sophageal echocardiography, and, through measurement of pulmonary venous Doppler flow characteristics, severity of mitral regurgitation was assessed. Postmortem examination of the heart confirmed all echocardiographic findings. This case of NBTE is unusual in several respects. First, all four valves were affected by the process. While the mitral valve was most involved by thrombus, discrete vegetations were seen on all four valves by biplane transesophageal echocardiography and this was confirmed at autopsy. Pathologically, these vegetations were fibrinous and nondestructive. In a recent review of NBTE, the incidence of quadrivalvular involvement in a compilation of 747 cases was 0.1 percent. I Second, the large vegetations developed rapidly. The preoperative echocardiogram showed no valvular abnormalities, but with. the development of DIe postoperativel~ large amounts of thrombus quickly formed on the cardiac valves, as demonstrated by transesophageal echocardiography on the seventh day after surger~ There is little information available on the time course of vegetation growth in NBTE, and no systematic prospective studies have been performed. This report demonstrates that thrombus formation may be rapid and extensive. Third, this case ofNBTE caused significant valvular insufficienc~ In general, because inflammatory reactions are not present in NBTE vegetations, leaflet destruction or perforation is rare, and valvular dysfunction seldom occurs. 4 In this patient, however, the large thrombotic vegetations caused marked mitral valvular distortion, abnormal leaflet coaptation, and severe regurgitation. In summar~ this case illustrates several points. NBTE vegetations may develop rapidly, and the presence of significant valvular dysfunction does not rule out the diagnosis. When clinically indicated, transesophageal echocardiography may be quite helpful in demonstrating valvular vegetations, especially if the lesions are small and transthoracic imaging is technically difficult. Although the procedure is semi-invasive, it is quite safe, 7 and should be considered if other techniques are nondiagnostic and clinical suspicion of NBTE remains high. REFERENCES 1 Lopez JA, Ross RS, Fishbein MC, Siegel RJ. Nonbacterial thrombotic endocarditis: a review Am Heart J 1987; 113:773-84 2 Rogers LR, Cho E-S, Kempin S, Posner JB. Cerebral infarction from non-bacterial thrombotic endocarditis: clinical and pathologic study including the effects of anticoagulation. Am J Med 1987; 83:746-56 3 Ziegler R. Uber den Bau die Entstehung Endocaritischer Effiorescenzen. Werh Dtsch Kong Intern Med 1888; 7:399 4 MacDonald RA, Robbins SL. The significance of nonbacterial - thrombotic endocarditis: an autopsy and clinical study of78 cases. Ann Intern Med 1957; 46:255-73 5 Lopez JA, Fishbein MC, Siegel RJ. Echocardiographic features of nonbacterial thrombotic endocarditis. Am J Cardioll987; 59: 478-80 6 Mugge A, Daniel WG, Frank G, Lichtlen PR. Echocardiographic diagnosis of infective endocarditis: reassessment of prognostic implications of vegetation size determined by the transthoracic and the transesophageal approach. J Am Coli Cardioll989; 14: 631-38 7 Daniel WG, Erbel R, Kasper ~ et ale Safety of transesophageal echocardiography: a multicenter survey of 10,419 examinations. Circulation 1991; 83:817-21

958

HIV-Associated Perlcardial

Effusions·

Mark] Eisenberg, M.D.; Amy Nelson B. Schiller, M.D.

