The Jet Lesion in Aortic Valve Endocarditis

Transcription

1 The Jet Lesion in Aortic Valve Endocarditis Lorenzo Gonzalez-Lavin, M.D., and Donald N. Ross, F.R.C.S. ABSTRACT Twenty patients with jet lesions of the mitral valve secondary to aortic valve endocarditis have been operated upon. In 16 patients the aortic valve lesion involved the noncoronary cusp or adjacent commissure. The jet lesions in the mitral valve were confined to the anterior leaflet in all patients. Conservative repair of the mitral valve was feasible in 12. There were 2 hospital and 3 late deaths. The surviving 15 patients are well six months to five years after operation. Surgical attention to both valves is imperative to achieve complete eradication of infection and to obtain good hemodynamic results. uring the course of infective endocarditis, the aortic valve is frequently affected and becomes regurgitant. The resulting jet of blood disseminates the infecting bacteria in a retrograde fashion, and the anterior leaflet of the mitral valve, due to its proximity, is vulnerable to invasion (Fig. 1). The destructive effects of this secondary infection usually result in mitral valve regurgitation and aggravate the already compromised left ventricular function in these patients. Awareness of the coexisting jet lesion is essential, as surgical attention to both valves is imperative to achieve complete eradication of the infection and to obtain good hemodynamic results. In recent years we have operated on 20 patients with jet lesions of the mitral valve secondary to aortic valve endocarditis. The first 10 patients have been previously reported [4]. The purpose of this communication is to present our experience regarding the operative treatment and results in these 20 patients. Materials and Methods INCIDENCE OF JET LESION From June, 1963, to July, 1971, 322 patients with aortic regurgitation were operated upon by the authors and surgical registrars at the National Heart Hospital in London. In 99 of the patients the regurgitation was a result of bacterial endocarditis. Twenty of these 99 patients were found to have secondary involvement of the mitral valve. From the Departments of Surgery, Institute of Cardiology and National Heart Hospital, London, England. We wish to thank Miss J. Brunner, R.N., for the diagrams appearing here and Miss V. Adler, B.A., for her valuable assistance. Presented at the Eighth Annual Meeting of The Society of Thoracic Surgeons, San Francisco, Calif., Jan , Address reprint requests to Dr. Gonzalez-Lavin, Division of Thoracic Surgery, Henry Ford Hospital, 2799 W. Grand Blvd., Detroit, Mich VOL. 14, NO. 4, OCTOBER,

2 GONZALEZ-LAVIN AND ROSS FIG. 1. Anatomical relationship between the noncoronary cusp of the aortic valve and the anterior leaflet of the mitral valve. Arrow depicts pathway of retrograde infection. (RCO = right coronary ostium; LCO = left coronary ostium.) There were 17 male patients and 3 female patients. Their ages ranged from 11 to 64 years with an average age of Eight patients had known preexisting valvular heart disease; the other 12 were without clinical evidence of a cardiac lesion prior to the onset of bacterial endocarditis. All patients had had at least one documented episode of bacterial endocarditis; 3 of them had had two recognized episodes; and 1 had experienced three episodes. In all patients the diagnosis was confirmed by blood cultures (Table). The portal of entry for bacterial infection was clear in 8 patients. Infection followed dental manipulation or extraction in 6, 1 patient presented with acute bacterial endocarditis and periodontal abscesses, and 1 had had a respiratory infection two months prior to developing Klebsiella endocarditis. According to the New York Heart Association Functional Classification, 5 patients were in Class I1 at the time of operation. Seven were in Class 111, and the other 8 had overt signs of congestive failure and consequently were designated Class IV. Clinical findings were those of predominant aortic regurgitation in all patients except 2, in whom the evidence of mitral regurgitation surpassed that of aortic valve disease. Ten other patients had a pansystolic murmur at the apex. The remaining 8 patients exhibited no clinical evidence of mitral valve disease. Radiological and electrocardiographic evidence of left ventricular enlargement was present in all patients. A left ventriculogram was performed in 10 patients. Severe mitral regurgitation was found in 3 patients, minimal 398 THE ANNALS OF THORACIC SURGERY

