May of 1975, after a physician heard munnurs of aortic stenosis and insufficiency on a routine physical examination. An echocardiogram revealed increased reflectance from the aortic leaflets ( Fig IA). The patient was not seen again until her final admission, when she was acutely ill, febrile, and dyspneic. Raised purpuric lesions were noted over both ankles, and the patient was in moderate congestive failw-e. An electrocardiogram suggested an interim infarction of the anterior wall. An echocardiogram revealed an increase in aortic valvular reflectance suggestive of vegetations ( Fig IB), and imaging just superior to the valvular leaflets (Fig IC) revealed a freely moving structure which traversed the aortic root dUiing systole. Administration of gentamicin and penicillin and therapy for failure were begun. Two of the cultures of blood taken at admission grew Propionobacterium species. The course of the patient's illness stabilized; however, three weeks after admission, she died suddenly. At postmortem examination a thiclcened, tricuspid aortic valve was found. Vegetations were present on all three cusps, with predominance on the left. In addition, the left cusp contained a gelatinous, darlc-red, freely movable vegetation that projected 1.3 em above the valve ( Fig 2). On openmg the aorta, this vegetation was inserted into and completely occluded the left coronary ostium. There was no evidence of coronary embolus, significant atherosclerosis, or other cause for sudden death.

©@~~UlJ~O©&trO@~® TO TH8 eDITOR

Communications for this section will be published as lfHJC8 and priorities permit. The comments should not exceed 500 words in length, with a maximum of five references; one figure or table can be printed. Exceptions may occur under particular circumstances. Contributions may include comments on articles published in this periodical, or they may be reports of unique educational character. Specific permission to publish should be cited in a covering letter or appended as a postscript.

Sudden ·Death Endocarditis

1n

Infective

To the Editor: In patients suffering from infective endocarditis, sudden death is not an uncommon occurrence. Recent reports have stressed that a full four-week to six-week course of antibiotic therapy need not be completed before valvular replacement is undertaken. Consequently, the identification of subjects who are at increased risk of sudden death takes on added importance. We report the clinical, serial echocardiographic, and necropsy findings in a patient with aortic valvular endocarditis in order to call attention to a complication which is not usually appreciated, namely, occlusion of the coronary ostia by valvular vegetations.

DISCUSSION

Sudden death due to coronary ostial occlusion is a rarely reported complication of aortic valvular endocarditis; however, the incidence of this complication may be underestimated, particularly in patients with large vegetations. Coronary ostial occlusion was first demonstrated by Lamb1 in 1913. Since that time, only scattered reports have appeared;H however, these reports mentioned no features by which patients at risk for this complication could be identified short of postmortem examination. Dillon et al8 first demonstrated that valvular vegeta-

CASE REPoRT

A 87 -year-old woman was admitted on Oct 20, 1975, with infective endocarditis. She had previously been evaluated in

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,~~v~~·... .. FIGURE 1. A (left), Echocardiogram five months prior to admission. Thickening of valvular leaflets is seen. Aortic root is slightly dilated. CPT, Carotid pulse tracing; LA, left atrium; and PCG, phonocardiogram. B (center), Echocardiogram during final admission. Increased thiclcening of leaflets suggestive of vegetation is noted. C (right), Echocardiogram with supravalvular transducer angulation. Highly mobile structure is noted during systole. This probably represents reflectance from vegetation seen at necropsy.

794 COMMUNICAnONS TO THE EDITOR

CHEST, 71: 6, JUNE, 1977

Reprint requests: Dr. Greenberg, Dioision of Cardiology, U~ versify of California Medical Center, Third and Pamassus Avenues, San Francisco 94122

fu:FERENCES 1 Lamb A: Acase of occlusion of the left coronary artery by a pedunculated vegetation of the aortic valve. NY Pathol Soc 13:15-18, 1913 2 Latscha B, Lenegre J. Mathivat A: Un cas d'embolie et un cas d'occlusion ostiale coronarieene au cours de I'endocardite maligne lente. Arch Mal Coeur 42:729-740, 1949 3 Walker B: Coronary embolism and coronary occlusion in bacterial endocarditis. Br Heart J 14:144-146, 1951 4 Von Althoff H: Isolierter Rechtsherzinfarkt bei residivierender Koronarembolie und Tamponade des Koronarostiums. Z KreislauHorsch 57:1204-1212, 1968 5 Bozio A, Loiri R: L'incarceratioo ostia1e coronarieene de vegetations d'endocardite infectieuse aortique. Arch Mal Coeur 66:1557-1562, 1973 6 Dillon G, Feigenbaum H, Konecki L, et al : Echocardiographic manifestation of valvular vegetations. Am Heart J 86:698-704, 1973

Respiratory Intensive Care Units To the Editor:

FIGURE 2. Thick vegetations are seen on left cusp of bicuspid aortic valve. Large gelatinous structure is seen extending to level of ostium of left coronary artery ( LCA). At postmortem examination, vegetation was inserted into and occluded ostium. Fusion of right and left cusps is also noted. RCA, Right coronary artery.

tions of sufficient size could be demonstrated echocardiographically. The changes in the serial echocardiogram in our patient strongly suggested the presence of vegetations. In addition, supravalvular imaging suggested the presence of a large, highly mobile vegetation in the aortic root, and this finding was confirmed at necropsy. The significance of echocardiographic demonstration of such a large and mobile vegetation remains to be proved by further investigation. Nevertheless, such findings in a patient with bacterial endocarditis should concern the physician and may, indeed, be a compelling indication for early surgical therapy. ACKNOWLEDGMENT: This work was supported in part by program project grant HL 06285 from the National Institutes of Health. Barry H. Greenberg, M.D.; Peter Hoffman, M.D.; NeLson B. Schiller, M.D.; Meredith Miller, M.D.; and Kanu Chatterjee, M.D. Departments of Medicine and Pathology and the Cardiovascular Research Institute University of California, San Francisco

CHEST, 71: 6, JUNE, 1977

I am writing in regard to an editorial entitled 'Who Should Supervise Respiratory Intensive Care Units?" by Zwillich and Petty (Chest 70:323-325, 1976) . Also, I am writing to comment on two articles1 •2 which prompted the editorial because I believe that the series of exchanges between the authors of these articles may be detrimental to the further development of rapport between specialties meeting at the bedside of critically ill patients. First, the report by Zwillich et al1 is a good review by a well-known group whose extensive experience and interest in this area qualify theDJ to comment on the complications of assisted ventilation. Their report serves to remind us all that well-recognized and sometimes avoidable complications may occur in the best of circumstances. This article was then abstracted and commented upon in another journal. 2 The commentary by Coppel2 accompanying the abstract r~ a number of delicate and disturbing issues. Hidden among the truths of Coppers2 commentary are statements sufficient to bother even the most unbiased reader, because some are poorly documented and some are delivered in an inappropriately abrasive manner. As Coppel2 states, the 10 percent incidence of endobronchial intubation missed by physical examination and noticed only after a chest x-ray film is alarming, even though, as Zwillich and Petty point out, the incidence of this complication under similar circumstances elsewhere is lacking. It is also true that nasal necrosis is a horrible complication of prolonged nasotracheal intubation in patients surviving episodes of assisted mechanical ventilation. On the other hand, nasal necrosis is relatively minor if the patient had a deformity of the jaw or facial trauma precluding any other route for a necessary rapid intubation. As one who trained in an excellent Canadian intensive

COMMUNICAnONS TO THE EDITOR 795

Sudden death in infective endocarditis.

May of 1975, after a physician heard munnurs of aortic stenosis and insufficiency on a routine physical examination. An echocardiogram revealed increa...
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