Ann Thorac Surg 2000;70:278-282
© 2000 The Society of Thoracic Surgeons
Case report
Mechanical bridge to recovery in fulminant myocarditis
Stephen Westaby, FRCSa,
Takahiro Katsumata, MD, PhDa,
David Pigott, MDb,
Xu Y. Jin, MD, PhDa,
Kjell Saatvedt, MD, PhDa,
Matthew Horton, FRCASa,
Richard E. Clark, MDa
a Department of Cardiac Surgery, John Radcliffe Hospital, Oxford, England, United Kingdom
b Department of Anesthesiology, John Radcliffe Hospital, Oxford, England, United Kingdom
Address reprint requests to Dr Westaby, Oxford Heart Centre, John Radcliffe Hospital, Oxford OX3 9DU, England
e-mail: swestaby{at}ahf.org.uk
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Abstract
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A patient with acute fulminant lymphocytic myocarditis and cardiogenic shock was successfully treated by mechanical offloading of the left ventricle. A nonpulsatile left-heart bypass was undertaken with an implantable centrifugal blood pump. Careful weaning resulted in device removal on the seventh day. Left and right ventricular function is sustained at 7 months. Widespread application of this method depends on the availability of an inexpensive user friendly blood pump, appropriate weaning protocols and emerging strategies to promote sustainabile myocardial recovery.
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Introduction
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Fulminant myocarditis may progress rapidly to biventricular failure and death. In the acute setting, a viraemic patient with hepatorenal dysfunction is rarely offered cardiac transplantation. The potential for complete recovery was recently recognized in young myocarditis patients who were sustained by biventricular support with extra corporeal blood pumps [1]. In this case report, we describe early myocardial and renal recovery during nonpulsatile support with a new implantable left-ventricular assist device (LVAD). Our findings suggest that mechanical circulatory support with a careful weaning strategy is an alternative to transplantation for patients with terminal acute myocarditis.
An otherwise healthy 21-year-old woman (body weight 51 kg) presented with a febrile illness and cardiogenic shock. The electrocardiogram showed widespread ST segment elevation and second-degree heart block. Two-dimensional echocardiography showed cardiac dilatation with biventricular hypokinesia and an akinetic anterolateral left-ventricular wall. There was moderate mitral (MR) and tricuspid regurgitation (TR). Inotropic support was begun, but the systolic blood pressure fell to 50 mm Hg and an intra-aortic balloon pump was inserted.
Coronary angiography showed markedly slow filling of the left-anterior descending coronary but normal coronary anatomy. Multifocal ventricular ectopic beats were noted and, with deteriorating consciousness through cardiogenic shock, the patient was intubated and an atrioventricular sequential pacing system inserted. She was then quickly transferred to Oxford for mechanical circulatory support.
On arrival, the patient was anuric with barely perceptible blood pressure. She was taken immediately to the operating room, where a sternotomy and a conventional cardiopulmonary bypass were instituted to sustain life.
The AB-180 (Cardiac Assist Technologies Inc, Pittsburgh, PA) centrifugal (nonpulsatile) blood pump (Fig 1) was then implanted in the right pleural cavity, with the outflow graft to the ascending aorta and the 40-Fr inflow cannula inserted into the left atrium via a Dacron and homograft sleeve [2] (Fig 2). The blood pump itself contains a polysulfone six-bladed, 25-mm-diameter impeller that rotates within the upper housing at speeds of 2500 to 4500 rpm. All blood-contacting surfaces are not heparin coated. The pump has a low-flow (10 mL/hr) infusion system of sterile water that contains heparin to provide both fluid dynamic hydraulic bearing surfaces and local anticoagulation within the pump. A balloon occluder system prevents backflow from the aorta to the left atrium should the pump fail.
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Fig 2. (A) Chest x-ray on admission showing cardiomegaly and severe pulmonary congestion. (B) On day 5 with the AB-180 in the right pleural cavity. The heart size is reduced, and there is no pulmonary congestion. (C) Seven months after LVAD removal, the heart remains small with clear lung fields.
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Air was removed from the system. With a pump flow of 4 L/min and epinephrine infusion to improve right ventricular ejection, the patient was weaned from cardiopulmonary bypass. Pump flow was calculated using the pressure/flow chart (nomogram) built up on the results of serial in vitro tests [3]. Transoesophageal echocardiography showed the left ventricle to be fully off-loaded as the aortic valve remained closed. The right ventricle was a hypokinetic conduit with the tricuspid and pulmonary valves remaining open in the presence of low pulmonary vascular resistance.
The AB-180 flow rate was gradually increased to 5.5 L/min (4000 rpm). A continuous infusion of heparin was used directly into the device and produced a systemic activated clotting time of 150 seconds. Hemofiltration was initiated, and the patient was transferred to the cardiac recovery area. Magnesium sulphate and amiodarone hydrochloride were used as antidysrhythmics. Immunosuppression was commenced with prednisolone (50 mg/day). The intra-aortic balloon pump was removed.