3 Jet Lesion in Aortic Valve Endocarditis ORGANISMS ISOLATED FROM BLOOD CULTURES IN 20 PATIENTS WITH AORTIC VALVE ENDOCARDITIS Initial Episode Second Episode Third Episode No. of No. of No. of Pa- Pa- Patients Organism tients Organism tients Organism 13 Streptococcus, 1 Staphylococcus, 1 Streptococcus, viridans type Group G unspecified 1 Streptococcus, viridans type 1 Staphylococcus albus 2 Staphylococcus aureus 2 Klebsiella 1 Beta-hemolytic 1 Staphylococcus streptococcus aureus 1 Enterococcus 1 Staphylococcus albus mitral regurgitation was seen in 5, and a normally functioning mitral valve was found in the other 2 patients. A left heart catheterization was abandoned in 1 more patient because of repeated bouts of paroxysmal atrial tachycardia. Half of the patients underwent operation within a year of the first episode of bacterial endocarditis. One patient underwent an emergency procedure because of intractable pulmonary edema three weeks after the onset of endocardi tis. OPERATION A median sternotomy is the routine approach for all cardiopulmonary bypass procedures. The aortic valve is assessed first and then is excised and cultured. The mitral valve is approached through a longitudinal incision on the left atrium. In some patients the actual involvement of the mitral valve can be suspected by viewing the ventricular aspect of the anterior leaflet of the mitral valve from the aortic annulus. Anoxic arrest is limited to 30 to 40 minutes during mitral valve repair or replacement. Coronary perfusion is instituted for the insertion of the aortic valve. In 16 of the 20 patients in this series the aortic valve lesions involved the noncoronary cusp or adjacent commissure (Fig. 2). The jet lesions in the mitral valve were confined to the anterior leaflet in all patients (Fig. 3). Aortic Vulve. Ten patients underwent homograft replacement of the aortic valve. In 4 more a supported fascia lata valve was inserted. Three VOL. 14, NO. 4, OCTOBER,

4 GONZALEZ-LAVIN AND ROSS FIG. 2. Site of main aortic valve lesion in 20 patients with jet lesions of the mitral valve. (LCC = left coronary cusp; NCC = noncoronary cusp; N/RCC = commissure between noncoronary and right coronary CUSPS.) other patients had a pulmonary valve autograft, and in the other 3 a Starr- Edwards prosthesis was used. Mitrul Valve. In 12 patients reparative procedures to the mitral valve were possible. Annuloplasty or repair, or both, of ruptured chordae tendineae was performed in 6 patients; repair consisted of reattaching the chordae to the corresponding papillary muscle, either by direct suture or by incorporating a sling of pericardium. Excision of a mycotic aneurysm from the anterior cusp was performed in 2 more patients. In another 3 patients, perforation of the anterior leaflet was repaired by pericardial patch in 2 and a fascia lata patch in 1. In all 3 patients there was no evidence of active infection. In 1 additional patient, fibrous vegetations distorting the anterior leaflet were excised. In 2 others an ulceration of the anterior leaflet was found; no corrective procedure was necessary. In the remaining 6 patients replacement of the mitral valve was necessary, in 2 because of active infection. Three patients received a fascia lata valve, 2 a stented aortic valve homograft, and 1 a Starr-Edwards ball-valve prosthesis. Results There were 2 hospital deaths, both due to neurological damage (10% hospital mortality). Three other patients died after discharge from the hos- 4-Aneurysm / 7-Ulcer or Vegetations / FIG. 3. Various types of jet lesion found in the anterior leaflet of the mitral ualue in 20 patients. B-Ruptured Chdm (7 essociated wirh anorher lesion) 400 THE ANNALS OF THORACIC SURGERY

