The authors present the case of an 81-year-old patient with severe aortic stenosis who experienced left ventricular embolization of an aortic bioprosthesis during transapical aortic valve implantation. The authors discuss reasons for prosthesis embolization and reinforce the attention to technical details and the widespread use of multimodality imaging techniques. In this context, transesophageal echocardiography appears indispensable in the detection and management of procedure-related complications.
Minimally invasive beating-heart transapical transcatheter aortic valve implantation (TA-AVI) represents a new alternative to the current standard, open-heart aortic valve replacement, in the treatment of symptomatic aortic valve stenosis in a selected high-risk patient population. To date, several groups have demonstrated their perioperative results, reporting high rates of procedural success and significant improvements in the New York Heart Association functional classes of their patients at early follow-up. Nevertheless, TA-AVI is a technically challenging procedure, requiring a particularly careful imaging assessment of all cardiac structures, especially the left ventricular (LV) outflow tract (LVOT) and the thoracic aorta, to implant the balloon-expandable bioprosthesis in the correct position. Because of the impossibility of repositioning, life-threatening complications can occur in case of suboptimal prosthesis deployment.
Here, we present a rare case of TA-AVI in which the bioprosthesis embolized into the left ventricle because of malpositioning at a too low level with respect to the aortic valve annulus. Transesophageal echocardiography (TEE) was decisive in the immediate detection of the cause of hemodynamic deterioration and in guiding emergent procedural and medical management.
Case Presentation
An 81-year-old man with severe symptomatic aortic valve stenosis and high risk for conventional surgery (logistic European System for Cardiac Operative Risk Evaluation score, 69%; Society of Thoracic Surgeons mortality risk score, 9.9%) was admitted to our institution to be evaluated for TA-AVI. He presented in New York Heart Association class III, stable angina pectoris (Canadian Cardiovascular Society class III), and permanent atrial fibrillation. Risk factors included coronary artery disease with previous bypass grafting and stent implantation. A single-chamber permanent pacemaker (VVI mode) had been implanted previously because of sinus arrest. Additional risk factors included chronic renal failure with long-term hemodialysis, insulin-dependent diabetes mellitus, peripheral artery occlusive disease, and parenchymal lung disease with elevated pulmonary vascular resistance (502 dynes/sec · cm −5 ).
Preoperative transthoracic echocardiography had revealed LV hypertrophy with poor systolic function (ejection fraction, 20%) and diastolic dysfunction (classification moderate according to Canadian consensus guidelines), resulting in severe global hypokinesia. The right ventricle was not dilated, and right ventricular (RV) systolic function was only mildly reduced (RV fractional area change, 30%; tricuspid annular plane systolic excursion, 18 mm). Mild tricuspid regurgitation was noted (proximal isovelocity surface area radius, 0.40 cm; systolic dominance of hepatic vein flow) in the presence of the pacemaker lead, which allowed the estimation of systolic pulmonary pressure at 48 mm Hg. The aortic valve was high-grade calcified, resulting in severe stenosis, with a mean pressure gradient of 23 mm Hg and a valve orifice area of 0.6 cm 2 (determined by continuity equation). The aortic annular diameter was 24 mm on preoperative computed tomography and TEE.
TA-AVI was performed off pump in standard fashion, as recently described in detail. On TEE, after visualizing the aortic root in the midesophageal aortic valve long-axis view, the severity of aortic valve stenosis was assessed, and the aortic annular diameter was measured repeatedly. Likewise, the exact positioning of the guidewire, the balloon valvuloplasty catheter, and the valve delivery system was monitored by both fluoroscopy and TEE. Following dilatation (balloon valvuloplasty) of the native aortic valve during rapid ventricular pacing (RVP), the selected bioprosthesis (Edwards SAPIEN Ø 26 mm; Edwards Lifesciences, Irvine, CA) was transapically advanced under fluoroscopic and transesophageal echocardiographic guidance into the aortic annulus in a manner such that the annulus bisected the midportion of the stainless steel stent. The prosthesis was deployed during RVP. This interventional phase was guided by fluoroscopy alone because the transesophageal probe had been slightly withdrawn for improved fluoroscopic visualization of the LVOT, aortic root, and ascending aorta.
Immediately upon termination of RVP and restoration of cardiac ejection, hemodynamic compromise became apparent. Marked diastolic hypotension on invasive arterial monitoring suggested severe aortic regurgitation (AR). TEE confirmed complete retrograde prosthesis embolization in the left ventricle ( Figure 1 , Videos 1A and 1B ). The resultant AR was severe and accompanied by progressively impaired LV contractility, necessitating inotropic support. A second prosthesis of the same size was immediately prepared. It was implanted transapically into the correct position using the guidewire of the first prosthesis and passing the second valve through the embolized first one ( Figure 2 , Video 2 ). The positioning of the second prosthesis was correct on the first attempt. However, the deterioration of hemodynamics continued. The midesophageal aortic valve long-axis view demonstrated moderate central AR through the second valve. In this phase, the guidewire was pulled back to reduce volume overload of the left ventricle and to improve hemodynamics. Unfortunately, this maneuver led to liberation of the first prosthesis from the guidewire. The embolized valve became free floating and was self-positioned in front of the correctly implanted valve in the LVOT ( Figure 3 , Video 3 ) apparently impairing LV ejection. After several attempts using bursts of RVP, a fixation at the LV apex succeeded with Teflon-reinforced sutures ( Figure 4 , Video 4 ). This interventional solution was necessary because conversion to open-heart aortic valve replacement on cardiopulmonary bypass had been declined by the patient during preoperative evaluation.
However, at the end of the intervention, TEE demonstrated, as a new finding, severe dilatation of the right ventricle with pronounced right-to-left bowing of the interatrial septum and a paradoxical ventricular septal motion (tricuspid annular plane systolic excursion, 8 mm; midventricular diameter, 47 mm). In addition, severe tricuspid regurgitation (proximal isovelocity surface area radius, 0.9 cm; jet area, 10 cm 2 ) with systolic reversal of hepatic vein flow had ensued. Despite aggressive pharmacologic treatment in the intensive care unit, RV failure progressed and led to the patient’s death on the second postoperative day ( Table 1 ).
| Standard procedure | Presented case |
|---|---|
| Transapical insertion of balloon catheter with the crimped prosthesis | Yes |
| Exact positioning with fluoroscopy/TEE using landmarks | Yes |
| RVP for termination of cardiac ejection | Yes |
| Prosthesis deployment using volumetric inflation of the balloon catheter | Yes |
| Correct prosthesis placement | Prosthesis misplacement |
| Termination of RVP, return of cardiac ejection | Yes |
| Stable hemodynamics | Low diastolic pressure |
| Evaluation of prosthesis position using TEE/fluoroscopy | Yes |
| Prosthesis in correct position (aortic annulus) | Prosthesis embolization in left ventricle |
| No or mild paravalvular prosthesis incompetence | Severe AR |
| Correct second prosthesis implantation | |
| Poor hemodynamics | |
| Withdrawal of guidewire | |
| Free-floating first prosthesis embolizes in LVOT | |
| Impairment of LV ejection |
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