Volume

120

Number

6, Part

Brief Communications

1

Both fatal and symptomatic atherosclerotic coronary artery disease and aortic stenosis have been described in association with alkaptonuric ochronosis.4p 6-11O’Brien et a1.l found no increase in the frequency of either aortic stenosis or coronary artery disease in a large series of patients. Others, however, have suggested that the frequency of aortic stenosis may be increased8p l1 and that ochronotic pigment in the aortic valve may lead to acceleration of degenerative changes in that structure.l” Although the aortic valve in our patient was focally thickened by fibrous tissue, calcium, and ochronotic pigment, it was not stenotic. REFERENCES

1. O’Brien WM, LaDu BN, Bunim JJ. Biochemical, pathologic and clinical aspects of alcaptonuria, ochronosis and ochronotic arthropathy. Review of world literature (1584-19621. Am J Med 1963;34:813-38.

2. LeeSL, Stenn FF. Characterizationof mummyboneochronotic pigment. JAMA 1978;240:136-8. 3. Skinsnes OK. Generalized ochronosis. Report of an instance in which it was misdiagnosed as melanosarcoma, with resultant enucleation of an eye. JAMA 1942;120:552-8. 4. Lichtenstein L, Kaplan L. Hereditary ochronosis. Pathologic changes observed in two necropsied cases. Am J Path01 1954;30:99-119. 5. Nishimori I, Itoh J, Hakuno T. An autopsy case of alkaptonuria with ochronosis. Acta Path01 Jpn 1970;20:505-12. 6. Reginato A, Riera M, Martinez V, et al. Alcaptonuria, artropatia ochronotica y estenosis aortica. Rev Med Chil 1972;100:529-33. 7. Gould I+ Reddy CVR, DePalma D, et al. Cardiac manifestations of ochronosis. J Thorac Cardiovasc Surg 1976;72:788-91. 8. I,evine HD, Parisi AF, Holdsworth DE, et al. Aortic valve replacement for ochronosis of the aortic valve. Chest 197874: 466-7.

9. Ptacin M, Sebastian J, Bamrah VS. Ochronotic cardiovascular disease. Clin Cardiol 1985;8:441-5. 10. Vlay SC, Hartman AR, Culliford AT. Alkaptonuria and aortic stenosis [Abstract]. Ann Intern Med 1986;104:446. 11.

GainesJJ, Pai GM. Cardiovascular ochronosis. Arch Path01

12.

Lab Med 1987;111:991-4. Gaines JJ. The pathology of alkaptonuric Path01 1989;20:40-6.

ochronosis. Hum

Free-floating ball thrombus in left atrium after mitral valve replacement: Surgical removal following embolization to the aorta Wing-Hing Chow, MB, MRCP, Wai-Tsun Lee, BS, FRCS, Yau-Ting Tai, MB, MRCP, and King-Loong Cheung, MB, FRCP. Hong Kong

From

the Departments

Reprint Hospital, 4/4/24347

of Medicine

requests: Dr. Wing-Hing 125, Wong Chuk Hang

and Surgery,B Chow, Road,

The Grantham

Dept. of Medicine, Aberdeen, Hong

Hospital.

The Grantham Kong.

