary outcomes and mechanism of action of intravascular lithotripsy in calcified, femoropopliteal lesions: results of Disrupt PAD II. Catheter Cardiovasc Interv. 2019; 93:335–342.CrossrefMedlineGoogle Scholar
    • 24 Di Mario C, Chiriatti N, Stolcova M, Meucci F, Squillantini G. Lithoplasty‐assisted transfemoral aortic valve implantation. Eur Heart J. 2018. Available at: [Epub ahead of print].CrossrefGoogle Scholar
    • 25 Di Mario C, Goodwin M, Ristalli F, Ravani M, Meucci F, Stolcova M, Sardella G, Salvi N, Bedogni F, Berti S, Babaliaros VC, Pop A, Caparrelli D, Stewart J, Devireddy C. A prospective registry of intravascular lithotripsy‐enabled vascular access for transfemoral transcatheter aortic valve replacement. JACC Cardiovasc Interv. 2019; 12:502–504.CrossrefMedlineGoogle Scholar
    • 26 Van Mieghem NM, Latib A, van der Heyden J, van Gils L, Daemen J, Sorzano T, Ligthart J, Witberg K, de Kroon T, Maor N, Mangieri A, Montorfano M, de Jaegere PP, Colombo A, Roubin G. Percutaneous plug‐based arteriotomy closure device for large‐bore access. JACC Cardiovasc Interv. 2017; 10:613.CrossrefMedlineGoogle Scholar
    • 27 Jackson MWP, Muir DF, de Belder MA, Palmer S, Owens WA, Goodwin A, Hayat U, Williams PD. Transradial secondary access to guide valve implantation and manage peripheral vascular complications during transcatheter aortic valve implantation. Heart Lung Circ. 2019; 28:637–646.CrossrefMedlineGoogle Scholar
    • 28 Allende R, Urena M, Cordoba JG, Ribeiro HB, Amat‐Santos I, DeLarochelliere R, Paradis JM, Doyle D, Mohammadi S, Cote M, Abdul‐Jawad O, Del Trigo M, Ortas MR, Laflamme L, Laflamme J, DeLarochelliere H, Dumont E, Rodes‐Cabau J. Impact of the use of transradial versus transfemoral approach as secondary access in transcatheter aortic valve implantation procedures. Am J Cardiol. 2014; 114:1729–1734.CrossrefMedlineGoogle Scholar
    • 29 Grossman Y, Silverberg D, Berkovitch A, Chernomordik F, Younis A, Asher E, Barbash I, Halak M, Guetta V, Segev A, Fefer P. Long‐term outcomes of iliofemoral artery stents after transfemoral aortic valve replacement. J Vasc Interv Radiol. 2018; 29:1733–1740.CrossrefMedlineGoogle Scholar
    • 30 Barbanti M, Yang TH, Rodès Cabau J, Tamburino C, Wood DA, Jilaihawi H, Blanke P, Makkar RR, Latib A, Colombo A, Tarantini G, Raju R, Binder RK, Nguyen G, Freeman M, Ribeiro HB, Kapadia S, Min J, Feuchtner G, Gurtvich R, Alqoofi F, Pelletier M, Ussia GP, Napodano M, de Brito FS, Kodali S, Norgaard BL, Hansson NC, Pache G, Canovas SJ, Zhang H, Leon MB, Webb JG, Leipsic J. Anatomical and procedural features associated with aortic root rupture during balloon‐expandable transcatheter aortic valve replacement. Circulation. 2013; 128:244–253.LinkGoogle Scholar
    • 31 Eggebrecht H, Schmermund A, Kahlert P, Erbel R, Voigtlander T, Mehta RH. Emergent cardiac surgery during transcatheter aortic valve implantation (TAVI): a weighted meta‐analysis of 9,251 patients from 46 studies. EuroIntervention. 2013; 8:1072–1080.CrossrefMedlineGoogle Scholar
    • 32 Kapadia SR, Svensson LG, Roselli E, Schoenhagen P, Popovic Z, Alfirevic A, Barzilai B, Krishnaswamy A, Stewart W, Mehta A, Lal Poddar K, Parashar A, Modi D, Ozkan A, Khot U, Lytle BW, Murat Tuzcu E. Single center TAVR experience with a focus on the prevention and management of catastrophic complications. Catheter Cardiovasc Interv. 2014; 84:834–842.CrossrefMedlineGoogle Scholar
    • 33 Schymik G, Heimeshoff M, Bramlage P, Wondraschek R, Süselbeck T, Gerhardus J, Luik A, Posival H, Schmitt C, Schröfel H. Ruptures of the device landing zone in patients undergoing transcatheter aortic valve implantation: an analysis of TAVI Karlsruhe (TAVIK) patients. Clin Res Cardiol. 2014; 103:912–920.CrossrefMedlineGoogle Scholar
    • 34 Eggebrecht H, Mehta RH. Transcatheter aortic valve implantation (TAVI) in Germany 2008–2014: on its way to standard therapy for aortic valve stenosis in the elderly?EuroIntervention. 2016; 11:1029–1033.CrossrefMedlineGoogle Scholar
