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Ann Thorac Surg 1997;63:920-921
© 1997 The Society of Thoracic Surgeons
Department of Cardiology University of the Witwatersrand and Johannesburg Hospital Area 555 Parktown 2193 Republic of South Africa
Suite 103 Morningside Clinic Rivonia Rd Morningside 2057 Republic of South Africa
To the Editor:
Amsel and associates [1] report a pyrexial illness in a 19-year-old man principally comprising cardiac tamponade, severe myocardial dysfunction, hemodynamically unimportant valve lesions detected on Doppler echocardiography, widening of QRS complexes on the electrocardiogram with associated significant Q waves, and moderate interstitial edema as well as an inflammatory infiltrate on endomycardial biopsy. No Aschoff nodules were detected. The patient was treated with biventricular assist devices, penicillin, aspirin, and steroids. He eventually made a remarkable recovery with normalization of ventricular function and of the electrocardiographic abnormalities. At 3-month follow-up the patient was "doing fine and has taken up some of his former activities." The contribution of the ventricular assist devices was clearly life-saving.
Although all aspects of this isolated case were typical of a severe viral myopericarditis [2], Amsel and associates [1] elected to incriminate "acute rheumatic pancarditis." Their reasons for substantiating that decision are wanting but, regrettably, the case report will necessarily contribute to the furtherance of two ongoing myths. The first relates to a myocardial factor, so-called rheumatic myocarditis, as an important cause of heart failure and death in patients with active rheumatic carditis [3]. The second relates to the administration of steroids as a "life-saving measure" in young patients dying of that condition. We deprecate the title of this case report and are critical of your referees who sanctioned its publication. We suspect that neither Amsel and associates in Belgium nor your referees have meaningful experience with fulminating rheumatic carditis, nor did they take cognizance of current literature, although at least one relevant article was cited [4].
Active rheumatic carditis remains prevalent in developing countries [5], including South Africa [6, 7], and its medical and surgical management are ongoing major challenges in our environment [8]. It is a common cause of pure severe mitral regurgitation, which, in turn, is the principal valve lesion resulting in heart failure in children and young adults. The primary defect caused by active rheumatic carditis is dilatation of the mitral annulus with consequent anterior mitral leaflet prolapse and hence mitral regurgitation [5, 6, 8]. The hemodynamic overload on the heart of the mitral regurgitation exacerbates the rheumatic activity [5]. Despite medical therapy, including diuretics and vasodilators, intractable heart failure often supervenes and sole effective therapy is then surgical. We operate on approximately 40 such patients every year and succeed with mitral repair, preferable to replacement, in at least 80% of cases [5]. The rheumatic activity abates dramatically during the first few weeks of the postoperative period, heart size decreases, and the patients gain weight.
In contradistinction to viral myopericarditis, during three decades of observation we have yet to encounter heart failure due to rheumatic carditis without a hemodynamically important valve lesion! We submit that observations on hemodynamically severe so-called rheumatic myocarditis were made [3, 9] when the crucial contribution of mitral regurgitation could well have been underestimated. We remain unconvinced, in fact, that a rheumatic myocardial factor [10] directly affects left ventricular contractility at all [5–7].
In a report [4] from this environment, cited by Amsel and associates [1], it was demonstrated, on echocardiographic evaluation 3 months after a successful operation, that a significant decrease in left ventricular diastolic dimension with preservation of systolic function occurred in all of the 32 patients who had had active rheumatic carditis, severe regurgitant valve lesions, and heart failure. Although those results are indeed in accord with an absence or unimportance of any rheumatic myocardial factor, we are uncertain of the details of patient selection, but an inference that significant and sometimes irreversible myocardial contractile dysfunction is never encountered preoperatively or postoperatively in our rheumatic patients subjected to operation would be both incorrect and misleading. Cardiopulmonary bypass, especially if prolonged, may have caused or aggravated postoperative myocardial dysfunction in a few. In the majority, however, we favor that prolonged volume overload is the relevant factor [6] just as it is in patients with nonrheumatic mitral [11] or aortic [12] regurgitation.
Finally, we reiterate what we have observed and emphasized for years [5, 6]. Intractable heart failure and death in young patients with fulminant rheumatic carditis are caused by a hemodynamically severe valve lesion. This is invariably mitral regurgitation. Contrary to misleading doctrine [3, 9, 10] based on no meaningful data, steroid therapy is not indicated [5]. It is valve repair or replacement that are life-saving, and these should not be delayed [6–8].
References
Department of Cardiac Surgery University Hospital of Antwerp Wilrijkstraat 10 B-2650 Antwerp-Edegem, Belgium
Reply
To the Editor:
We thank Barlow and associates for their comments and for sharing with us their extensive experience with acute rheumatic fever in South Africa. A few points require clarification.
First, through an oversight at some stage between preparation and publication of our article, left-sided valvular regurgitation in our patient was inadvertently reported to have been mild. In fact both mitral and aortic (and tricuspid) regurgitation were initially severe and became less severe later on. We apologize for this error. We agree with Barlow and associates that valvular lesions should be present in severe acute rheumatic carditis, and they were. These acute valvular lesions argue against a viral cause of the disease. A significant myocardial factor in heart failure in rheumatic fever is controversial [1, 2]. Our patient's heart failure had a myocardial and a valvular component. The first was too severe, however, to even consider a valvular operation.
Second, we did not wish to imply that steroid therapy is recommended for the treatment of acute rheumatic fever. Aspirin is, but led to severe bleeding in our patient, who was on assisted circulation. We therefore elected, in this specific clinical instance, to administer steroids as an alternative to aspirin, because some older literature suggests they may play a useful role [3, 4].
Third, the elevated antistreptolysin O titer mentioned in our article indicates a recent streptococcal infection and argues for acute rheumatic fever. It should be mentioned that myocardial histology in our case was not specific for rheumatic carditis. The absence of Aschoff nodules so early in the disease was to be expected.
Fourth, although, as Barlow and associates correctly state, autochthonic acute rheumatic fever is a rare entity in Belgium, our patient had been living in Israel, where the disease has a higher incidence [5]. This fact increases his a priori odds of suffering from acute rheumatic fever.
Fifth, myocardial contractility began improving only after initiation of aspirin therapy after 3 days of assisted circulation. The accelerated improvement is more compatible with acute rheumatic fever than with viral carditis.
In summary, we believe that our patient had severe acute rheumatic carditis and intend to continue recommending monthly injection of long-acting penicillin. Initial medical treatment of acute rheumatic fever should include rest, penicillin, and aspirin.
References
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