Ann Thorac Surg 1996;62:267-269
© 1996 The Society of Thoracic Surgeons
Case Report
Biventricular Assist for Severe Acute Rheumatic Pancarditis
Bram J. Amsel, MD,
Herbert De Raedt, MD,
Inez E. Rodrigus, MD,
Luc Haenen, MD,
Patrick Druwé, MD,
Anne Vorlat, MD,
Cecile G. Colpaert, MD,
Adrian C. Moulijn, MD, PhD
Departments of Cardiac Surgery, Intensive Care, and Pathology, University Hospital of Antwerp, Antwerp-Edegem, Belgium
Accepted for publication January 16, 1996.
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Abstract
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Severe heart failure in acute rheumatic myocarditis is rare. It may be rapidly reversible with treatment, so maximal medical treatment and, if necessary, mechanical support should be given before heart transplantation is considered.
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Introduction
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Even in developed countries acute rheumatic fever continues to appear [1]. There is controversy as to whether valvular or myocardial involvement of carditis is most responsible for heart failure when it occurs [2]. We report here a case of rheumatic pancarditis with such severe myocardial failure that biventricular circulatory assist was necessary to save the patient.
A 19-year-old Ashkenazi Jewish man who had been studying in Israel returned home to Belgium with a 2-week history of a sore throat and bronchitis. One month earlier he had been hospitalized with diarrhea and dehydration, from which he recovered rapidly but with significant weight loss. Two days after arrival he was hospitalized elsewhere with fever and cardiac tamponade. Pericardiocentesis yielded 1,700 mL of hemorrhagic but nondiagnostic fluid, but echocardiography demonstrated very poor cardiac function. The anti-streptolysine O titer was 647 IU/L. Viral serologic screening was negative. Because of rapidly worsening cardiogenic shock, the patient was transferred to the University Hospital of Antwerp. Echocardiography showed end-diastolic and end-systolic left ventricular internal dimensions of 60 and 53 mm, respectively, and an estimated left ventricular ejection fraction of 0.26 with very poor right ventricular function (Fig 1
). The atria were also dilated and did not contribute to ventricular filling. Color-coded Doppler echocardiography showed grade II aortic and grade III tricuspid regurgitation and grade I mitral regurgitation. The electrocardiogram demonstrated sinus tachycardia, first degree atrioventricular block, low voltages, right-sided conduction delay with a QRS-duration of 0.11 seconds, and broad Q waves in leads II, III, aVF, V1, and V2. After administration of norepinephrine (13 µg•kg-1•min-1, dopamine (36 µg•kg-1•min-1), and dobutamine (13 µg•kg-1•min-1) and sufficient volume loading, systolic blood pressure was 80 mm Hg and cardiac output 1.9 L/min. Plasma creatinine and lactate levels were 1.6 and 6.6 mg/L, respectively. Levels of aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase were 510, 330, and 2,204 U/L, respectively (normal values = 17, 22, and 241 U/L). Biventricular assist using ABIOMED (Danvers, MA) BVS 5000 pumps was started, immediately yielding good systemic and pulmonary blood flow and diuresis and normalization of hepatic enzyme levels and acid-base balance. Biopsy specimens of the left ventricle (Fig 2A), right atrium, and right atrial appendage (Fig 2B) taken during the operation showed a myocardial, pericardial, and subendocardial inflammatory infiltrate consisting of lymphocytes, histiocytes, and polymorphonuclear leukocytes with interstitial edema, most pronounced in the atrium. There were no Aschoff's nodules.
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Fig 1. . End-diastolic (A) and end-systolic (B) transesophageal echocardiographic frames demonstrating biventricular dilatation and poor contractile function.
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Fig 2. . (A) Light microscopy of left ventricular endomyocardial biopsy specimen showing focal interstitial edema and a sparse to moderately dense inflammatory infiltrate in myocardium and endocardium (right). (B) More pronounced interstitial edema in the right atrial appendage. (Hematoxylin and eosin; x250 before 35% reduction.)
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The patient was treated with penicillin, but antiinflammatory treatment was withheld until day 3, at which time cardiac function had not improved. Acetylsalicylic acid (100 mg•kg-1•day-1) was then given, but administration was stopped because of increased bleeding, and methylprednisolone (10 mg•kg-1•day-1) was given. Three repeat sternotomies were performed for bleeding during the first 9 days. From day 5, ie, 2 days after the start of antiinflammatory treatment, progressively improving echocardiographic myocardial function and left ventricular ejection component to the arterial blood pressure curve were noted, and on day 9 the assist devices were successfully explanted without any need for inotropic drugs. Administration of acetylsalicylic acid (100 mg• kg-1•day-1) was restarted, and methylprednisolone administration continued.