    • 35 Pasic M, Unbehaun A, Buz S, Drews T, Hetzer R. Annular rupture during transcatheter aortic valve replacement: classification, pathophysiology, diagnostics, treatment approaches, and prevention. JACC Cardiovasc Interv. 2015; 8:1–9.CrossrefMedlineGoogle Scholar
    • 36 Aksoy O, Paixao AR, Marmagkiolis K, Mego D, Rollefson WA, Cilingiroglu M. Aortic annular rupture during TAVR: mini review. Cardiovasc Revasc Med. 2016; 17:199–201.CrossrefMedlineGoogle Scholar
    • 37 Hansson NC, Nørgaard BL, Barbanti M, Nielsen NE, Yang TH, Tamburino C, Dvir D, Jilaihawi H, Blanke P, Makkar RR, Latib A, Colombo A, Tarantini G, Raju R, Wood D, Andersen HR, Ribeiro HB, Kapadia S, Min J, Feuchtner G, Gurvitch R, Alqoofi F, Pelletier M, Ussia GP, Napodano M, Sandoli de Brito F, Kodali S, Pache G, Canovas SJ, Berger A, Murphy D, Svensson LG, Rodés‐Cabau J, Leon MB, Webb JG, Leipsic J. The impact of calcium volume and distribution in aortic root injury related to balloon‐expandable transcatheter aortic valve replacement. J Cardiovasc Comput Tomogr. 2015; 9:382–392.CrossrefMedlineGoogle Scholar
    • 38 Condado JF, Corrigan FE, Lerakis S, Parastatidis I, Stillman AE, Binongo JN, Stewart J, Mavromatis K, Devireddy C, Leshnower B, Guyton R, Forcillo J, Patel A, Thourani VH, Block PC, Babaliaros V. Anatomical risk models for paravalvular leak and landing zone complications for balloon‐expandable transcatheter aortic valve replacement. Catheter Cardiovasc Interv. 2017; 90:690–700.CrossrefMedlineGoogle Scholar
    • 39 Hayashida K, Bouvier E, Lefèvre T, Hovasse T, Morice MC, Chevalier B, Romano M, Garot P, Farge A, Donzeau‐Gouge P, Cormier B. Potential mechanism of annulus rupture during transcatheter aortic valve implantation. Catheter Cardiovasc Interv. 2013; 82:E742–E746.CrossrefMedlineGoogle Scholar
    • 40 Girdauskas E, Owais T, Fey B, Kuntze F, Lauer B, Borger MA, Conradi L, Reichenspurner H, Kuntze T. Subannular perforation of left ventricular outflow tract associated with transcatheter valve implantation: pathophysiological background and clinical implications. Eur J Cardiothorac Surg. 2017; 51:91–96.CrossrefMedlineGoogle Scholar
    • 41 Azarrafiy R, Albuquerque FN, Carrillo RG, Cohen MG. Coil embolization to successfully treat annular rupture during transcatheter aortic valve replacement. Catheter Cardiovasc Interv. 2018; 92:1205–1208.CrossrefMedlineGoogle Scholar
    • 42 Hamm CW, Mollmann H, Holzhey D, Beckmann A, Veit C, Figulla HR, Cremer J, Kuck KH, Lange R, Zahn R, Sack S, Schuler G, Walther T, Beyersdorf F, Bohm M, Heusch G, Funkat AK, Meinertz T, Neumann T, Papoutsis K, Schneider S, Welz A, Mohr FW; Board GA‐E . The German Aortic Valve Registry (GARY): in‐hospital outcome. Eur Heart J. 2014; 35:1588–1598.CrossrefMedlineGoogle Scholar
    • 43 Gaede L, Blumenstein J, Liebetrau C, Dorr O, Kim WK, Nef H, Husser O, Elsasser A, Hamm CW, Mollmann H. Outcome after transvascular transcatheter aortic valve implantation in 2016. Eur Heart J. 2018; 39:667–675.CrossrefMedlineGoogle Scholar
    • 44 Ludman P. UK TAVI audit data 2007 to 2015. 2016.Google Scholar
    • 45 Ludman P.UK TAVI audit data 2007 to 2017. 2018.Google Scholar
    • 46 Auffret V, Lefevre T, Van Belle E, Eltchaninoff H, Iung B, Koning R, Motreff P, Leprince P, Verhoye JP, Manigold T, Souteyrand G, Boulmier D, Joly P, Pinaud F, Himbert D, Collet JP, Rioufol G, Ghostine S, Bar O, Dibie A, Champagnac D, Leroux L, Collet F, Teiger E, Darremont O, Folliguet T, Leclercq F, Lhermusier T, Olhmann P, Huret B, Lorgis L, Drogoul L, Bertrand B, Spaulding C, Quilliet L, Cuisset T, Delomez M, Beygui F, Claudel JP, Hepp A, Jegou A, Gommeaux A, Mirode A, Christiaens L, Christophe C, Cassat C, Metz D, Mangin L, Isaaz K, Jacquemin L, Guyon P, Pouillot C, Makowski S, Bataille V, Rodes‐Cabau J, Gilard M, Le Breton H; FRANCE TAVI Investigators . Temporal trends in transcatheter aortic valve replacement in France: FRANCE 2 to FRANCE TAVI. J Am Coll Cardiol. 2017; 70:42–55.CrossrefMedlineGoogle Scholar