s. Gordon; and

Following a case of cardiac tamponade in a patient with the acquired immunode6ciency syndrome (AIDS), we examined the frequency and clinical spectrum of pericardial etTusions associated with human immunode6ciency virus infection (HIV) at our institution. or 187 hospitalized patients documented to have pericardial effusions over a one-year period, 14 (7 percent) were known to be HIVpositive at the time of their ecbocardiograms. One patient presented with a large effusion and cardiac tamponade, three had moderate effusions, and ten had small eff'usions. The probable effusion etiology was established in four cases and included endocarditis (2), lymphoma (1), and myocardial infarction (1). In hospital mortality was 29 percent (4 of 14). From our study, as well as a growing number of reports in the literature, we conclude that HIV-associated pericardia) eff'usioDS are frequently seen and that their clinical spectrum is broad. (Cheat 1992; 102:956-58) the 1 human immunodeficiency virus I nfectionhaswithbeen associated with a variety of cardiac (HIV)

type

complications, including myocarditis, endocarditis, and dilated cardiomyopath~ In addition to these complications, a number of reports have described pericardial effusions associated with HIV infection. 1•14 Following a recent case of cardiac tamponade in an AIDS patient, we examined the frequency and clinical spectrum of HIV-associated pericardial effusions at our institution. CASE REPORT A 36-year-old man with AIDS presented with four days of fevers, chills~

night sweats, and progressive dyspnea. He had been treated

for pulmonary tuberculosis during the previous six months but had discontinued his medications one month before admission. On physical examination, the patient was in moderate distress with a heart rate of 112 bpm~ a blood pressure of 94/76 mm Hg, a respiratory rate of281m in, and a temperature of38.1°C. Examination was also remarkable for oral thrush, bilateral basilar rales, elevated jugular venous pressure, and distant heart sounds. Initial laboratory test results were unremarkable. A chest roentgenogram, however, revealed an enlarged cardiac silhouette, bilateral pleural effusions, and apical scarring. Subsequently, an echocardiogram showed a large pericardia1 effusion associated with right ventricular collapse, right atrial collapse, inferior vena cava plethora with blunted response to respiration, and respiratory variation of mitral inflow velocities. Because of the patient's hemodynamic instability, a pericardiocentesis was performed. More than 1,000 ml of serosanguineous fluid was drained, and blood pressure rose to 115185 mm Hg. The next day, a pericardial window was created but subsequent laboratory examination of pericardial tissue and fluid showed only ·~"?m the Cardiovascular Research Institute, the Cardiology DiVISIon of ~e Department of Medicine, and The John Henry Mills

Echocanbograpliy Laboratory of the University of California San Francisco. ' Supported by an Institutional National Research Service award HL 07192, Training Program in Heart and Vascular Disease~ NHLBI, Bethesda. Reprint requests: Dr. Eisenberg, Box 1214 Moffitt-Umg Hospital, 505lbmassus Avenue, San Francisco 94143 HIV-Associated PericardiaI Effusions (EIsenberg, Gordon, SChiller)

Table I-H~ ftIIienta tDitla HIV-AaocitJted PericIJnIW EJfuaiou s.n ooer tJ One-Year Period· Age

Sex

HlVStatus (Risk Factor)

IntenmreDt Illnesses

Beasoob Admission

:I)

M

AIDS (IV drug

liposis san:oma,

Cardiac tampooade

Altered mental

Possible sepsis vs trusfusioo

Feve~

33

M

user)

ARC (unbown)

herpes simplex keratitis NODe

reactioo

34

34

M

M

AIDS (IV drug user) HIV+ (IV drug user)

Oral thrush, esophageal

caodidiasis

PDeumococcaI meningitis

Possible Pneumocystis pneumonia

Signs and Symptoms

E8'usioo Size

Etiology

(Diagnosis)

Large

Idiopathic

Small

Idiopathic

Pericardiocentesis x2, pericardiotomy IV Fluids,

Small

Idiopathic

Empiric antibiotic

~cyanosis.

pdsus paradox

cbiUs.

myalgias, dyspnea 1day after tnnsfusion Dyspnea, fever,

cough, pharyngitis, neck pain

Small

Idiopathic

Aggressive diuresis

Died (day 2)

Fever, hypotension

Small

Prosthetic valve endocarditis

Aortic valve

Died (day 11)

PericardiaI e8'usioo

Cough, dyspnea on exertion

Moderate

(autopsy) Idiopathic

Supportive

Discharged

RetiDal

Decreased vision

Small

Idiopathic

Diuresis and

Transferred (day 31)

