**3. Complications in valve-in-valve TAVR**

#### **3.1 Prosthesis-patient mismatch**

Valve-in-valve TAVR could cause prosthesis-patient mismatch especially when there was severe bioprosthetic valve stenosis. It was also pointed out that valvein-valve TAVR was an independent predictor of valve hemodynamic deterioration (defined as an increase in mean aortic valve gradient ≥10 mm Hg) [13].

Herrmann et al. reviewed 62,125 patients in the Society of Thoracic Surgeons/ American College of Cardiology TVT registry and reported that severe prosthesispatient mismatch occurred in 12% [14]. Patients with severe prosthesis-patient mismatch had higher mortality rate compared to patients with moderate or no prosthesis-patient mismatch.

On the contrary, Dvir et al. reported that severe prosthesis-patient mismatch occurred in 31.8% of patients surviving aortic valve-in-valve TAVR [4]. However, one-year survival was not affected by having severe prosthesis-patient mismatch.

The long-term transaortic gradient has not been reported. In the Partner II registry, mean transaortic gradient was 16.6 mmHg at 3-year follow-up [7].

#### **3.2 Coronary obstruction**

Coronary obstruction is a rare, but life-threatening complication associated with TAVR. Its incidence in native valve TAVR was reported as less than 1% [15]. However, it occurs more frequently in valve-in-valve TAVR.

Ribeiro et al. reviewed 1,612 patients from the Valve-in-Valve International Data Registry [16]. Coronary obstruction occurred in 37 patients (2.3%), and the 30-day mortality was 52.9% among the patients who had coronary obstruction. Coronary obstruction happened more frequently in stented valves with externally mounted leaflets or stentless valves compared to stented valves with internally mounted leaflets.

Multiple detector computed tomography is a standard diagnostic modality in the planning of TAVR [17]. A virtual transcatheter valve to coronary ostium distance <4 mm is considered a high risk of coronary obstruction [16].

In the case of anticipated high risk of coronary obstruction, a placement of a coronary guidewire with coronary balloon or undeployed stent in the targeted *The Current Perspectives in Valve-in-Valve Transcatheter Aortic Valve Replacement DOI: http://dx.doi.org/10.5772/intechopen.97521*

coronary arteries before deploying TAVR is a good option for coronary protection, since the emergent percutaneous coronary intervention for coronary obstruction is challenging. Ribeiro et al. reported that percutaneous coronary intervention was successful only in 81.8% [15].

Delayed coronary obstruction is a rare complication following TAVR that accompanies with high in-hospital mortality. Jabbour et al. reported that the incidence of delayed coronary obstruction was 0.22% in 17,092 TAVR procedures and the overall in-hospital mortality was 50% [18]. Percutaneous coronary intervention was successful only in 68.8%. It occurred more frequently after valve-in-valve TAVR compared to native valve TAVR (0.89% vs. 0.18%) and it occurred more frequently in self-expandable valves compared to balloon-expandable valves (0.36% vs. 0.11%).

#### **3.3 Self-expandable valve versus balloon-expandable valve**

Self-expanding valves are usually associated with lower postprocedural gradients. Rogers et al. reported that hemodynamics of self-expandable valves were superior to that of balloon-expandable valves in patients with small aortic annulus [19].

In the meantime, Dvir et al. reported that elevated postprocedural gradients were happened more frequently in balloon expandable valves compared with selfexpandable valves [4].

Pibarot et al. reported that pre-existing prosthesis-patient mismatch of the failed surgical valve was strongly and independently associated with increased risk for mortality following valve-in-valve TAVR [9]. Elevated pressure gradients are seen in more than 70% of patients who present with baseline prosthesis-patient mismatch if treated with balloon-expandable valves.

The optimal deployment height would be important to avoid postprocedural high gradients. Simonato et al. reported that lower gradients and greater effective orifice areas were achieved with higher deployment positions than lower deployment in vitro study [20]. Hatoum et al. reported that supra-annular axial deployment is associated with lower pressure gradients, and sub-annular deployment is associated with more favorable sinus hemodynamics [21].

When severe prosthesis-patient mismatch is present, a self-expanding device in a supra-annular position would be the preferred treatment strategy. Dvir et al. suggested an implant depth of up to 3 mm for the self-expandable valve; Evolut (Medtronic, Minneapolis, Minnesota), and up to 20% frame depth for the balloonexpandable valve; SAPIEN 3 (Edwards Lifesciences, Irvine, California) [22].

#### **3.4 Structural valve deterioration after TAVR**

Bioprosthetic valve dysfunction happens both in surgical AVR and TAVR. However, bioprosthetic valve dysfunction is a broad term that encompasses structural and non-structural valve deterioration [23]. It is very important to distinguish between two of them. Structural valve deterioration is the principal etiological factor, and it can lead to irreversible valve dysfunction, whereas non-structural valve deterioration includes reversible dysfunction such as valve thrombosis or endocarditis.

The long-term durability of valve-in-valve TAVR has been unknown. One of the longest follow-up data was reported from Partner II registry [7]. Among 337 patients who could be followed for 3 years, 5 patients underwent repeat aortic valve replacement for aortic valve dysfunction after valve-in-valve procedure. Moderate hemodynamic valve deterioration occurred in 2 out of 160 patients

(1.3%), and severe hemodynamic valve deterioration also occurred in 2 out of 160patients (1.3%) at 3 years.

## **3.5 Valve thrombosis**

Valve thrombosis following TAVR has been increasingly recognized. Valve thrombosis is associated with reduced leaflet motion, and leads to high chance of strokes and transient ischemic attacks. Subclinical leaflet thrombosis is manifested by either hypo-attenuated leaflet thickening or reduced leaflet motion [24].

Del Trigo et al. reported that the incidence of valve hemodynamic deterioration following TAVR was 4.5% in 1,521 patients, and a valve-in-valve procedure was an independent predictor for valve hemodynamic deterioration [25].

Vahidkhah et al. analyzed computational three-dimensional models for the surgical aortic valve and transcatheter aortic valve [26]. They found that geometric confinement of the transcather aortic valve by the leaflets and the frame of the degenerated bioprosthesis that circumferentially surround the transcatheter aortic valve stent increased the blood residence time on the leaflets, which could act as a permissive factor in the leaflet thrombosis after valve-in-valve TAVR.

#### **3.6 Antiplatelet/anticoagulation therapy after TAVR**

The optimal antiplatelet/anticoagulation management after TAVR has been controversial [23, 27].

Most of the societies such as American Heart Association and Society of Thoracic Surgeons recommend lifelong-aspirin and 6 months of Clopidogrel after TAVR. In terms of anticoagulant therapy, it may be considered in patients with chronic atrial fibrillation or other indications. Vitamin K antagonist may be considered in the first 3 months after procedure in patients at risk for atrial fibrillation or valve thrombosis.

Overtchouk et al. reviewed 11,469 patients in French registry, and found that anticoagulation decreased the risk of bioprosthetic valve dysfunction, whereas chronic renal failure and prosthesis size ≤23 mm were associated with the risk of bioprosthetic valve dysfunction [28].
