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Cardiovasc Intervent Radiol (1998) 21:91–92

CardioVascularand InterventionalRadiologyq Springer-Verlag New York Inc. 1998

Letter to the Editor

Fig. 2. AP supine portable abdomen radiograph shows the ball em-bolus positioned over the lower midabdomen (refer to autopsy re-port).

Fig. 1. AP supine portable chest radiograph shows a fracture (arrow)through the apex of the strut; no steel ball is identified within thecage.

Re: Starr–Edwards Aortic Valve Strut Fracturewith Ball Embolus

We report an incidence of actual strut fracture with ballembolus of a Starr–Edwards aortic valve prosthesis. Aliterature review of major experiences with ball valveprostheses indicates no previously reported strut frac-ture/ball embolus with the Starr–Edwards valve.

A 72-year-old male experienced excruciating chestpain 2 hr prior to admission on May 27, 1990. The painmigrated to the back and was unrelieved by nitroglyc-erin. Physical examination revealed a systolic bloodpressure of 80 mmHg in the right arm and 108 mmHgin the left arm, a respiratory rate of 40, a heart rateof 100, distended neck veins, bilateral absence of fem-oral pulses, and bilateral lower extremity paralysis. Anosculation revealed a regular rhythm, a soft 2/6 systolicmurmur, no definite valve click, and bilateral diffuserales over both lungs.

Pertinent previous history included Starr–Edwardsaortic valve replacement (AVR) 18 years previously in

1971 for severe aortic stenosis and aortic insufficiencysecondary to rheumatic heart disease and bacterial en-docarditis. Following valve placement the patient hadbeen maintained on coumadin anticoagulation, withone documented episode of bacterial endocarditis in1987, but no thromboembolic events. He had beenevaluated and treated for congestive heart failure 1week prior to his penultimate admission and at that timecine fluoroscopy of the valve revealed no mechanicalabnormalities. His past medical history was also sig-nificant for coronary artery disease and oxygen-requir-ing chronic obstructive pulmonary disease.

Admission chest radiographs demonstrated theprosthesis but no poppet (ball) within the cage (Fig. 1).An anteroposterior AP supine radiograph of the abdo-men demonstrated the metallic ball at about the levelof the aortic bifurcation (Fig. 2). The patient subse-quently experienced a rapid downhill course, de-veloping acute renal failure with severe aorticregurgitation and eventual heart flutter; he expired onthe day of admission.

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Letter to the Editor92

A limited autopsy (restricted by the family)showed detachment of the strut at the level of the leftaortic cusp, this detachment from the apex to the ringbase (chest radiographs clearly show the left strut de-tachment at the apex only and it is likely that the find-ings at autopsy were associated with dissectiondislodgement). The right and posterior valve strutswere intact, i.e., firmly attached at the apex and at themetallic ring base. The cloth covering of the strut anda portion of the ring were largely worn away but rem-nants were identified. A perivalvular leak with an in-ferior defect measuring 1.2 1 0.2 cm communicatedwith a superior defect of 0.6 1 0.2 cm located at theright posterior lateral junction of the valve and myo-cardium. The poppet, described as a gray metal ball,was lodged in the very distal portion of the abdominalaorta occluding the aortic lumen. The renal arteriesand the inferior mesenteric artery were widely patent.Due to autopsy restrictions, more complete evaluationof abdominal and retroperitoneal organs could not bepursued. Specific comment by the pathologist indi-cates that the patient’s prosthesis was either a model2310 or 2320.

The first generation Starr–Edwards aortic valveprosthesis, model 1000, was introduced in 1961. Sub-sequent modifications in 1965, that virtually eliminatedthe problem of ball variance, resulted in models 1200and 1260. The valves pertinent to this case were intro-duced in 1971 (models 2310 and 2320). By 1985 there

were an estimated 33,000 prosthetic mitral or aorticvalves implanted yearly in the US [1].

Long-term complications of these prostheses in-clude perivalvular leak, thrombosis, endocarditis, he-molysis, tissue overgrowth, and degeneration and/ormechanical failure of the prosthesis [2, 3]. Given theserisks our patient’s survival for 18 years after AVR isnoteworthy, as valve-related mortality after 20 years isabout 13% [4]. The incidence of actual strut fracturewith ball embolus is rare [3], and has not, to our knowl-edge, been previously reported as a complication of aStarr–Edwards aortic valve prosthesis.

Andrew J. Meholic, M.D.Matthew M. Jaksha, M.D.

University of New MexicoHealth Sciences Center

Albuquerque, New Mexico, USA

References

1. Schoen FJ, Hobson CE (1985) Anatomic analysis of removedprosthetic heart valves: Causes of failure of 33 mechanical valvesand 58 bioprostheses, 1980 to 1983. Hum Pathol 16(6):549–559

2. Katz A, Fraser D, Weitzman S, Gueron M (1989) Follow-up ofisolated aortic valve prosthesis 1964 to 1986. Isr J Med Sci25(10):564–567

3. Swanson JS, Starr A (1989) The ball valve experience over threedecades. Ann Thorac Surg 48(3):S51–S52

4. Cobanoglu A, Fessler CL, Guvendik L, Grunkemeier G (1988)Aortic valve replacement with the Starr–Edwards prosthesis: Acomparison of the first and second decades of follow-up. AnnThorac Surg 45(3):248–252