Primary left ventricular mural endocarditis diagnosed by transesophageal echocardiography

Primary Left Ventricular Mural Endocarditis Diagnosed by Transesophageal Echocardiography Jamshid Shirani, MD, Kelly Keffler, MD, Enriquc Gerszten, MD, Carolyn S. Gbur, MD, and James A. Arrowood, MD, Richmond, Virginia

Primary left ventricular mural abscess was detected by transesophageal echocardiography and was confirmed at necropsy in a 44-year-old w o m a n with Staphylococcus aureus bacteremia and cerebrovasoalar embolism. In two occasions, transthoracic echocardiography failed to show the mural abscess in this patient. Because o f the aggressive nature o f primary mural endocarditis, early use o f transesophageal echocardiography is recommended in patients with Staphylococcal bacteremia and suspected endocarditis even in the absence o f valvular abnormalities detectable by the transthoracic approach. (J AM Soc ECHOCAV.DIOGR1995;8:554-6.)

Infection

involving the nonvalvular endocardium (mural endocarditis) is r a r e ) W h e n such an infection occurs, it is often secondary and thus associated with valvular vegetations, myocardial abscesses, endocardial plaques, or cardiac structural abnormalities such as ventricular septal defect. 1-s Primary mural endocarditis is extremely rare. T o o u r knowledge, there has been only one report describing a patient in w h o m this diagnosis was made during life. 6 W e herein report a patient with primary left ventricular mural endocarditis in w h o m this diagnosis was first suggested by transesophageal echocardiography (TEE) and subsequently confirmed at necropsy. CASE REPORT A 44-year-old woman was admitted to the hospital after an episode of syncope. On admission she was febrile and had a right central facial nerve palsy, nystagmus, and multiple infected lower extremity ulcers as a result of chronic venous insufficiency. Other relevant clinical and laboratory findings on admission are listed in Table 1. Computerized tomography of the brain showed multiple cerebellar infarcts. Cultures of blood and the lower extemity ulcers were obtained and the patient was given antibiotics. On day 2 o f admission a transthoracic echocardiogram showed nor-

From The Department of Medicine, Division of Cardiology., and the Department of Pathology, Medical College of Virginia. Reprint requests: Jamshid Shirani, MD, Albert Einstein College of Medicine, Division of Cardiology, Forschheimer Bldg., Room G-42, 1300 Morris Park Ave., Bronx, NY 10461. Copyright 9 1995 by the American Society of Echocardiography. 0894-7317/95 $3.00 + 0 27/4/59737 554

Table 1 Certain clinical findings and laboratory test results on hospital admission in a patient with primary mural endocarditis History Intravenous drag user Lower extremity venous insufficiency Syncope on day of admission Physical examination Temperature 102.4~ F, pulse rate 115 beatshnin, blood pressure 162/71 mm Hg, mild respiratory distress Clear lungs, grade II/VI systolic ejection murmur at left lower sternal border, tenderness in right upper quadrant of abdomen, infected ulcers in both lower extremities Alert and oriented, central right facial nerve palsy, nystagmus Laboratory test results White blood cell count 14,600/mm 3 (86% polymorphonuclear leukocytes), hemoglobin 8.7 gm/dl, hematocrit 26%, platelet count ll8,000/mm 3, microcytic indexes, blood urea nitrogen 10 mg/dl, serum creatinine 1.2 mg/dl Chest roentgenogram: normal heart size, dear lung tields Electrocardiogram: sinus tachycardia, left ventricular hypertrophy

mal left ventricular size and systolic function and no valvular regurgitation or vegetation. During the next 2 days, the patient's temperature decreased but her neurologic stares worsened. All blood and soft tissue cultures grew methicillin-sensitive Staphylococcus aureus. On day 4 of admission, transthoracic echocardiography was repeated and showed no changes compared with the study done 2 days earlier (see above). A TEE was then performed that showed normal ca)diac chamber sizes, hypertrophy of the left ven-

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Figure 1 Heart of 44-year-old woman (MCV A94-11) who died ofcerebellar and cerebral emboli from left ventricular infective mural vegetation. Two-dimensional diastolic (A), and systolic (B) frames from transesophageal four-chamber view of heart show large echogenic mass (a) attached to thickened, echogenic posteromedial papillary muscle (p). Mitral valve leaflets appear to be normal. C, Four-chamber view of heart at necropsy shows left ventricular mural abscess (a). No myocardial lesions or valvular vegetations are seen. LA, Left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

tricle without segmental wall motion abnormalities, and structurally normal cardiac valves without vegetations or significant regurgitation. A large, oval, and echogenic mass was seen in the left ventricular cavity that appeared to be attached to a thickened and echogenic posteromedial papillary muscle (Figure 1, A and B). No masses or thrombi were present in other cardiac chambers. Antibiotics and supportive care were continued; however, the patient died of progressive neurologic deterioration caused by recurrent cerebral and cerebellar emboli. POSTMORTEM EXAMINATION