The patient sustained the following complications: atelectasis of the left lower lobe improving over 6 weeks, a mild sacral pressure ulcer, a grand mal epileptic fit considered unrelated to salicylate treament, salt-losing nephritis, and late cytomegaloviral hepatitis. A gated blood pool scan showed a left ventricular ejection fraction of 0.60 with only septal hypokinesis. Echocardiographic end-diastolic and end-systolic internal left ventricular diameters had decreased to 49 and 32 mm, respectively. Right ventricular function was normal. There was grade II aortic and grade I mitral regurgitation and a normal tricuspid valve at color-coded Doppler examination. The electrocardiogram showed normal atrioventricular conduction, a QRS-duration of 0.08 seconds, absence of Q waves, and generalized inverted T waves. At 3-month follow-up the patient is doing fine and has taken up some of his former activities.
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Comment
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In spite of effective antibiotic prophylaxis being available, rheumatic fever still occurs worldwide [1]. It is an expression of an immunologic sequel to a group A streptococcal upper respiratory tract infection. Carditis is one of its complications, but it is clear that heart failure in the acute setting is usually due to valvular destruction [2]. The diagnosis is made according to the presence of an elevated anti-streptolysin O titer and the revised Jones criteria [3]. The cardiac biopsies in our case showed pathologic changes consistent with the diagnosis, although, because of the early presentation, no Aschoff's nodules were found [4]. Our patient had severe myocarditis and demonstrable valvulitis and pericarditis, the first being so severe as to require mechanical circulatory support to sustain life.
Cardiac transplantation, which was considered initially and which became unnecessary because of the rapid improvement of biventricular function, has been performed in acute rheumatic fever with death due to acute rejection on the 45th day [5]. This death was possibly related to an activated immune state, and, if so, cardiac transplantation may not be suitable treatment for active rheumatic fever. Steimle and associates [6] have found significant improvement in left ventricular function in 13 of 49 patients with acute cardiomyopathies of different causes and have cautioned against premature transplantation, but clearly our case presented with such severe biventricular myocardial failure that further treatment without circulatory support would rapidly have led to a fatal outcome. In severe myocardial failure due to rheumatic myocarditis, early ventricular mechanical assist should be considered in addition to antiinflammatory treatment when necessary. A possible role for cardiac transplantation, when improvement of ventricular function does not occur, is uncertain at present.
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Footnotes
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Address reprint requests to Dr Amsel, Department of Cardiac Surgery, University Hospital of Antwerp, Wilrijkstraat 10, B-2650 Antwerp-Edegem, Belgium.
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References
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- Bisno AL. Group A streptococcal infections and acute rheumatic fever. N Engl J Med 1991;325:783–93.
- Essop MR, Wisenbaugh T, Sareli P. Evidence against a myocardial factor as the cause of left ventricular dilation in active rheumatic carditis. J Am Coll Cardiol 1993;22:826–9.[Abstract]
- Dajani AS, Ayoub E, Bierman FZ, et al. Guidelines for the diagnosis of rheumatic fever: Jones criteria, updated 1992. Circulation 1993;87:302–7.
- Ursell PC, Albala A, Fenoglio JJ. Diagnosis of acute rheumatic carditis by endomyocardial biopsy. Hum Pathol 1982;13:677–9.[Medline]
- Silva LMMF, Mansur AJ, Bocchi EA, Stolf NAG, Bellotti G. Unsuspected rheumatic fever carditis ending in heart transplantation. Thorac Cardiovasc Surg 1994;42:191–3.[Medline]
- Steimle AE, Stevenson LW, Fonarow GC, Hamilton MA, Moriguchi JD. Prediction of improvement in recent onset cardiomyopathy after referral for heart transplantation. J Am Coll Cardiol 1994;23:553–9.[Abstract]
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J. B. Barlow, S. J. Middlemost, R. H. Kinsley, B. J. Amsel, I. E. Rodrigus, L. Haenen, and A. C. Moulijn
Biventricular Assist for Severe Acute Rheumatic Pancarditis
Ann. Thorac. Surg.,
March 1, 1997;
63(3):
920 - 921.
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Abstract
Introduction
