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Florida College of Medicine, Gainesville, Florida, USA. Summary: Infective endocarditis is an infrequent but serious complication in hcart transplant recipients.
Clin. Cardiol. 19,672-674 (1 996)

Aortic Valve Endocarditis in an Acutely Rejecting Orthotopic Heart Transplant Recipient R. BRIAN FMSA, M.D., ROGERM. MILLS, JR.,M.D.,C. RICHARDCONTI,M.D., EDWARDD. STAPLES, M.D.

Cardiac Transplant Program, Shands Hospital at the University of Florida and the Departments of Medicine and Surgcry,University 0 1 Florida College of Medicine, Gainesville,Florida, USA

Summary: Infective endocarditis is an infrequent but serious complication in hcart transplant recipients. We report successful treatment for this serious complication. Key words: heart transplant, infective endocarditis, immunosuppression.humoral rejection

Introduction As the number of surviving heart transplant recipients grows, complications occur more frequently. Infection is the leading cause of early death in numerous reports,I4 with the highest risk during the first 2 months post-transplant. Bacterial infections predominate in the first month, and viral in the second.5Endocarditis rarely attacks the allograft, probably because donor hearts are carefully screened to exclude predisposing structural abnormalities.Thus, optimal management of this problem is not clear. This report presents successful medical and surgical treatment of apatient with bacterial endocarditis.

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Address for reprints: R. Brian Fazia, M.D. University of Florida College of Medicine Department of Medicine I600 SW Archer Road, Box 100277 Gninesville, FL 32610-0277, USA Received: December 11, 1994 Accepted with revision: May 15, 1995

Case Report A 35-year-old gravida 0 licensed practical nurse tirst experienced biventricularheat failure in 1986. In 1990. episodes of nonsustained ventricular tachycardia prompted automatic implantable cardioverter-defibrillator(AICD) implantation. In 1993, her heart failure worsened to New York Heart ADsociation (NYHA) class IV. She was maintained on milrinone, sotalol, and vasodilators, and was listed with the United Network for Organ Sharing as Status I for cardiac transplant. In September, she underwent orthotopic heart transplantation with explantation of her AICD generator. Pathology of the explanted heart was consistent with mildly dilated congestive cardiomyopathy.6 OKT3 induction for 9 days was followed by standard cyclosporine therapy. The immediate post-transplant echocardiogram showed normal left ventricular (LV) size and function without valvular abnormalities. On October 1 1, she returned with a new S4 gallop and peripheral edema; endomyocardial biopsy was normal. The echocardiogram showed global hypokinesis with LV ejection fraction of 34%. She was admitted with a clinical diagnosis of humoral rejection and received methylprednisolone lg intravenously (IV) daily for 3 days. Echocardiogram on hospital Day 3 showed no significant changes. On hospital Day 4, she underwent cardiac catheterization and endomyocardial biopsy. The coronary arteries were normal. Pulmonary capillary wedge pressure was 24 mmHg, and cardiac output was 3.6 Vmin. Endomyocardial biopsy was again International Society for H e d u n g Transplantation (ISHLT) Grade 0 with negative stains for IgC and complement. Plasmapheresis was initiated via the right subclavian vein on hospital Day 4 and she underwent plasmapheresis every other day for six treatments. On hospital Day 11, she developed fever (38.5"C), chills, and leukocytosis ( W C 24,000); two blood cultures grew Sruph. aureus. She was empirically treated with vancomycin

R. B. Fazia et 01.: Aortic valve endocarditis in heart transplant

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no change in the vegetation. The patient was considered as a candidate for retransplantation. Aggressive inotropic and vasodilatory support was maintained, with anticipation of emergent aortic valve replacement if her aortic insufficiency became unmanageable. No donor became available. On hospital Day 28, echocardiogram showed moderate global hypokinesis, LV ejection fraction of 35%, trace mitral regurgitation, mild aortic insufficiency, and a less prominent aortic vegetation. She was discharged on hospital Day 44 and completed an 8-week course of IV vancomycin, followed by 4 weeks of ciprotloxacin orally. Transesophageal echocardiography on December 29, 1 month after discharge,showed mild thickening of the aortic valve, but no vegetation. Left ventricular function remained moderately reduced with an estimated ejection fraction of 35%. FKi. I Two-dimensional echocardiographic parasternal long-axis view of’vegetation on right cusp of aortic valve. LV = left ventricular cavity, VEG =vegetation.

