Radi PressureWire Rupture and Embolization to the Right Common Carotid Artery After Crossing a Bjork-Shiley Mechanical Aortic Valve

ABSTRACT: Direct measurement of the left ventricular pressure in patients with mechanical prosthetic aortic valve is an important technical challenge. In the past, transseptal puncture or direct left ventricular accesses were the only available methods. The use of a pressure wire through mechanical aortic prosthesis has been described to be feasible and safe. We report the first case report of pressure guidewire entrapment through a single tilting disk valve (Bjork-Shiley), which resulted in hemodynamic collapse, rupture, and embolization of the pressure wire tip to the right common carotid artery and its successful snaring.

J INVASIVE CARDIOL 2013;25(10):E191-E193

Key words: thromboemboli, endovascular therapy

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Accurate invasive assessment of the left ventricular pressure in patients with mechanical prosthetic aortic valve replacement (AVR) is often mandated in cases of repeat cardiac surgery or intervention decisions. The value of echocardiography is limited by the acoustic shadowing and in patients with multiple structural cardiac abnormalities (shunts, mixed valve disease, and combined aortic and mitral valvulopathy).¹ Computed tomography (CT) offers excellent imaging of the cardiac anatomy, but data regarding hemodynamics are limited.²

Traditionally, a transseptal or rarely a direct left ventricular puncture is needed to invasively measure the left ventricular pressure.^3,4 The passage of a standard catheter through a mechanical valve may cause fatal hemodynamic collapse or threaten the mechanical valve integrity.^5,6 The successful use of a retrograde left ventricular assessment using a pressure wire has been described as a safe alternative in patients with bileaflet prosthetic aortic valves.⁷ 

We report a case of entrapment, rupture, and embolization of the pressure-wire tip to the right common carotid artery in a patient with a Bjork-Shiley prosthetic valve. 

Case Report. A 75-year-old female was admitted with progressive dyspnea for 3 weeks. She had a history of rheumatic heart disease with a mechanical Bjork-Shiley AVR implantation (Shiley) 30 years ago, moderate mitral stenosis (MS) known for 6-7 years, mild-to-moderate pulmonary hypertension (PHTN) according to her last echocardiogram 3 years ago, and chronic atrial fibrillation post atrioventricular (AV) nodal ablation and a single-chamber pacemaker placement the same year of her surgery (30 years ago) with several battery changes. The patient did not have any other percutaneous or surgical interventions since then. She denied any chest pain, hemoptysis, hoarseness, syncope, infections, or thrombo-embolic phenomena.

She appeared well-nourished and well-developed, without apparent mitral facies in mild respiratory distress. Her physical examination was significant for jugular venous distention with an estimated right atrial pressure of 18 mm Hg, bibasilar crackles, with a normal non-displaced point of maximal impulse. There was a regular rate and rhythm, increased S1, a mechanical A2 and a discrete P2 increased in intensity without an S3 or S4. An opening snap was auscultated with an early decrescendo diastolic murmur, increasing with expiration.   

A transthoracic echocardiogram revealed moderate concentric left ventricular hypertrophy with a normal left ventricular ejection fraction (LVEF) >60%. The Bjork-Shiley AVR appeared to function normally, with a mean pressure gradient of 10 mm Hg and absence of aortic insufficiency. The mean mitral valve gradient was estimated to be 12 mm Hg, with a calculated mitral valve area (MVA) of 1.1 cm² and a Wilkins score of 7 with only mild mitral regurgitation. The right ventricular systolic pressure (RVSP) was calculated to be 60 mm Hg with only mild-to-moderate tricuspid insufficiency.

The patient was referred to the catheterization lab for a diagnostic coronary angiography, invasive evaluation of the mitral stenosis, and possible mitral valvuloplasty. The invasive assessment of the mitral stenosis was planned to be a simultaneous pressure of the left ventricle with a pressure wire and the left atrial pressure after a transseptal puncture. 