5 Jet Lesion in Aortic Valve Endocarditis pital, 1 of them five months after operation due to a myocardial infarction. The other 2 patients died eight and nine months, respectively, after operation. In both, the cause of death was a further episode of bacterial endocarditis precipitating severe heart failure; reoperation was refused by both patients. The surviving 15 patients are well and have been followed for six months to five years. Two of them, however, have had a further episode of bacterial infection: Stu~hylococcus albus was isolated in 1 at three months and streptococcus viridans in the other at three years after operation. Both patients were treated successfully. Of the entire group, 3 patients have a moderate degree of aortic regurgitation. One has a prosthetic valve, and the other 2 have homograft aortic valves. All 3 have remained asymptomatic. Three other patients have evidence of moderate mitral regurgitation. All underwent annuloplasty, and 2 of them also had repair of ruptured chordae tendineae. They have remained well and show increased exercise tolerance and no evidence of congestive failure. Comment The retrograde dissemination of infection in patients with aortic valve endocarditis has been well documented from postmortem examinations [3, 5, 101; however, it has been less commonly recognized in clinical practice. Recent reports of patients operated upon for infective endocarditis indicate that its occurrence is not rare. Braniff, Shumway, and Harrison [2] reported that in 1 of their 5 patients a perforation of the mitral valve was repaired with sutures at the time of aortic valve replacement. Kaiser and collaborators [7] described 1 of their 5 patients in whom positive blood cultures persisted after aortic valve replacement. The patient died five days after operation, and at postmortem examination the mitral valve was found to be actively infected and perforated. They also reviewed the literature and found 12 patients operated upon during active bacterial endocarditis. In 9 of these patients the aortic leaflets were perforated, and in 6 of the 9 the infection extended to the sinus of Valsalva or the mitral valve or both. In the report of Manhas and his associates [S], 2 of their 14 patients appear to have developed a jet lesion in the mitral valve. The incidence of this phenomenon has been more than impressive in our own experience, as 20 of 99 patients operated on for aortic regurgitation due to bacterial endocarditis presented with jet lesions of the mitral valve. In 16 of these patients, mitral regurgitation was of hemodynamic importance. Mitral valve involvement should be suspected in a patient who, in the course of bacterial endocarditis to the aortic valve, develops a pansystolic murmur at the apex coinciding with clinical deterioration of his cardiovascular condition. Left ventricular angiography is helpful in outlining the VOL. 14, NO. 4, OCTOBER,

6 GONZALEZ-LAWN AND ROSS mitral valve involvement, although in some of our patients there was a disparity between the angiographic findings and the actual degree of regurgitation found at operation. In patients with severe heart failure who are in urgent need of operation, angiography is not indispensable and may even be ill-advised, as it is known to precipitate acute pulmonary edema. There are three indications for surgical intervention in patients with bacterial endocarditis, the most common being overt heart failure due to important valvular destruction. The most pressing determinant of the actual time of operation is the hemodynamic state of the patient. Recent reports advocate early intervention [6, 9, 111. Persistent infection despite adequate antibiotic treatment is, at present, a clear indication for operation, and here again there is evidence that valve replacement should be undertaken despite active infection when the hemodynamic status of a patient is uncontrollable [12, 131. Systemic embolism of an infected valve is another definite indication for operation. Healed bacterial endocarditis with severe hemodynamic disturbances due to valve destruction has been the most common indication for operation in our series. However, the 2 most recent patients were operated upon in the presence of active infection. From the surgical point of view, jet lesions to the mitral valve were most often found when the aortic valve lesion was located in the noncoronary cusp or an adjacent commissure. The location of a lesion of endocarditis in this cusp should perhaps be, by itself, an indication for exploration of the mitral valve. Most lesions in the mitral valve are located in the anterior leaflet, and they vary from weakening of the leaflet substance with ulceration or aneurysm formation to perforation of the cusp and ruptured chordae tendineae. As seen in our present series and in the reports of others [Z], a conservative operation can often be performed; however, in the presence of active infection or severe valvular damage, replacement of the mitral valve is necessary. Patients in whom the mitral valve was reconstructed by conservative measures or replaced with a biological tissue valve underwent aortic valve replacement with a biological valve. In patients in whom the mitral valve was replaced with a prosthetic valve (mainly because of the lack of an appropriate-sized homograft valve), the aortic valve was also replaced by a prosthetic valve. The variety of valve substitutes used in this group of patients reflects our preference for biological valves and our criteria for evaluating usefulness and long-term function of the different valves in these challenging cases. Hospital mortality has been low and is comparable to that of some other reports [l, 81. The long-term results have been satisfactory, although recurrence of infection is high in these patients. In view of our experience and that of others, a plea is made for awareness of the coexisting jet lesion in aortic valve endocarditis. Surgical atten- 402 THE ANNALS OF THORACIC SURGERY