Myocardial histology showed widespread infiltration by lymphoid cells of variable density. The appearance suggested a severe active lymphocytic myocarditis in keeping with viral infection.
Myocardial performance was documented daily by electrocardiography, invasive hemodynamic monitoring and transesophageal echocardiography (TEE). The cavity size of both ventricles, regional wall motion and valve function were assessed. The main findings are summarized in Table 1.
During the first 24 hours, the left ventricle was completely off-loaded with a cavity dimension of 1 cm and persistently closed mitral and aortic valves. With recovery of left-ventricular contraction from 48 hours onward, we reduced pump flow to keep the left-ventricular end-diastolic dimension (LVEDD) at around 4 cm. The flow reduction allowed opening and closing of the mitral (but not the aortic) valve and prevented stasis in the left atrium. Initially (48 to 72 hours), the right-ventricular function worsened through increased preload and further dilation. The tricuspid and pulmonary valves remained wide open in the presence of high left-sided output and low pulmonary vascular resistance. Mean pulmonary artery pressure was between 15 and 22 mm Hg (mean 18 mm Hg).
Systemic blood flow remained pulseless for 36 hours; mean pressure was 70 mm Hg. A small pulse wave appeared during day 2. Urine flow resumed on day 3, and hemofiltration was discontinued on day 4. By day 6, left ventricular fractional shortening (LVFS) had recovered to 26%, further increasing to 30% as the AB-180 flow rate was reduced by 20%. On day 7, the weaning process produced a consistent increase in LVFS as pump flow was reduced from 5.2 L/min to 2.6 L/min (by 50%). Right-ventricular contraction also improved, although moderate TR persisted. Balancing further benefit versus risk, the patient was returned to the operating room and the pump removed. There were no thrombus in the device and no bleeding complications.
Serum creatinine returned to normal within a week of pump removal. The angiotensin-converting enzyme (ACE) inhibitor (lisinopril 5 mg/day) was prescribed, and prednisolone was withdrawn over a 3-week period. The patient was discharged from the hospital 16 days after discontinuing left-ventricular support. Two months after device removal, left-ventricular ejection fraction (LVEF) was 40% with no mitral or tricuspid regurgitation (transthoracic echo). By 3 months she was New York Heart Asociation class 1. The ACE inhibitor was increased to 10 mg/day at 5 months, and at 12 months LVEF improved to 50%.
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Comment
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We identified 11 other cases of fulminant nonrheumatic lymphocytic myocarditis with eventual weaning from ventricular assist devices (Tables 2 and 3) [4–10]. Most patients had external pulsatile biventricular pumps connected to the right and left heart through long lengths of tubing. These external devices have a substantial complication rate through infection, bleeding and thromboembolism. A small implantable centrifugal pump with short extracardiac connections may solve some of these problems.
Weaning from mechanical assist is a complex process in which detailed TEE plays a vital role. From 72 hours, we found sustained improvement in left-ventricular contraction, probably in response to improved coronary blood flow. We then explored the response of both ventricles to a temporary reduction in AB-180 pump flow (stepwise by 5% to a total of 40%). By day 6, LVFS increased to normal levels and LVEDD increased from 4 to 5 cm, as the pump flow was reduced by 40%. Right-ventricular contraction was also maintained with closure of the tricuspid and pulmonary valves. When this finding was reproduced on day 7, we decided to remove the LVAD. This was the first successful outcome with the AB-180, a device developed primarily for post cardiotomy support or post infarction cardiogenic shock.
In comparison with other reports (Table 2) our duration of support was relatively short. We speculate that this brief period might be due to the rigorous weaning protocol with a device whose flow is easily controlled, and perhaps to the influence of steroids on myocardial edema and coronary blood flow. The issue of long-term nonpulsatile systemic blood flow needs further exploration. Our patient’s renal function was restored during nonpulsatile flow, and we found no adverse effects in sheep supported for up to 7 months with the nonpulsatile Jarvik 2000 axial flow impeller pump (Jarvik Heart Inc, New York, NY) [11].
It is uncertain whether immunosuppressive therapy assists recovery in viral myocarditis. Clinical reports are equivocal with similar rates of improvement with and without immunosuppression [12]. We were concerned that immunosuppression might retard viral clearance, but prescribed prednisolone in an attempt to reduce inflammatory edema and to promote myocardial blood flow.
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Acknowledgments
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We are grateful to Cardiac Assist Technologies, Inc, Pittsburgh, PA, who provided the AB-180 device free of charge and covered the hospital and research costs for this patient. Our anesthesiologists, Drs Michael Sinclair and Rhys Evans, maintained the extremely high standards of care required for a successful outcome in this case. We thank Dr Derek Roskell for his detailed pathological examination. We are grateful to our dedicated nurses, particularly Mrs Desiree Robson.
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References
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Accepted for publication November 16, 1999.
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Abstract
Introduction