The diagnostic angiography revealed normal coronary arteries. A Radi PressureWire (St Jude Medical, Inc) was easily advanced in the left ventricle via an AL1 guiding catheter and the left ventricular pressure was invasively measured in real time (Figure 1). Twenty seconds later, the Radi wire monitor showed abrupt loss of pressure. In fluoroscopy, the valve appeared to be stalled in closed position with an intact pressure wire in the left ventricle. The patient arrested and cardiopulmonary resuscitation was initiated. Attempt to pull the wire was unsuccessful, as it appeared to be trapped in the closed Bjork-Shiley valve. More aggressive pulling of the wire resulted in the rupture of the distal segment of the Radi fractional flow reserve (FFR) in the valve (Figure 2). The valve resumed its normal function and the patient was stabilized hemodynamically and clinically. In the next fluoroscopic picture, the FFR fragment was not visualized in the valve. With fluoroscopic scan of the aortic course, the FFR fragment was “found” in the right common carotid artery. A JR4 guiding catheter was engaged in the ostium of the right common carotid artery and a selective angiographic image was taken. The Radi wire fragment was successfully retrieved with a use of a snare (Figure 3).

The patient recovered and was discharged in 2 days with clinical improvement on medical therapy, without neurologic deficits after an unchanged echocardiogram, carotid ultrasound, and head magnetic resonance imaging.

Discussion. In the past, concerns have been addressed about the possibility of pressure-wire dysfunction when used for mechanical valve hemodynamic assessment.⁷ Visible kinking of the 0.014˝ pressure wire has been described after crossing mechanical valves, raising the possibility of pressure-wire dysfunction when used for mechanical valve hemodynamic assessment.⁸ 

Kern et al demonstrated the feasibility and safety of a retrograde pressure wire placement through bileaflet mechanical aortic valve prosthesis for invasive left ventricular hemodynamic assessment.⁷ In 2010, Owan et al published the first report of this pressure-wire technique to assess hemodynamics across a Bjork-Shiley single-tilting disk valve.⁹  

We report the first case report of guidewire entrapment through a single-tilting disk valve. The valve “stalled” in closed position, resulting in hemodynamic collapse. Normal valve function resumed only after aggressive pulling of the pressure wire, which resulted in the rupture of its tip and consequently its embolization to the right common carotid artery.  

The mechanism of entrapment of the FFR wire in a Bjork-Shiley valve at a closed position is unclear. Although “kinking” and dysfunction of the pressure wire have been described in ex vivo studies,⁸ a similar finding has not been previously reported. Kinking of the pressure wire between the struts and the disc of the mechanical valve or between the disc and the support ring may have resulted in that iatrogenic complication. 

Conclusion. The use of a 0.014˝ pressure wire to invasively measure the left ventricular pressure in patients with aortic mechanical prosthesis is an easy procedure and it is thought to be safe and less complex that a transseptal or direct left ventricular puncture. Although the use of this technique in bileaflet mechanical prosthesis has proved to be safe, insufficient data exist about its safety in patients with single-tilting disk valve. Entrapment of the pressure wire may lead to fatal hemodynamic collapse, valve dysfunction, rupture, or embolization of the wire tip. Structural interventional cardiologists should be aware of this complication and consider alternative methods. More data are needed for the generalized use of pressure wires through single-tilting disk mechanical prosthesis.

References

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From the ¹Citizens Memorial Hospital, Heart and Vascular Institute, Bolivar,
Missouri and ²Arkansas Heart Hospital, Little Rock, Arkansas.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure
of Potential Conflicts of Interest. The authors report no conflicts of interest regarding
the content herein.

Manuscript submitted March 26, 2013, provisional acceptance given May 16,
2013, final version accepted May 21, 2013.

Address for correspondence: Konstantinos Marmagkiolis, MD, FACC, RPVI
Citizens Memorial Hospital, Heart and Vascular Institute, 1500 N Oakland Ave,
Bolivar MO, 65613. Email: c.marmagiolis@gmail.com