1463

Thrombus formation in the left atrium can be recognized aseither an early or a late complication of mitral valve replacement. Free-floating ball thrombus in the left atrium, without attachment to the atria1wall or to the mitral prosthesis,is reported to occur very rarely.lp 2To avoid complications, prompt surgical removal is mandatory. We describe a patient with a free-floating ball thrombus in the left atrium after mitral valve replacementwho had a spontaneouscure following embolization to the aorta. A 46-year-old housewife with chronic rheumatic heart diseasewasreferred to our hospital for evaluation. Over the previous 6 months she had considerable deterioration in exercisecapacity and had been hospitalized twice because of heart failure. On examination, she had mild peripheral edemaand a malar flush. Her jugular venous pressurewas elevated. Blood pressuremeasured110/70mm Hg and the pulse wasirregular at 80 beats/min. The first heart sound wasloud and a long mid-diastolic rumble could be heard at the cardiac apex. The chest was clear and the liver was mildly enlarged. Electrocardiogram revealed atrial fibrillation with a ventricular rate of 80 beats/min. Chest radiograph showed a heart in mitral stenosisand pulmonary congestion.Cross-sectionalechocardiographyrevealed the presenceof a stenotic and calcific mitral valve with an estimated area of 0.9 cm2.The left atrium wasenlarged and thrombus wasnot seen.The patient agreedto surgery. Mitral valve replacement (Medtronic-Hall No. 27, Medtronic Inc., Minneapolis, Minn.) was performed 2 days later uneventfully. Intracardiac thrombus wasnot seenintraoperatively and warfarin sodium anticoagulation was started immediately after the operation. The patient remained well and stable. Routine cross-sectionalechocardiography in multiple views on the fifth postoperatively day revealed a free-floating mass moving randomly within the left atrium (Fig. 1). It floated in and out of the field of view, gently rolling and tumbling around the left atrium aswell asbouncing off its walls. A free-floating ball thrombus was diagnosedand she was prepared for open-heart surgery. Two hours later, however, she complained of sudden, severepain in both legs.The color in both extremities was white below the groin, and both legswere cold and pulseless.A repeat cross-sectionalechocardiogramin multiple views showeddisappearanceof the free-floating ball thrombus. A diagnosisof an aortic saddleemboluswasmadeand the patient was brought immediately to the operating room. A Fogarty catheter was inserted in succession through incisionsin both groins and a thrombus, measuring 2 x 2 cm, wasremoved from the abdominal aorta. Histologic examination showedthe presenceof red blood cells mixed with fibrin strands and confirmed the diagnosisof a thrombus. No foreign body was identified within the thrombus. Postoperatively, the patient was treated with heparin and warfarin sodium and was in a good clinical condition. Repeat cross-sectionalechocardiography (Fig. 2) showedabsenceof thrombus in the left atrium and she wasdischarged 2 weekslater. The formation of a free-floating ball thrombus in the left atrium is uncommon. It usually occursin an enlarged left atrium associatedwith a diseasedmitral valve’ or after mi-

1464

Brief Communications

American

December 1990 Heart Journal

Fig. 1. Cross-sectionalechocardiographyin the short-axis view showsthe presenceof a free-floating ball thrombus demonstrating random mobility (A, B, and C) in the left atrium (LA).

Fig. 2. Postoperative cross-sectionalechocardiogram in

the short-axis view showsabsenceof thrombus in the left atrium (LA).

tral valve replacement.2The estimated autopsy incidence of a free-floating ball thrombus is about 1 in 2000to 3000.3 To receive the designation, a free-floating ball thrombus must be larger than the orifice of the valve, and it must have

a smoothsurface with no signsof attachment to the atria1 wall. Nevertheless, the distinction between a large mural thrombus and a free-floating ball thrombus is academic and may be dangerousif it is allowedto influence management. Both manifestations can causemitral valve orifice obstruction and emholization, leading to suddendeath or heart failure. Cross-sectionalechocardiography remains the investigational tool of choiceto identify the presenceof a free-floating ball thrombus in the left atriume4Multiple views of the left atrium are required, becausethere may be no singleplane in which the thrombus isconstantly imaged. The causefor formation of a free-floating ball thrombus in the left atrium after mitral valve replacement in our patient despite anticoagulation wasunclear. We initially suspected the presenceof a foreign body that served as a nidus for thrombus formation, although this possibility was excluded after careful histologic examination of the thrombus. The other possibility-that of dislodging a left atria1 appendagethrombus at the time of surgery asa causefor formation of the thrombus-was thought to be unlikely, as no intracardiac thrombus had been detected intraoperatively. Once the diagnosisof a free-floating ball thrombus in the left atrium is established,prompt surgical removal is mandatory in order to avoid complications5 Our patient with a free-floating ball thrombus in the left atrium after

Volume Number

120 6, Part

Brief Communications

1

mitral valve replacement is unique in that she had been fortunate enough to have a spontaneous cure following embolization to the abdominal aorta. After successful removal of the thrombus by a Fogarty catheter, repeat open-heart surgery was unnecessary and she has remained well. REFERENCES 1. 2.

3.

Read JL, Porter RR, Russi S, Kriz JR. Occlusive auricular thrombi. Circulation 1955;12:250-8. Blanche C. Chaux A. Kass RM. Helfenstein J. Suearman G. Free-floating ball thrombus in’the left atrium aflter mitral valve replacement: successful surgical management. Ann Thorat Surg 1985;39:566-8. Lie JL. Entman ML. “Hole-in-one” sudden death: mitral stenosis and left atria1 ball thrombus. AM HEART J 1976; 91:798-804.

4.

5.

Fraser AG, Angelini GD, Ikram S, Butchart EG. Left atria1 ball thrombus: echocardiographic features and clinical implications. Eur Heart J 1988;9:672-7. Hedenmark J, Dubiel TW, Landelius J, Lidell C, Nystrom SO, Tyden H. Persistent cardiac failure after mitral valve replacement due to free-floating intracardiac thrombus formation. Case report. Acta Anaesthesiol Stand 1987;31:661-3.

