Peripheral contrast angiography is the most practical, readily available, and cost effective modality for assessing the peripheral vasculature. In contrast, MSCT can be associated with a higher contrast load, higher radiation exposure, and greater expense. However, MSCT provides greater appreciation of vessel size, tortuosity, and calcific burden [44, 45] (Fig. 10.3). Using contrast angiography, a SFAR ratio ≥1.05 (i.e., outer Sheath diameter to Femoral Artery minimal luminal diameter Ratio) has been identified as a predictor of major vascular complications and 30-day mortality [46, 47]. In non-calcified vessels, the ratio is increased to 1.10 and, in the presence of calcium, it is decreased to 1.00. The utility of the SFAR criteria in MSCT is unclear. It should be noted that MSCT technology and techniques continue to advance, with a focus on reducing the quantity of radiation and contrast delivered to patients.

The aortic valve annulus corresponds to a virtual plane defined by the basal attachment points of the three leaflets [48] (Fig. 10.4). This plane is a surrogate for the transition from the left ventricular outflow tract into the aortic root, but does not represent the anatomic ventriculo-arterial junction nor the hemodynamic junction between the left ventricular outflow tract and the aortic root. The non-circular shape of the aortic valve annulus has generated much debate about how best to measure its diameter for the purposes of transcatheter aortic valve size selection [49–51] (Fig. 10.5). Currently, MSCT appears to be the most suitable method for assessment of aortic annulus dimensions due to its 3D nature and high spatial resolution. Additionally, MSCT allows for multiplanar reconstructions of the original images, which can provide reformatted coronal, sagittal, and axial images of the aortic root [52, 53]. This reformatting results in oblique coronal, oblique sagittal, and double-oblique axial images, which are en face with the aortic annular plane. On the double-oblique axial view, the maximum and orthogonal minimum diameters, perimeter, and area of the annulus can be measured. According to MSCT data, the mean difference between the maximum and orthogonal minimum diameter of the non-circular aortic annulus is 6.5 mm (95% confidence interval, 5.7–7.2) [49, 50]. Depending on the orientation, 2D echocardiography appreciates only one view of the aortic annulus, and usually underestimates the annulus diameter with respect to MSCT. With this in mind, the use of 2D measurements (TTE, TEE, contrast aortography) for transcatheter valve sizing is potentially problematic. Nevertheless, 2D echocardiography remains the most commonly used method to assess the aortic valve annulus diameter, though a shift towards MSCT is emerging.

A degree of post-implant aortic regurgitation (paravalvular or transvalvular) is observed in 70–90% of TAVI recipients, though less than 5% of cases have moderate to severe aortic regurgitation [92–98]. Mechanisms of aortic regurgitation include: (1) transcatheter valve undersizing [97, 99]; (2) mal-positioning [100, 101]; (3) mal-apposition, underexpansion or recoil of the transcatheter valve [102–104]; and (4) mal-coaptation or immobility of the valve leaflets [105–107]. Delayed severe aortic regurgitation has also been reported [108–110]. The Valvular Academic Research Consortium (VARC) recommends using an integrative echocardiographic approach when quantifying aortic regurgitation [111, 112].

Management of significant aortic regurgitation depends on the underlying mechanism; treatment may include post-implant dilation, implantation of a second valve, or repositioning of the frame using a snare (Fig. 10.14). Conversion to surgical aortic valve replacement is required in less than 1% of cases.

The anatomical proximity of the aortic valvar complex and the conduction system explains the potential for conduction disturbances following TAVI [48] (Fig. 10.15). Indeed, the average distance between the nadir of the non-coronary aortic valve leaflet and the left bundle branch is only 6.3  ±  2.7 mm (Fig. 10.15) [113]. New-onset left bundle branch block occurs in 30–65% of patients after Medtronic CoreValve implantation and in 7–18% [114–131] after Edwards SAPIEN implantation [132–134]. The long-term implications of new-onset left bundle branch block after TAVI are currently unknown, however anecdotal evidence suggests that it has a negligible impact on 1-year survival. Approximately 15–47% [114–131] and 4–21% [132–134] of patients require a new permanent pacemaker after CoreValve and Edwards SAPIEN implantation, respectively. The most important predictors for new-onset conduction abnormalities after CoreValve implantation include a pre-existing right bundle branch block, baseline QRS duration (msec), and the depth of prosthesis implantation (mm) [114–120, 123–125, 127–129, 131, 135, 136]. Temporary pacing should be maintained for 48–72 h, especially after CoreValve implantation, as a small percentage of patients may present with delayed conduction block. Indications for permanent pacemaker implantation after TAVI are based upon the European Society of Cardiology guidelines [137, 138].

Occlusion of the left main coronary following TAVI occurs in less than 1% of cases [139–149]. Unsurprisingly, it frequently induces sudden hemodynamic compromise and death. The diagnosis is usually suspected on the basis of hemodynamics, ECG pattern, and/or contrast aortography. Hemodynamic support and re-establishment of coronary perfusion is critical. The nature and severity of the coronary obstruction and hemodynamic status determines the mode of revascularization (percutaneous or surgical).

Possible mechanisms for coronary obstruction include: (1) impingement of the coronary ostia by the valve support structure; (2) displacement of native aortic valve leaflets towards the coronary ostia during valve deployment; and (3) embolization from calcium, thrombus, air, and/or endocarditis. The width and height of the sinus of Valsalva, height of the coronary ostia, and bulkiness of the native leaflets play important roles in the pathogenesis of coronary occlusion following TAVI.