At necropsy, multiple septic embolic infarcts were present in the brain, kidneys, spleen, mad liver. The heart weighed 450 gm. The epicardium was normal. All four major epicardial (left main, left anterior descending, left circumflex, and right) coronary arteries were free of atherosclerosis. Both atria were mildly

dilated. Left and right ventricular cavities were norreal. The mitral valve was mildly and diffusely thickcned and the tricuspid valve had redundant leaflets. Aortic and pulrnonic valves appeared structurally normal. No valvular vegetation, perforation, chordal rupture, or other evidence o f valvular infective endocarditis was present. There was no morphologic evidence o f hypertrophic cardiomyopathy, including left ventricular outflow tract fibrous plaques. A large mural abscess (1.0 • 1.0 • 1.5 cm) with a thick capsule was attached to the posteromedi~ papillary muscle (Figure 1, C). Multiple small vegetations and thrombi were attached to the outer surface of this abscess and projected into the left ventricular cavity. Histologically, the abscess contained inflammatory cells (predominantly polymorphonuclear leukocytes), gram-positive cocci, and clot debris. The ventricular septal myocardium adjacent to the abscess was not involved.

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DISCUSSION

REFERENCES

In recent years, echocardiography, especially TEE, has added an important dimension to the management o f patients with valvular infective endocarditis. 7-9 Because of its rarity, primary nonvalvular (mural) endocarditis has not been addressed, s,9 In 1992 Shenoy et al. 6 reported a 53-year-old woman with bacteremia and an echogenic mass attached to the midportion o f the left ventricular surface o f the ventricular septum on TEE. There were no valvular vegetations, regurgitation, or myocardial abnormalities in this patient, and the "mural vegetation" resolved by appropriate antibiotic therapy. 6 More recently, Habib et al.10 have described a 22-year-old man with bacteremia, ruptured left ventricular anterolateral papillary muscle, and severe mitral regurgitation detected by transthoracic and echocardiography and TEE. Vegetations were found at the site o f papillary muscle rupture at surgery. N o mention was made of any valvular vegetation and thus this patient also may have had primary mural endocarditis. S. a u r e u s was responsible for infective endocarditis in the two patients mentioned above 6,1~and the one reported here. Because o f the aggressive nature of primary mural endocarditis, early use o f TEE should be considered in patients with S. a u r e u s bacteremia and suspected endocarditis in the absence o f valvular abnormalities on transthoracic echocardiography.

1. Buchbinder NA, Roberts WC. Active infective endocarditis confined to mural endocarditun. Arch Pathol 1972;93:43540. 2. Milstoc M, Berger AR. True bacterial mural endocarditis. Chest 1971;59:103-5. 3. Kuhn C, Weber N. Mural bacterial endocarditis of a ventricular friction lesion. Arch Pathol 1973;95:92-3. 4. LeJemtel TH, Factor SM, Koenigsberg M, O'Reilly M, Frater R, Sonnenblick EH. Mural vegetations at the site of endocardial trauma in infective endocarditis complicating idiopathic hypertrophic subaortic stenosis. Am J Cardiol 1979;44:569-74. 5. Herzog CA, Carson P, Michand A, Asinger RW. Two-dimensional echocardiographic imaging of left ventricular mural vegetations. Am Heart J 1988;115:684-6. 6. Shenoy MM, Kalakota M, Uddin M, Siegel S. Left ventricular mural bacterial endocarditis: diagnosis by transesophageal echocardiography. Can J Cardiol 1992;8:57-9. 7. Martin RP. The diagnostic and prognostic role of cardiovascular ultrasound in endocarditis: bigger is not better. J Am Coil Cardiol 1990; 15:1234-7. 8. Sanfilippo AJ, Picard MH, Newell JB, et al. Echocardiographic a s s e s s m e n t of patients with infectious endocarditis: prediction of risk for complications. J Am Coil Cardiol 1991;18:1191 9. 9. Shively BK, Gurule FT, Roldan CA, Leggert JH, Schiller NB. Diagnostic value of transesophageal compared with transthoracic echocardiography in infective endocarditis. J Am Coil Cardiol 1991;18:391-7. 10. Habib G, Guidon C, Tricoire E, Djiane V, Monties J, Luccioni R. Papillary muscle rupture caused by bacterial endocarditis: role of transesophageal echocardiography. J AM Soc ECHOCARDIOGR1994;7:79-81.