    • 47 Holmes DR, Nishimura RA, Grover FL, Brindis RG, Carroll JD, Edwards FH, Peterson ED, Rumsfeld JS, Shahian DM, Thourani VH, Tuzcu EM, Vemulapalli S, Hewitt K, Michaels J, Fitzgerald S, Mack MJ; STS/ACC TVT Registry . Annual outcomes with transcatheter valve therapy: from the STS/ACC TVT registry. J Am Coll Cardiol. 2015; 66:2813–2823.CrossrefMedlineGoogle Scholar
    • 48 Nkomo VT, Suri RM, Pislaru SV, Greason KL, Sinak LJ, Holmes DR, Mathew V, Rihal CS. Delayed transcatheter heart valve migration and failure. JACC Cardiovasc Imaging. 2014; 7:960–962.CrossrefMedlineGoogle Scholar
    • 49 Pang PYK, Chiam PTL, Chua YL, Sin YK. A survivor of late prosthesis migration and rotation following percutaneous transcatheter aortic valve implantation. Eur J Cardiothorac Surg. 2012; 41:1195–1196.CrossrefMedlineGoogle Scholar
    • 50 Radu C, Raffoul R, Brochet E, Himbert D. Delayed migration of a transfemorally implanted aortic bioprosthesis. J Thorac Cardiovasc Surg. 2012; 143:e1–e3.CrossrefMedlineGoogle Scholar
    • 51 Pilgrim T, Lee JKT, O'Sullivan CJ, Stortecky S, Ariotti S, Franzone A, Lanz J, Heg D, Asami M, Praz F, Siontis GCM, Vollenbroich R, Räber L, Valgimigli M, Roost E, Windecker S. Early versus newer generation devices for transcatheter aortic valve implantation in routine clinical practice: a propensity score matched analysis. Open Heart. 2018; 5:e000695.CrossrefMedlineGoogle Scholar
    • 52 Fournier S, Monney P, Roguelov C, Ferrari E, Eeckhout E, Muller O, Durko A, Van Mieghem NM, Kappetein AP, Margey R. How should I treat an Edwards SAPIEN 3 aortic valve embolisation during a transaortic transcatheter aortic valve implantation?EuroIntervention. 2017; 13:495–498.CrossrefMedlineGoogle Scholar
    • 53 Barbash IM, Bogdan A, Fefer P, Spiegelstein D, Raanani E, Beinart R, Guetta V, Segev A. How should I treat a left ventricular outflow tract‐migrated balloon‐expandable transcatheter heart valve?EuroIntervention. 2016; 11:1442–1445.CrossrefMedlineGoogle Scholar
    • 54 Giannini F, Ruparelia N, Del Furia F, Romano V, Ancona M, Mangieri A, Regazzoli D, Latib A, Godino C, Ancona F, Candilio L, Jabbour R, Colombo A, Montorfano M. A novel technique for prosthetic valve retrieval after transcatheter aortic valve embolization. Can J Cardiol. 2017; 33:951.e1–951.e3.CrossrefMedlineGoogle Scholar
    • 55 Tiroch K, Schleiting H, Karpettas N, Schmitz E, Vetter HO, Seyfarth M, Vorpahl M, Thomas M, Abdel‐Wahab M, Sier H, Richardt G. How should I treat dislocation of a TAVI SAPIEN prosthesis into the left ventricle?EuroIntervention. 2015; 10:1370–1372.CrossrefMedlineGoogle Scholar
    • 56 Nicolino A, Vischi M, Moshiri S, Salsano A, Passerone G, Chiarella F, Santini F. Valve migration into the left ventricular outflow tract managed by coaxial double‐valve alignment. JACC Cardiovasc Interv. 2014; 7:822–824.CrossrefMedlineGoogle Scholar
    • 57 Ribeiro HB, Webb JG, Makkar RR, Cohen MG, Kapadia SR, Kodali S, Tamburino C, Barbanti M, Chakravarty T, Jilaihawi H, Paradis JM, de Brito FS, Canovas SJ, Cheema AN, de Jaegere PP, del Valle R, Chiam PT, Moreno R, Pradas G, Ruel M, Salgado‐Fernandez J, Sarmento‐Leite R, Toeg HD, Velianou JL, Zajarias A, Babaliaros V, Cura F, Dager AE, Manoharan G, Lerakis S, Pichard AD, Radhakrishnan S, Perin MA, Dumont E, Larose E, Pasian SG, Nombela‐Franco L, Urena M, Tuzcu EM, Leon MB, Amat‐Santos IJ, Leipsic J, Rodes‐Cabau J. Predictive factors, management, and clinical outcomes of coronary obstruction following transcatheter aortic valve implantation: insights from a large multicenter registry. J Am Coll Cardiol. 2013; 62:1552–1562.CrossrefMedlineGoogle Scholar
    • 58 Dvir D, Leipsic J, Blanke P, Ribeiro HB, Kornowski R, Pichard A, Rodes‐Cabau J, Wood DA, Stub D, Ben‐Dor I, Maluenda G, Makkar RR, Webb JG. Coronary obstruction in transcatheter aortic valve‐in‐valve implantation: preprocedural evaluation, device selection, protection, and treatment. Circ Cardiovasc Interv. 2015; 8:e002079.LinkGoogle Scholar
    • 59 Maggio S, Gambaro A, Scarsini R, Ribichini F. Preventive left main and right coronary artery stenting to avoid coronary ostia occlusion in high‐risk stentless valve‐in‐valve transcatheter aortic valve implantation. Interact Cardiovasc Thorac Surg. 2017; 25:147–149.CrossrefMedlineGoogle Scholar