Delayed presentation of cardiac perforation after apparently successful catheter ablation for incessant ventricular tachycardia Stanley Hwang, MD, William G. Stevenson, MD, Isaac Weiner, MD, and C. Todd Sherman, MD. Los Angeles,

Calif.

Percutaneouscatheter ablation of ventricular tachycardia foci using high voltage direct-current shocksis an investigational technique that has been useful in controlling refractory ventricular tachycardia in somepatients.l Despite the potential for generation of high pressureshock waves exceeding 2 atm at the catheter-electrode-tissue interface,s the incidence of cardiac perforation had been low.’ We report a caseof cardiac rupture and death after successfulablation in a patient with incessantventricular tachycardia associatedwith a markedly thinned ventricular scar. A 71-year-old man with incessantventricular tachycardia wastransferred to UCLA Medical Center for endocardial catheter ablation. He had sustained an anterior wall myocardial infarction and had undergonecoronary artery bypasssurgery in 1974.He did well until 4 months prior.to admission,when he developedventricular tachycardia that was initially controlled with type I antiarrhythmic medications. He wasadmitted to another hospital with increasingly frequent episodesof ventricular tachycardia with From Reprint UCLA, 4/4/24351

The Division

of Cardiology,

UCLA

School

requests: William G. Stevenson, MD, CHS 47-123, Los Angeles, CA 90024.

of Medicine. Division

of Cardiology,

1465

hemodynamic deterioration requiring cardioversion. Ventricular tachycardia recurred following cardioversion despite withdrawal of all ant&rhythmic drugs and trials of procainamide, quinidine, lidocaine, bretylium, and overdrive pacing. Tachycardia had been incessantfor 18 hours prior to transfer to UCLA Medical Center, but with intravenousprocainamide infusion the tachycardia rate slowed to 140 to 170 beats/min and was hemodynamically tolerated with the patient supine. Echocardiography during ventricular tachycardia showedan estimated left ventricular ejection fraction of 40% and dyskinesia of the left ventricular apex and hypokinesia of the anteroinferior and distal lateral walls and interventricular septum. On arrival at UCLA, the patient was experiencing ventricular tachycardia at a rate of 150 beats/min. Following his informed consent,he wastaken on an emergencybasis to the cardiac catheterization laboratory for attempted endocardial catheter ablation, following the protocol approved by the UCLA Human Subject Protection Committee in April 1985. Endocardial catheter mapping showed presystolic ventricular activation at the inferolateral border of a left ventricular apical aneurysm. Programmed ventricular stimulation at that site entrained the tachycardia with little or no changein the surface electrocardiogram QRS morphology, in a manner consistent with stimulation at or near an areaof slowconduction in the tachycardia circuit.3 A single shock of 200joules was delivered between an electrode positioned at the left ventricular site (cathode) and a cutaneous back electrode patch (anode).Sinus rhythm wasimmediately restored. Immediately following the shock, systolic blood pressurefell from 130to 100mm Hg but slowly returned to 130mm Hg, with a sinus rhythm at 90 to 110 beats/min. The 12-lead electrocardiogram showedright bundle branch block with left axis deviation, Q wavesin the lateral precordium, and new 3 mm ST elevation in leadsII, III, and AVF, which resolved over 15 minutes. Fifteen minutes after the shock, programmed electrical stimulation with up to two extra stimuli at basicdrive lengths of 500and 400 msecfailed to initiate ventricular tachycardia. The patient was transferred to the cardiac care unit awake and alert, complaining of left shoulder pain that improved with massageover the area. His blood pressurethen remained stable for 90 minutes, when he suddenly complained of dizziness and lost consciousness.The electrocardiogram showed sinus bradycardia, but there was no palpable pulse or blood pressure.Atropine and epinephrine produced sinustachycardia without a palpable pulse.Pericardiocentesisyielded a small amount of clotting blood without restoring peripheral perfusion. Resuscitative efforts were unsuccessful. Necropsy examination was performed. The pericardium was tense but contained only 25 ml of loculated partially clotted blood dissectingalong epicardial-pericardial adhesions.The heart wasenlarged,weighing725gm.A large left ventricular apical aneurysm consisting of fibrotic tissue waspresent, which wasthinned to 3 mm in thickness (Fig. 1). No discrete hole wasidentified, although there were areasof hemorrhagedissectinginto myocardium within and adjacent to the aneurysm and clotted blood wasadherent to the epicardial surface of the aneurysm. Two coronary

Free-floating ball thrombus in left atrium after mitral valve replacement: surgical removal following embolization to the aorta.

Volume 120 Number 6, Part Brief Communications 1 Both fatal and symptomatic atherosclerotic coronary artery disease and aortic stenosis have bee...
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