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Ann Thorac Surg 2000;69:284-286
© 2000 The Society of Thoracic Surgeons

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Case Reports

Bridge to recovery with a left ventricular assist device for fulminant acute myocarditis

^a Heart and Lung Transplant Service, Alfred Hospital, Melbourne, Victoria, Australia

Address reprint requests to Dr Esmore, Heart and Lung Transplant Service, Alfred Hospital, Commercial Rd, Prahran, Melbourne, Victoria 3181, Australia

	Abstract

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Acute fulminant myocarditis frequently causes circulatory collapse that is resistant to conventional therapy. We describe a case in which a patient with histologically confirmed viral myocarditis was supported by a left ventricular assist device (LVAD) as a bridge to recovery. The LVAD was successfully weaned 3 weeks later.

	Introduction

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Acute fulminant myocarditis frequently causes rapidly progressive cardiac decompensation and circulatory collapse, associated with high mortality. In the last decade, ventricular assist devices have been available for management of severe heart failure, which is refractory to high-dose inotropic infusion with or without intraaortic balloon pumping (IABP) support. We report a case with profound heart failure secondary to acute myocarditis, which was successfully supported by the left ventricular assist device (LVAD), allowing patient recovery and weaning from the device.

A previously healthy 34-year-old man presented with recurrent collapse following a week of flulike symptoms. He was admitted to the regional hospital. Echocardiography showed a pericardial effusion and poor left ventricular (LV) function, and he was transferred to our institution for further care. On arrival he was hypotensive, his systolic blood pressure was 75 mm Hg and tachycardic, and his heart rate was 110/min, regular. An electrocardiogram showed no ischemic ST-T change. Repeated transthoracic echocardiography revealed severely impaired LV systolic function, fractional shortening of 16%, a nondilated ventricle, end-diastolic LV diameter of 4.1 cm, and a pericardial effusion, consistent with a diagnosis of myopericarditis. The patient remained tachycardic, tachypneic, and oliguric, and developed acute cardiogenic shock, requiring cardiopulmonary resuscitation including endotracheal intubation and mechanical ventilation. Despite high-dose intropic support with dobutamine at 10 µg · kg^-1 · min^-1, adrenaline at 40 µg/min, and noradrenaline at 5 µg/min, as well as IABP support, hemodynamic data showed a right atrial pressure of 20 mm Hg, a pulmonary artery wedge pressure of 20 mm Hg, and a cardiac index of 1.6 L · min^-1 · min^-2. Endomyocardial biopsy (EMB) showed a diffuse mild lymphocytic myocardial infiltration with intact myocardial fibers, which were compatible with viral myocarditis (Fig 1). Three days after admission, a decision was made to implant Thoratec LVAD (Thoratec Laboratories Corporation, Pleasanton, CA) because of failure to improve.

View larger version (139K): [in this window] [in a new window]   Fig 1. Endomyocardial biopsy specimen before implantation of LVAD reveals a characteristic infiltration of lymphocytes, histiocytes, and a few neutrophils in a mildly edematous interstitium. The myocardial fibers appear generally intact. (Hematoxylin and eosin; x400 before 52% reduction.)

View larger version (144K): [in this window] [in a new window]   Fig 2. Endomyocardial biopsy specimen 1 month after removal of LVAD reveals a diffuse but unevenly developed increase in cellularity because of a light influx of mononuclear cells, lymphocytes, and histiocytes within the interstitium. Slight vacuolar change can be seen within some fibers. (Hematoxylin and eosin. x400 before 52% reduction.)

	Comment

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Correlation between histologic manifestations on EMB and recovery of ventricular function has been controversial. In two cases, repeat EMBs from the right ventricle (RV) showed resolving interstitial lymphocytic infiltration on days 6 and 15 after the initial EMBs [1, 2]. In the case of an infant, repeat EMB was not performed [3]. In another two reports, EMB from the RV failed to determine a cause of acute heart failure [4, 5]. In our case, although remarkable improvement in LV contractility was already observed on the echocardiogram 2 weeks after implantation of the LVAD, the EMB did not show substantial histologic resolution of lymphocytic infiltration even 50 days after the initial biopsy. Therefore, EMB from the RV may not always correlate well with severity of cardiac dysfunction, especially LV dysfunction, in cases of acute myocarditis.

It is important to decide whether an LVAD alone or a biventricular assist device (BVAD) is necessary to treat severe heart failure caused by acute fulminant myocarditis. Most surgeons prefer to initially support such patients with LVAD alone to reduce the potentially increased risks associated with BVAD implantation. There have been three cases of LVAD [2–4] and two cases of BVAD [1, 5] implantation in the literature. Jett and colleagues [1] implanted BVAD simultaneously because the right atrium and RV were markedly dilated before placement on cardiopulmonary bypass, associated with marked lymphocytic infiltration and myocytolysis on EMB from the RV. Martin and colleagues [5] added RV assist device implantation because of a dilated RV and increasing right-sided filling pressure soon after weaning from CPB after LVAD implantation [5]. The other three patients were well supported with LVAD alone [2–4].

Recently, Farrar and colleagues [6] in a multicenter review of 213 Thoratec implants demonstrated that severity of renal, hepatic, and respiratory dysfunction was predictive of the need for BVAD [6]. They also suggested that the earlier the VAD was implanted, the more likely the patient could be supported by LVAD alone [6]. Our approach has been to support these patients with LVAD alone whenever possible and to aggressively unload the RV pharmacologically with inhaled nitric oxide and inotropic agents. In 36 VAD implants, we have required only 2 BVADs.

The patient described in this report demonstrated the potential for recovery in acute fulminant myocarditis and the essential role of LVAD support.

	References

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1. Jett G.K., Miller A., Savino D., Gonwa T. Reversal of acute fulminant lymphocytic myocarditis with combined technology of OKT3 monoclonal antibody and mechanical circulatory support. J Heart Lung Transplant 1992;11:733-738.[Medline]
2. Rockman H.A., Adamson R.M., Dembitsky W.P., Bonar J.W., Jaski B.E. Acute fulminant myocarditis. Am Heart J 1991;121:922-926.[Medline]
3. Chang A.C., Hanley F.L., Weindling S.N., Wernovsky G., Wessel D.L. Left heart support with a ventricular assist device in an infant with acute myocarditis. Crit Care Med 1992;20:812-815.
4. Holman W.L., Bourge R.C., Kirklin J.K. Case report. J Thorac Cardiovasc Surg 1991;102:932-934.[Medline]
5. Martin J.M., Sarai K., Schindler M., van de Loo A., Toshitake M., Beyersdorf F. MEDOS HIA-VAD biventricular assist device for bridge to recovery in fulminant myocarditis. Ann Thorac Surg 1997;63:1145-1146.[Abstract/Free Full Text]
6. Farrar D., Hill J.D., Pennington D.G., et al. Preoperative and postoperative comparison of patients with univentricular and biventricular support with the Thoratec ventricular assist device as a bridge to cardiac transplantation. J Thorac Cardiovasc Surg 1997;113:202-209.[Abstract/Free Full Text]

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