    • 60 Zivelonghi C, Pesarini G, Scarsini R, Lunardi M, Piccoli A, Ferrero V, Gottin L, Vassanelli C, Ribichini F. Coronary catheterization and percutaneous interventions after transcatheter aortic valve implantation. Am J Cardiol. 2017; 120:625–631.CrossrefMedlineGoogle Scholar
    • 61 Khan JM, Greenbaum AB, Babaliaros VC, Rogers T, Eng MH, Paone G, Leshnower BG, Reisman M, Satler L, Waksman R, Chen MY, Stine AM, Tian X, Dvir D, Lederman RJ. The BASILICA trial: prospective multicenter investigation of intentional leaflet laceration to prevent TAVR coronary obstruction. JACC Cardiovasc Interv. 2019; 12:1240–1252.CrossrefMedlineGoogle Scholar
    • 62 Babaliaros VC, Greenbaum AB, Khan JM, Rogers T, Wang DD, Eng MH, O'Neill WW, Paone G, Thourani VH, Lerakis S, Kim DW, Chen MY, Lederman RJ. Intentional percutaneous laceration of the anterior mitral leaflet to prevent outflow obstruction during transcatheter mitral valve replacement: first‐in‐human experience. JACC Cardiovasc Interv. 2017; 10:798–809.CrossrefMedlineGoogle Scholar
    • 63 Muralidharan A, Thiagarajan K, Van Ham R, Gleason TG, Mulukutla S, Schindler JT, Jeevanantham V, Thirumala PD. Meta‐analysis of perioperative stroke and mortality in transcatheter aortic valve implantation. Am J Cardiol. 2016; 118:1031–1045.CrossrefMedlineGoogle Scholar
    • 64 Grube E, Van Mieghem NM, Bleiziffer S, Modine T, Bosmans J, Manoharan G, Linke A, Scholtz W, Tchetche D, Finkelstein A, Trillo R, Fiorina C, Walton A, Malkin CJ, Oh JK, Qiao H, Windecker S; FORWARD Study Investigators . Clinical outcomes with a repositionable self‐expanding transcatheter aortic valve prosthesis: the international FORWARD study. J Am Coll Cardiol. 2017; 70:845–853.CrossrefMedlineGoogle Scholar
    • 65 Wendler O, Schymik G, Treede H, Baumgartner H, Dumonteil N, Ihlberg L, Neumann FJ, Tarantini G, Zamarano JL, Vahanian A. SOURCE 3 registry: design and 30‐day results of the European postapproval registry of the latest generation of the SAPIEN 3 transcatheter heart valve. Circulation. 2017; 135:1123–1132.LinkGoogle Scholar
    • 66 Forrest JK, Mangi AA, Popma JJ, Khabbaz K, Reardon MJ, Kleiman NS, Yakubov SJ, Watson D, Kodali S, George I, Tadros P, Zorn GL, Brown J, Kipperman R, Saul S, Qiao H, Oh JK, Williams MR. Early outcomes with the Evolut PRO repositionable self‐expanding transcatheter aortic valve with pericardial wrap. JACC Cardiovasc Interv. 2018; 11:160–168.CrossrefMedlineGoogle Scholar
    • 67 Mollmann H, Hengstenberg C, Hilker M, Kerber S, Schafer U, Rudolph T, Linke A, Franz N, Kuntze T, Nef H, Kappert U, Walther T, Zembala MO, Toggweiler S, Kim WK. Real‐world experience using the ACURATE neo prosthesis: 30‐day outcomes of 1,000 patients enrolled in the SAVI TF registry. EuroIntervention. 2018; 13:e1764–e1770.CrossrefMedlineGoogle Scholar
    • 68 Pagnesi M, Martino EA, Chiarito M, Mangieri A, Jabbour RJ, Van Mieghem NM, Kodali SK, Godino C, Landoni G, Colombo A, Latib A. Silent cerebral injury after transcatheter aortic valve implantation and the preventive role of embolic protection devices: a systematic review and meta‐analysis. Int J Cardiol. 2016; 221:97–106.CrossrefMedlineGoogle Scholar
    • 69 Miller DC, Blackstone EH, Mack MJ, Svensson LG, Kodali SK, Kapadia S, Rajeswaran J, Anderson WN, Moses JW, Tuzcu EM, Webb JG, Leon MB, Smith CR; PARTNER Trial Investigators and Patients, PARTNER Stroke Substudy Writing Group and Executive Committee . Transcatheter (TAVR) versus surgical (AVR) aortic valve replacement: occurrence, hazard, risk factors, and consequences of neurologic events in the PARTNER trial. J Thorac Cardiovasc Surg. 2012; 143:832–843.e13.CrossrefMedlineGoogle Scholar
    • 70 Kleiman NS, Maini BJ, Reardon MJ, Conte J, Katz S, Rajagopal V, Kauten J, Hartman A, McKay R, Hagberg R, Huang J, Popma J; CoreValve Investigators . Neurological events following transcatheter aortic valve replacement and their predictors: a report from the CoreValve trials. Circ Cardiovasc Interv. 2016; 9:e003551.LinkGoogle Scholar