Fevers, chills,

Small

Idiopathic

Antibiotics

Discharged (day 11)

Fever, dyspnea, chest pain, cbiUs. night sweats,

Small

Idiopathic

Acyclovir and

Discharged

Moderate

Lymphoma (autopsy)

Pericardiocentesis, antibiotics and

Died (day 1)

Small

Idiopathic

Antibiotics

Didarged

Small

MI (clinical)

Medical therapy forMIandCHF

Discharged (day 14)

AIDS (homosemaI)

lIposi's sarcoma

Possible

Poeumocystis pneumonia

Poeumocystis

Fevers, obtundation,

nuchal rigidity

Fevers, increasing

Moderate

endocarditis (surgery)

40

M

AIDS (unbown)

sinusitis

productive cough

en~

VSD CMV retinitis,

~CGriraii

AIDS cardiomyopathy, CMV retinitis, oral

thrush,

dissemioated MAl 41

43

45

51

&»

M

M

M

M

M

AIDS (homosexual) ABCt (IV drug user)

Porcine valve

liposis sarcoma,

CMVretinitis, esopbageaI

candidiasis

Oral thrush, probable

esophageal candidiasis

detadunent, anasarca

Possible central line infection, pIDCYtopenia

Feverrl unbown origin

AIDS (homosemaI)

Lymphoma, dissemioated MAl

Possible

AIDS (homosemaI)

DissemiDated MAl, oral thrush, scro£uJa,

Pneumonia

HIV+ (bisexua1)

Pneumocystis pneumonia

Asthma, hypertension

pneumonia

Possible Poeumocystis

replacement and

right eye, dyspnea, orthopnea,

masarca

weight loss, fatigue, cough, dyspnea

weight loss Cough, dyspnea, fatigue, weight loss, pleuritic chest pain Fever, dyspnea, chest pain, productive cough Chest pUn, dyspnea

(day 50)

aortic root reamtruction

dyspnea, recurrent

pneumonia

liposis sarcoma,

Discharged

Dyspnea,

M

AIDS {bomosemaI)

medical advice (day 12)

Discharged

36

M

against

Antibiotics

Possible

:rr

Left hospital

Idiopathic

Oral thrush

Nooe

therapy

Discharged (day 13)

Small

ABCt (homosexual)

HIV+ (bomosemal)

antibiotics

Died (day 2)

Aortic valve

dehisceoce

M

M

vasopressors, empiric

Outcome

Prosthetic valve

Aortic valve

36

36

Treatment

for CHF and dilated

cardiomyopathy

replacement, VSDpatch

afterload reduction

ketocooazole

(day 9)

(day 2)

(dayS)

steroids

(day 42)

poeumooia,

COPD

tARe =AIDS-rellted complel; CHF =coogestne heIIt fiiIure; CMV =cytomegalovirus; MAl = 1I,eobtJcterium. . .~ ; VSD = ventriculoseptal defect. evidence of a nonspecific pericarditis. The patient was treated for a patients are seen at our institution, most of these patients in the presumed tuberculous etJusion and was discharged after seven days San Francisco area are treated at another UCSF affiliate. Thus, in hospital. Moffitt-Long Hospital subserves a patient population not unlike those of many other university hospitals in the United States. METHODS To examine the frequency and clinical spectrum of HIV-associated MofBtt-Long Hospital is the main teaching hospital for the pericardial effusions at our institution, we searched the UCSF University of California at San Francisco. Although HIV-positive CHEST I 102 I 3 I SEPTEMBER, 1992

157

Echocardiography Database for all hospitalized patients who were documented to have pericardial effusions over a one-year period. We then examined the hospital charts of these patients, identified those known to be HIV-positive (at the time of their echocardiograms), and reviewed their echocardiograms and clinical courses. Effusion size was graded as follows: large, a circumferential effusion ~1 em in width (in any view); moderate, a circumferential effusion