Discussion

and ceftazidime. The right subclavian pheresis catheter was removed and replaced with a left subclavian pheresis catheter. Chest x-ray showed a left pleural effusion. Echocardiogram on hospital Day 14 showed a 1 cm vegetation on the right coronary cusp of the aortic valve (Fig. I). Left ventricularejection fraction decreased to 25% with mild aortic insufficiency. On the basis of laboratory sensitivities, IV vancomycin was continued and ceftazidime was discontinued. Thoracentesisrevealed purulent fluid. A 2 cm induration at the upper sternal incision appeared; aspiration yielded St@. UIIIPIIS. Urgent mediatinal exploration revealed a large retrostemal collection of purulent fluid. Adhesions to the heart were dissected free, and an omental flap was laid over the heart and ascending aorta. Medical management included cyclospotine by continuous infusion to maintain a level in the 200-250 ng/ml range (Table I). Methylprednisolone was decreased to 25 mg IV daily. Repeat endomyocardial biopsy on hospital Day 25 showed ISHLT Grade 0 histology. Echocardiogramshowed worsening of the aortic insufficiency with

Bacterial endocarditis developed in an orthotopic heart transplant recipient undergoing plasmapheresis for suspected humoral rejection. OKT3 induction has been associated with an increased frequency of humoral rejection in transplanted patients, and significantly poorer graft and patient survival is seen with humoral than with cellular reje~tion.’.~ Early, aggressive plasmapheresis appears to offer benefit in the treatment of acute humoral rejection in heart transplant recipients.” Although central venous access and multiple treatments are required, infection with plasmapheresis is rare. l o Optimal treatment for infective endocarditis in this setting is uncertain. Retransplantation, valve replacement, and medical management are all logical options. Counihan ern/.]’described successful medical treatment of a mitral valvular vegetation 7 months following orthotopic heart transplantation. We considered retransplantation; however, her heart failure improved, and we elected to pursue all other reasonable options. Had acute severe aortic insufficiency ensued, emergent aortic valve replacementwould have been readily available.In summary, successful management included surgical drainage and debridement of the sternal infection, parenteral antibiotic therapy, decreased immunosuppression,and nutritional support. She continued to improve with this therapy, making retransplantation and valve replacement unnecessary.

TABLE 1 Mean serum cyclosporine(CYA) levels (ng/ml) following

Acknowledgement

t r i m plantation

Days post transplant 10 20 30 40 50 60 70

Average CYA level (ng/ml) 350 300 250 200 x I50

x

80

Special thanks to Trina King for secretarial assistance in preparation of this manuscript.

References

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1. Stinson EB, Bieber CP, Griepp RB, Clark DA, Shumway NE,

Remington JS: Infectious complications after cardiac transplantation in man. Ann hrem Med 74.22-36 (197I )

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2. Gentry LO, Zelutl’BJ: Diagnosis and treatment of infection in cardiac transplant patients. Surg Chi ofNorfhAmerica 66(3), 459465 ( 1986) 3. Hoftlin JM. Potasman I,Baldwin JC, Oyer PE: Infectious complications in heart transplant recipients receiving cyclosporine and corticosteroids. Ann 61ternMed 106,209-2 I6 ( 1987) 4. Linder J: Infection as a complication of heart transplantation. J Hem1 Tiunsp/ 7,39&394 (1988) 5. Miller LW, Naftel DC. Bourge RC, Kirklin JK, Bronzena SC. Jarcho J, Hohhs RE, Mills RM: Infection following cardiac transplantation: A multi-institutional study. J Heart Lung Transpl 81, 506-S I 7 (in press) 6 . Keren A. Gottlieb S,Tzivoni D, Stem S, Yarom R, Billingham ME, Popp RL: Mildly dilated congestive cardiomyopathy, use of prospective diagnostic criteria and description of the clinical course without heart transplantation. Circularion 8 I , 5 0 6 5 17 (1990) 7. Hammond EH, Wittwer CT, Greenwood J, Knape WA, Yowell RL, Menlove RL. Craven C, Renlund DG, Bristow MR, DeWitt CW,