    • 71 Dangas GD, Lefevre T, Kupatt C, Tchetche D, Schafer U, Dumonteil N, Webb JG, Colombo A, Windecker S, Ten Berg JM, Hildick‐Smith D, Mehran R, Boekstegers P, Linke A, Tron C, Van Belle E, Asgar AW, Fach A, Jeger R, Sardella G, Hink HU, Husser O, Grube E, Deliargyris EN, Lechthaler I, Bernstein D, Wijngaard P, Anthopoulos P, Hengstenberg C; BRAVO‐3 Investigators . Bivalirudin versus heparin anticoagulation in transcatheter aortic valve replacement: the randomized BRAVO‐3 trial. J Am Coll Cardiol. 2015; 66:2860–2868.CrossrefMedlineGoogle Scholar
    • 72 Testa L, Latib A, Casenghi M, Gorla R, Colombo A, Bedogni F. Cerebral protection during transcatheter aortic valve implantation: an updated systematic review and meta‐analysis. J Am Heart Assoc. 2018; 7:e008463. DOI: 10.1161/JAHA.117.008463.LinkGoogle Scholar
    • 73 Bagur R, Solo K, Alghofaili S, Nombela‐Franco L, Kwok CS, Hayman S, Siemieniuk RA, Foroutan F, Spencer FA, Vandvik PO, Schaufele TG, Mamas MA. Cerebral embolic protection devices during transcatheter aortic valve implantation: systematic review and meta‐analysis. Stroke. 2017; 48:1306–1315.LinkGoogle Scholar
    • 74 Lansky AJ, Schofer J, Tchetche D, Stella P, Pietras CG, Parise H, Abrams K, Forrest JK, Cleman M, Reinohl J, Cuisset T, Blackman D, Bolotin G, Spitzer S, Kappert U, Gilard M, Modine T, Hildick‐Smith D, Haude M, Margolis P, Brickman AM, Voros S, Baumbach A. A prospective randomized evaluation of the TriGuard HDH embolic DEFLECTion device during transcatheter aortic valve implantation: results from the DEFLECT III trial. Eur Heart J. 2015; 36:2070–2078.CrossrefMedlineGoogle Scholar
    • 75 Demir OM, Iannopollo G, Mangieri A, Ancona MB, Regazzoli D, Mitomo S, Colombo A, Weisz G, Latib A. The role of cerebral embolic protection devices during transcatheter aortic valve replacement. Front Cardiovasc Med. 2018; 5:150. DOI: 10.3389/fcvm.2018.00150.CrossrefMedlineGoogle Scholar
    • 76 Barbanti M, Gulino S, Tamburino C, Capodanno D. Antithrombotic therapy following transcatheter aortic valve implantation: what challenge do we face?Expert Rev Cardiovasc Ther. 2016; 14:381–389.CrossrefMedlineGoogle Scholar
    • 77 Coughlan JJ, Fleck R, O'Connor C, Crean P. Mechanical thrombectomy of embolised native aortic valve post‐TAVI. BMJ Case Rep. 2017; 2017:bcr2016218787.CrossrefMedlineGoogle Scholar
    • 78 Khatri PJ, Webb JG, Rodes‐Cabau J, Fremes SE, Ruel M, Lau K, Guo H, Wijeysundera HC, Ko DT. Adverse effects associated with transcatheter aortic valve implantation: a meta‐analysis of contemporary studies. Ann Intern Med. 2013; 158:35–46.CrossrefMedlineGoogle Scholar
    • 79 Auffret V, Puri R, Urena M, Chamandi C, Rodriguez‐Gabella T, Philippon F, Rodes‐Cabau J. Conduction disturbances after transcatheter aortic valve replacement: current status and future perspectives. Circulation. 2017; 136:1049–1069.LinkGoogle Scholar
    • 80 Mollmann H, Kim WK, Kempfert J, Walther T, Hamm C. Complications of transcatheter aortic valve implantation (TAVI): how to avoid and treat them. Heart. 2015; 101:900–908.CrossrefMedlineGoogle Scholar
    • 81 Toggweiler S, Stortecky S, Holy E, Zuk K, Cuculi F, Nietlispach F, Sabti Z, Suciu R, Maier W, Jamshidi P, Maisano F, Windecker S, Kobza R, Wenaweser P, Luscher TF, Binder RK. The electrocardiogram after transcatheter aortic valve replacement determines the risk for post‐procedural high‐degree AV block and the need for telemetry monitoring. JACC Cardiovasc Interv. 2016; 9:1269–1276.CrossrefMedlineGoogle Scholar
    • 82 Fadahunsi OO, Olowoyeye A, Ukaigwe A, Li Z, Vora AN, Vemulapalli S, Elgin E, Donato A. Incidence, predictors, and outcomes of permanent pacemaker implantation following transcatheter aortic valve replacement: analysis from the U.S. Society of Thoracic Surgeons/American College of Cardiology TVT Registry. JACC Cardiovasc Interv. 2016; 9:2189–2199.CrossrefMedlineGoogle Scholar