7 Jet Lesion in Aortic Valve Endocarditis tion to both valves is imperative to achieve complete eradication of the infection and to yield good hemodynamic results. References 1. Braimbridge, M. V. Cardiac surgery and bacterial endocarditis. Lancet 1: 1307, Braniff, B. A., Shumway, N. E., and Harrison, D. C. Valve replacement in active bacterial endocarditis. N. Engl. J. Med. 176:1464, Edwards, J. E. Acquired Diseases of the Heart and Great Vessels. Philadelphia: Saunders, P Gonzalez-Lavin, L., Lise, M., and Ross, D. N. The importance of the jet lesion in bacterial endocarditis involving the left heart. J. Thorac. Cardiovase. Surg. 59:185, Hudson, R. E. B. Cardiovascular Pathology. London: Arnold, Vol. 2, p Hutter, M. A., DeSanctis, R. W., Nathan, J. M., Buckley, M. G., Mundth, E. D., Daggett, W. M., and Austen, W. G. Aortic valve surgery as an emergency procedure. Circulation 41 :623, Kaiser, G. C., Willman, V. L., Thurmann, M., and Hanlon, C. R. Valve re lacement in cases of aortic insufficiency due to active endocarditis. J. T 1 orac. Cardiovasc. Surg. 54:491, Manhas, D. R., Hessel, E. A., Winterscheid, L. C., Dillard, D. H., and Merendino, K. A. Open heart surgery in infective endocarditis. Circulation 41: 841, Neville, W. E., Magno, M., Foxworthy, D. T., and Moffat, J. E. Emergency aortic valve replacement in bacterial endocarditis. J. Thorac. Cardiovasc. Surg. 61:916, Robard, S. Blood velocity and endocarditis. Circulation 27: 18, Scott, S. M., Fish, R. G., and Crutcher, J. C. Early surgical intervention for aortic insufficiency due to bacterial endocarditis. Ann. Thorac. Surg. 3: 158, Wallace, A. G., Young, W. G., and Osterhout, S. Treatment of acute bacterial endocarditis by valve excision and replacement. Circulation 31 :450, Wilson, L. C., Wilcox, B. R., Sugg, W. L., and Peters, R. M. Valvar regurgitation in acute bacterial endocarditis and early replacement. Arch. Surg. 101:756, D iscussio n DR. C. WALTON LILLEHEI (New York, N.Y.): This is an excellent clinical study of the problems associated with infection in heart valves. I would like to emphasize two points: The first is the importance of always inspecting the mitral valve during an aortic valve operation, which can be done very readily through the o n aortotomy. This inspection is greatly facilitated, as previously described (J. T r orac. Cardiovasc. Surg. 50:487, 1969, by having on the table a uterine curette. This instrument is ideal for picking up the leaflets of the valve individually and bringing them up into the visual field to check chordae, scarring, or perforations. The second point relates to a clearer understanding of the patho hysiology of persistent valvular infections resistant to antibiotics. I think, as B o the authors, that this situation is a clear-cut indication-in fact, an urgent indication -for immediate operation. Almost invariably, an infected valve or prosthesis has regurgitant leaks which greatly increase the mechanical work of the heart.

8 GONZALEZ-LAVIN AND ROSS Many clinicians don t realize the dreadful increase in susceptibility to cardiac infection that occurs with increased cardiac work. To illustrate this, I d like to refer to some experimental studies done twenty years ago involving the production of endocarditis with valvular deformities in dogs with peripheral arteriovenous fistulas (AVF) (Dis. Chest 24:421, 1953). The study animals had an iliac AVF on one side and a femoral AVF in the other leg. After a period of three months, these dogs were exposed to intravenous injections of bacteria. The control group consisted of normal dogs who were given the same bacteria. These AVF dogs received a total intravenous dose of to ml. of a 24-hour culture of beta-hemolytic streptococcus (Group D) over seven days, and all subsequently died of progressive vegetative endocarditis with pathological lesions indistinguishable from those found in man. The controls received up to a 350 ml. total intravenous dose of the same culture over seven days, and none got endocarditis. This represents a bacterial dose differential of 10,000 to 14,000 timeevery dramatic evidence of the huge difference in susceptibility induced by increased cardiac work. Interestingly, even though this was a very penicillin-susceptible culture of beta-hemolytic streptococcus, treatment of the study animals with huge doses of penicillin was of no avail unless the AVF was taken down. I believe these experiments are very pertinent to the problems of infected human cardiac valves and prostheses. Chronic cardiac overwork enormously increases the susceptibility to infection, and the chances of sterilizing the bloodstream under these conditions are very small. I think this is important because cardiologists invariably seem to want to wait for a sterile bloodstream before operating. While this is desirable if obtainable, it may be impossible in the face of either a sizable leak through the diseased natural valve or a paravalvular prosthetic leak. 404 THE ANNALS OF THORACIC SURGERY