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Ann Thorac Surg 2000;70:278-282
© 2000 The Society of Thoracic Surgeons
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
| Abstract |
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| Introduction |
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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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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.
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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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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 patients 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.
| Acknowledgments |
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