    • 83 Urena M, Webb JG, Cheema A, Serra V, Toggweiler S, Barbanti M, Cheung A, Ye J, Dumont E, DeLarochelliere R, Doyle D, Al Lawati HA, Peterson M, Chisholm R, Igual A, Ribeiro HB, Nombela‐Franco L, Philippon F, Garcia Del Blanco B, Rodes‐Cabau J. Impact of new‐onset persistent left bundle branch block on late clinical outcomes in patients undergoing transcatheter aortic valve implantation with a balloon‐expandable valve. JACC Cardiovasc Interv. 2014; 7:128–136.CrossrefMedlineGoogle Scholar
    • 84 van der Boon RM, Nuis RJ, Van Mieghem NM, Jordaens L, Rodes‐Cabau J, van Domburg RT, Serruys PW, Anderson RH, de Jaegere PP. New conduction abnormalities after TAVI–frequency and causes. Nat Rev Cardiol. 2012; 9:454–463.CrossrefMedlineGoogle Scholar
    • 85 Husser O, Pellegrini C, Kessler T, Burgdorf C, Thaller H, Mayr NP, Kasel AM, Kastrati A, Schunkert H, Hengstenberg C. Predictors of permanent pacemaker implantations and new‐onset conduction abnormalities with the SAPIEN 3 balloon‐expandable transcatheter heart valve. JACC Cardiovasc Interv. 2016; 9:244–254.CrossrefMedlineGoogle Scholar
    • 86 Webb J, Gerosa G, Lefevre T, Leipsic J, Spence M, Thomas M, Thielmann M, Treede H, Wendler O, Walther T. Multicenter evaluation of a next‐generation balloon‐expandable transcatheter aortic valve. J Am Coll Cardiol. 2014; 64:2235–2243.CrossrefMedlineGoogle Scholar
    • 87 Perrin N, Perrin T, Hachulla A‐L, Frei A, Müller H, Roffi M, Cikirikcioglu M, Ellenberger C, Licker M‐J, Burri H, Noble S. Conduction disorders using the Evolut R prosthesis compared with the CoreValve: has anything changed?Open Heart. 2018; 5:e000770.CrossrefMedlineGoogle Scholar
    • 88 Rampat R, Khawaja MZ, Byrne J, MacCarthy P, Blackman DJ, Krishnamurthy A, Gunarathne A, Kovac J, Banning A, Kharbanda R, Firoozi S, Brecker S, Redwood S, Bapat V, Mullen M, Aggarwal S, Manoharan G, Spence MS, Khogali S, Dooley M, Cockburn J, de Belder A, Trivedi U, Hildick‐Smith D. Transcatheter aortic valve replacement using the repositionable LOTUS valve: United Kingdom experience. JACC Cardiovasc Interv. 2016; 9:367–372.CrossrefMedlineGoogle Scholar
    • 89 Zaman S, McCormick L, Gooley R, Rashid H, Ramkumar S, Jackson D, Hui S, Meredith IT. Incidence and predictors of permanent pacemaker implantation following treatment with the repositionable Lotus transcatheter aortic valve. Catheter Cardiovasc Interv. 2017; 90:147–154.CrossrefMedlineGoogle Scholar
    • 90 Franzoni I, Latib A, Maisano F, Costopoulos C, Testa L, Figini F, Giannini F, Basavarajaiah S, Mussardo M, Slavich M, Taramasso M, Cioni M, Longoni M, Ferrarello S, Radinovic A, Sala S, Ajello S, Sticchi A, Giglio M, Agricola E, Chieffo A, Montorfano M, Alfieri O, Colombo A. Comparison of incidence and predictors of left bundle branch block after transcatheter aortic valve implantation using the CoreValve versus the Edwards valve. Am J Cardiol. 2013; 112:554–559.CrossrefMedlineGoogle Scholar
    • 91 Bernardi FL, Ribeiro HB, Carvalho LA, Sarmento‐Leite R, Mangione JA, Lemos PA, Abizaid A, Grube E, Rodes‐Cabau J, de Brito FS. Direct transcatheter heart valve implantation versus implantation with balloon predilatation: insights from the Brazilian Transcatheter Aortic Valve Replacement Registry. Circ Cardiovasc Interv. 2016; 9:e003605.LinkGoogle Scholar
    • 92 Schymik G, Tzamalis P, Bramlage P, Heimeshoff M, Wurth A, Wondraschek R, Gonska BD, Posival H, Schmitt C, Schrofel H, Luik A. Clinical impact of a new left bundle branch block following TAVI implantation: 1‐year results of the TAVIK cohort. Clin Res Cardiol. 2015; 104:351–362.CrossrefMedlineGoogle Scholar
    • 93 Katsanos S, van Rosendael P, Kamperidis V, van der Kley F, Joyce E, Debonnaire P, Karalis I, Bax JJ, Marsan NA, Delgado V. Insights into new‐onset rhythm conduction disorders detected by multi‐detector row computed tomography after transcatheter aortic valve implantation. Am J Cardiol. 2014; 114:1556–1561.CrossrefMedlineGoogle Scholar
    • 94 Urena M, Mok M, Serra V, Dumont E, Nombela‐Franco L, DeLarochelliere R, Doyle D, Igual A, Larose E, Amat‐Santos I, Cote M, Cuellar H, Pibarot P, de Jaegere P, Philippon F, Garcia del Blanco B, Rodes‐Cabau J. Predictive factors and long‐term clinical consequences of persistent left bundle branch block following transcatheter aortic valve implantation with a balloon‐expandable valve. J Am Coll Cardiol. 2012; 60:1743–1752.CrossrefMedlineGoogle Scholar