Cardiac perforation has been reported in 2–4% of patients undergoing TAVI [150–152]. Potential mechanisms include right or left ventricular injury due to the temporary pacemaker lead or stiff guidewire, respectively. Small hypertrophic left ventricular cavities (commonly seen in elderly females), or inadequate pre-shaping or positioning of the left ventricular support wire may increase the risk for this complication. Cardiac perforation and cardiac tamponade are usually suspected on the basis of hypotension and/or a new pericardial effusion, and are diagnosed using TTE. Percutaneous pericardiocentesis and reversal of the anticoagulation are recommended.

Rupture of the annulus or aortic root is rare (<1%). This life threatening complication is difficult to predict, but typically occurs during balloon inflation (pre-implant balloon aortic valvuloplasty or balloon-expandable valve implantation) (Fig. 10.16). A non-compliant aortic valvar complex, bulky calcification, and aggressive balloon/prosthesis oversizing are possible risk factors. Depending on its location, rupture may result in a ventricular septal defect, left ventricle to left atrial or right atrial shunt, or communication with the extracardiac space. Emergent cardiopulmonary bypass support and surgical exploration is the management of choice.

Prosthetic valve dysfunction may manifest as symptoms and signs of valvular stenosis or regurgitation. Careful clinical history and examination coupled with echocardiography (TTE or TEE) are suggested to evaluate valve dysfunction [111, 112]. Prosthetic valve dysfunction is graded as: (1) normal; (2) possible; or (3) significant according to the VARC criteria [111, 112]. To date, there are limited case reports describing degeneration of transcatheter valves [153, 154].

Transcatheter valve embolization usually occurs during valve implantation and appears to correlate with operator experience. Embolization may be caused by: (1) undersizing the prosthesis; (2) mal-placement of the prosthesis; (3) improper rapid pacing during valve deployment or post-implant dilation; (4) entanglement of a guidewire across the struts of the prosthesis during valve re-crossing; (5) entanglement of the nose cone with the inflow portion of the prosthesis upon retrieving the delivery catheter; and (6) inadequate release of the loading hooks of the frame from the delivery catheter. Delayed embolization, presenting with unexpected hemodynamic compromise and severe aortic regurgitation, has also been described [108, 109].

Valve thrombosis is defined as any thrombus attached to or near an implanted valve that interrupts blood flow, interferes with valve function, or is sufficiently large to warrant treatment. Post-mortem studies of patients implanted with the Edwards SAPIEN and CoreValve prostheses have observed thrombotic material attached to the frame and/or leaflets [155]. To date, transcatheter aortic valve thrombosis has been reported in only three individual case reports [156–158].

Currently, dual antiplatelet therapy (aspirin and clopidogrel) is recommended for 6 months following TAVI, with aspirin continued indefinitely [150, 159]. However, a single-center randomized study, observed no differences in clinical outcomes between groups who received dual antiplatelet therapy for 3 months vs. aspirin alone [160].

The diagnosis of prosthetic valve endocarditis can be made using the Duke Criteria for endocarditis, during reoperation, or on autopsy [111, 112]. Several case reports of bacterial or fungal transcatheter aortic valve endocarditis have been reported involving both the Edwards SAPIEN and Medtronic CoreValve [161–167]. These cases underline the importance of adequate dental care prior to TAVI, the importance of pre-procedural antibiotics, and sterile techniques during the procedure.

Mitral valve injury associated with retrograde TAVI is rare. Resistance during the passage of the delivery catheter into the left ventricle or observation of new mitral regurgitation on TEE should raise the suspicion of catheter entanglement within the mitral valve apparatus. Pre-procedural mitral regurgitation can be identified in up 75% of patients [168, 169], and improves in approximately one-third of patients, and worsens in one-third following TAVI. Mitral annular calcification and deep implantation of the transcatheter valve into the left ventricular outflow tract have been associated with worsening mitral regurgitation [168–171].

To date, observational series have reported 30-day stroke rates of 0–6% in patients undergoing TAVI [93, 150, 172–174]. In the randomized Placement of AoRTic TraNscathetER (PARTNER) Cohort A trial, the neurologic event rate (all strokes or transient ischemic attacks) was nearly twofold higher in the TAVI group compared to the surgical group at 30-day and 1-year follow-ups (5.5% vs. 2.4% at 30 days; 8.3% vs. 4.3% at 1 year) [159]. Similarly, in the randomized PARTNER Cohort B trial, the neurologic event rate was higher in the TAVI group compared to the medical therapy group at 30 days and 1 year (6.7% vs. 1.7% at 30 days, and 10.6% vs. 4.5% at 1 year). Interestingly, one-third to one-half of strokes occurred between 2 and 30 days after the index procedure [150, 159, 175]. A history of cerebrovascular disease is an independent predictor of neurologic injury after TAVI [176].

Post-TAVI magnetic resonance imaging (MRI) studies have observed new and multiple silent cerebral infarcts in 68–83% of cases [177–182] (Fig. 10.17). This suggests that most strokes after TAVI are embolic in nature, a hypothesis corroborated by a recent study using intraprocedural transcranial Doppler which found cerebral microemboli in all patients undergoing transapical TAVI [183]. Cerebral embolic protection devices such as the Embrella (Edwards LifeSciences) and Montage System (Claret Medical, Santa Rosa, CA, USA) have been developed to prevent cerebral embolization and have received European CE mark approval [184, 185] (Fig. 10.18). These devices have the potential to reduce the incidence of clinical stroke in TAVI recipients [186].