O’Connell JB: Relationship of OKT3 sensitization and vascular rejection in cardiac transplant patients receiving OKT3 rejection prophylaxis. Transplanfarion SO, 776782 ( 1990)

8. HammondEH, Yowell RL, Shinichi N, Menlove RL, Renlund DG. Bristow MR, Gay WA Jr, Jones KW, O’Connell JB: Vascular (htimoral) rejection in heart transplantation: Pathologic observations and clinical implications. J Heart Trans/>/8 . 4 3 W 3 ( 1989) 9. Malafa M, Mancini MC, Myles JL, Gohara A, Dickinson JM, Walsh T E Successful treatment of acute humoral rejection i n a heart transplant patient. J Heart Lung Trwqd I I,4 8 U 9 I ( 1992)

10. Mokrzycki MH, Kaplan AA: Therapeutic plasma exchange: Complications and management. Am J K i d n q Dis 23(6),8 17-827 ( 1994)

I I. Counihan PJ, Yelland A, de Belder MA, Pepper JR:Infective endccarditis in a heart transplant recipient. J Hear/ Lung Tr~in.sp/10. 275-279 (1991)

Clin. Cardiol. 19, 674-677 (1996)

Sustained Ventricular TachycardiasAssociated with Myotonic Dystrophy KOJITAMUKA, M.D., HISAKO TSUJI, M.D., YUMIE MATSU~, M.D., AKIRA MASUI, M.D., MAKOTO HIKOSAKA, M.D., MASAHIKO KARAKAWA, M.D.,TOSHIJI IWASAKA,M.D.,MITSUOINADA,M.D.

Second Department of Internal Medicine,Kansai Medical University, Osaka, Japan

Summary: Patients with myotonic dystrophy are reported to

have a higher frequency of sudden death than the general population. Although causes of sudden death in myotonic dystrophy are suggested to be due to conduction defects progressing, the HV interval cannot predict whether conduction system disease would develop or progress. We report two cases of myotonic dystrophy complicated with sustained monomorphic ventricular tachycardias (VT), which can cause sudden death. In Case No. 1, although the patient was treated successfully for sustained VT with verapamil in electrophysiologic studies, another sustained VT was confirmed 2 years later. In Case No. 2, the patient showed decreased left ventricular ejection fraction and late potentials, and induced sustained VT that was identical to clinically documented VT. Although VT is believed to be rare in patients with myotonic dystrophy, these cases suggest that VT is a possible cause of sudden death.

Address for reprints: Koji Tamura, M.D. Second Depatiment of Internal Medicine Kansai Medical University I -Fumizonocho. Moriguchi City Ohaka, S70. Japan Received: September 12, I994 Accepted with revision: April 20. 1995

Key words: late potentials, left ventricular function

Introduction Myotonic dystrophy is a multisystemic disease inherited in an autosomal dominant fashion. I The disease is charactcrized by variable expression and severity, and symptoms usually appear in patients between the ages of 20 and 50 years.’ There is electrocardiographic (ECG) evidence of heart disease in most patients with myotonic dystrophy.3 Although ECG abnormalities do not produce symptoms in most patients, some show symptoms as a result of conduction and rhythm abnormalities severe enough to need a permanent pacemaker and antiarrhythmic drugs. Moreover, patients with myotonic dystrophy are reported to have a higher frequency of sudden death than the general Although conduction defects are the main ECG findings in myotonic dy~trophy,~ we report two cases of myotonic dystrophy complicated with sustained monomorphic ventricular tachycardias (VT), which can cause sudden death.

Case No. 1 A 20-year-old man suffered from palpitation starting November 1990. Wide QRS tachycardia was documented on ECG in March 1991 and was treated with procainamide. To evaluate the wide QRS tachycardia, he was admitted to the second department of internal medicine of Kancai Medical University.