    • 95 Boerlage‐Van Dijk K, Kooiman KM, Yong ZY, Wiegerinck EM, Damman P, Bouma BJ, Tijssen JG, Piek JJ, Knops RE, Baan J. Predictors and permanency of cardiac conduction disorders and necessity of pacing after transcatheter aortic valve implantation. Pacing Clin Electrophysiol. 2014; 37:1520–1529.CrossrefMedlineGoogle Scholar
    • 96 Hein‐Rothweiler R, Jochheim D, Rizas K, Egger A, Theiss H, Bauer A, Massberg S, Mehilli J. Aortic annulus to left coronary distance as a predictor for persistent left bundle branch block after TAVI. Catheter Cardiovasc Interv. 2017; 89:E162–E168.CrossrefMedlineGoogle Scholar
    • 97 Regueiro A, Abdul‐Jawad Altisent O, Del Trigo M, Campelo‐Parada F, Puri R, Urena M, Philippon F, Rodes‐Cabau J. Impact of new‐onset left bundle branch block and periprocedural permanent pacemaker implantation on clinical outcomes in patients undergoing transcatheter aortic valve replacement: a systematic review and meta‐analysis. Circ Cardiovasc Interv. 2016; 9:e003635.LinkGoogle Scholar
    • 98 Ando T, Takagi H. The prognostic impact of new‐onset persistent left bundle branch block following transcatheter aortic valve implantation: a meta‐analysis. Clin Cardiol. 2016; 39:544–550.CrossrefMedlineGoogle Scholar
    • 99 Houthuizen P, van der Boon RM, Urena M, Van Mieghem N, Brueren GB, Poels TT, Van Garsse LA, Rodes‐Cabau J, Prinzen FW, de Jaegere P. Occurrence, fate and consequences of ventricular conduction abnormalities after transcatheter aortic valve implantation. EuroIntervention. 2014; 9:1142–1150.CrossrefMedlineGoogle Scholar
    • 100 Nazif TM, Williams MR, Hahn RT, Kapadia S, Babaliaros V, Rodes‐Cabau J, Szeto WY, Jilaihawi H, Fearon WF, Dvir D, Dewey TM, Makkar RR, Xu K, Dizon JM, Smith CR, Leon MB, Kodali SK. Clinical implications of new‐onset left bundle branch block after transcatheter aortic valve replacement: analysis of the PARTNER experience. Eur Heart J. 2014; 35:1599–1607.CrossrefMedlineGoogle Scholar
    • 101 Testa L, Latib A, De Marco F, De Carlo M, Agnifili M, Latini RA, Petronio AS, Ettori F, Poli A, De Servi S, Ramondo A, Napodano M, Klugmann S, Ussia GP, Tamburino C, Brambilla N, Colombo A, Bedogni F. Clinical impact of persistent left bundle‐branch block after transcatheter aortic valve implantation with CoreValve Revalving System. Circulation. 2013; 127:1300–1307.LinkGoogle Scholar
    • 102 Urena M, Webb JG, Eltchaninoff H, Munoz‐Garcia AJ, Bouleti C, Tamburino C, Nombela‐Franco L, Nietlispach F, Moris C, Ruel M, Dager AE, Serra V, Cheema AN, Amat‐Santos IJ, de Brito FS, Lemos PA, Abizaid A, Sarmento‐Leite R, Ribeiro HB, Dumont E, Barbanti M, Durand E, Alonso Briales JH, Himbert D, Vahanian A, Imme S, Garcia E, Maisano F, del Valle R, Benitez LM, Garcia del Blanco B, Gutierrez H, Perin MA, Siqueira D, Bernardi G, Philippon F, Rodes‐Cabau J. Late cardiac death in patients undergoing transcatheter aortic valve replacement: incidence and predictors of advanced heart failure and sudden cardiac death. J Am Coll Cardiol. 2015; 65:437–448.CrossrefMedlineGoogle Scholar
    • 103 Fraccaro C, Buja G, Tarantini G, Gasparetto V, Leoni L, Razzolini R, Corrado D, Bonato R, Basso C, Thiene G, Gerosa G, Isabella G, Iliceto S, Napodano M. Incidence, predictors, and outcome of conduction disorders after transcatheter self‐expandable aortic valve implantation. Am J Cardiol. 2011; 107:747–754.CrossrefMedlineGoogle Scholar
    • 104 Gonska B, Seeger J, Kessler M, von Keil A, Rottbauer W, Wohrle J. Predictors for permanent pacemaker implantation in patients undergoing transfemoral aortic valve implantation with the Edwards Sapien 3 valve. Clin Res Cardiol. 2017; 106:590–597.CrossrefMedlineGoogle Scholar
    • 105 Akin I, Kische S, Paranskaya L, Schneider H, Rehders TC, Trautwein U, Turan G, Bansch D, Thiele O, Divchev D, Bozdag‐Turan I, Ortak J, Kundt G, Nienaber CA, Ince H. Predictive factors for pacemaker requirement after transcatheter aortic valve implantation. BMC Cardiovasc Disord. 2012; 12:87.CrossrefMedlineGoogle Scholar
    • 106 Mauri V, Reimann A, Stern D, Scherner M, Kuhn E, Rudolph V, Rosenkranz S, Eghbalzadeh K, Friedrichs K, Wahlers T, Baldus S, Madershahian N, Rudolph TK. Predictors of permanent pacemaker implantation after transcatheter aortic valve replacement with the SAPIEN 3. JACC Cardiovasc Interv. 2016; 9:2200–2209.CrossrefMedlineGoogle Scholar
    • 107 van Rosendael PJ, Delgado V, Bax JJ. Pacemaker implantation rate after transcatheter aortic valve implantation with early and new‐generation devices: a systematic review. Eur Heart J. 2018; 39:2003–2013.CrossrefMedlineGoogle Scholar
    • 108 Rodriguez‐Olivares R, van Gils L, El Faquir N, Rahhab Z, Di Martino LF, van Weenen S, de Vries J, Galema TW, Geleijnse ML, Budde RP, Boersma E, de Jaegere PP, Van Mieghem NM. Importance of the left ventricular outflow tract in the need for pacemaker implantation after transcatheter aortic valve replacement. Int J Cardiol. 2016; 216:9–15.CrossrefMedlineGoogle Scholar
    • 109 Guetta V, Goldenberg G, Segev A, Dvir D, Kornowski R, Finckelstein A, Hay I, Goldenberg I, Glikson M. Predictors and course of high‐degree atrioventricular block after transcatheter aortic valve implantation using the CoreValve Revalving System. Am J Cardiol. 2011; 108:1600–1605.CrossrefMedlineGoogle Scholar
    • 110 Kim WJ, Ko YG, Han S, Kim YH, Dy TC, Posas FE, Lee MK, Kim HS, Hong MK, Jang Y, Grube E, Park SJ. Predictors of permanent pacemaker insertion following transcatheter aortic valve replacement with the CoreValve Revalving System based on computed tomography analysis: an Asian multicenter registry study. J Invasive Cardiol. 2015; 27:334–340.MedlineGoogle Scholar
    • 111 Hilling‐Smith R, Cockburn J, Dooley M, Parker J, Newton A, Hill A, Trivedi U, de Belder A, Hildick‐Smith D. Rapid pacing using the 0.035‐in. Retrograde left ventricular support wire in 208 cases of transcatheter aortic valve implantation and balloon aortic valvuloplasty. Catheter Cardiovasc Interv. 2017; 89:783–786.CrossrefMedlineGoogle Scholar
    • 112 Mohananey D, Jobanputra Y, Kumar A, Krishnaswamy A, Mick S, White JM, Kapadia SR. Clinical and echocardiographic outcomes following permanent pacemaker implantation after transcatheter aortic valve replacement: meta‐analysis and meta‐regression. Circ Cardiovasc Interv. 2017; 10:e005046.AbstractGoogle Scholar
    • 113 Brignole M, Auricchio A, Baron‐Esquivias G, Bordachar P, Boriani G, Breithardt OA, Cleland J, Deharo JC, Delgado V, Elliott PM, Gorenek B, Israel CW, Leclercq C, Linde C, Mont L, Padeletti L, Sutton R, Vardas PE, Zamorano JL, Achenbach S, Baumgartner H, Bax JJ, Bueno H, Dean V, Deaton C, Erol C, Fagard R, Ferrari R, Hasdai D, Hoes AW, Kirchhof P, Knuuti J, Kolh P, Lancellotti P, Linhart A, Nihoyannopoulos P, Piepoli MF, Ponikowski P, Sirnes PA, Tamargo JL, Tendera M, Torbicki A, Wijns W, Windecker S, Blomstrom‐Lundqvist C, Badano LP, Aliyev F, Bansch D, Bsata W, Buser P, Charron P, Daubert JC, Dobreanu D, Faerestrand S, Le Heuzey JY, Mavrakis H, McDonagh T, Merino JL, Nawar MM, Nielsen JC, Pieske B, Poposka L, Ruschitzka F, Van Gelder IC, Wilson CM. 2013 ESC guidelines on cardiac pacing and cardiac resynchronization therapy: the Task Force on cardiac pacing and resynchronization therapy of the European Society of Cardiology (ESC). Developed in collaboration with the European Heart Rhythm Association (EHRA). Eur Heart J. 2013; 34:2281–2329.CrossrefMedlineGoogle Scholar
    • 114 Schernthaner C, Kraus J, Danmayr F, Hammerer M, Schneider J, Hoppe UC, Strohmer B. Short‐term pacemaker dependency after transcatheter aortic valve implantation. Wien Klin Wochenschr. 2016; 128:198–203.CrossrefMedlineGoogle Scholar
    • 115 Marzahn C, Koban C, Seifert M, Isotani A, Neuss M, Holschermann F, Butter C. Conduction recovery and avoidance of permanent pacing after transcatheter aortic valve implantation. J Cardiol. 2018; 71:101–108.CrossrefMedlineGoogle Scholar


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