Ann Thorac Surg 2002;74:584-586
© 2002 The Society of Thoracic Surgeons
Case report
Echocardiographic evidence of right ventricular remodeling after transplantation
Holger K. Eltzschig, MDa,
Tomislav Mihaljevic, MDb,
John G. Byrne, MDb,
Raila Ehlers, MDc,
Brian Smith, RDCSa,
Stanton K. Shernan, MD*a
a Department of Anesthesiology, Perioperative and Pain Medicine, Boston, Massachusetts, USA
b Division of Cardiac Surgery, Boston, Massachusetts, USA
c Cardiovascular Division, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA
Accepted for publication February 27, 2002.
* Address reprint requests to Dr Shernan, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women’s Hospital, Harvard Medical School, 75 Francis St, Boston, MA 02115 USA
e-mail: shernan{at}zeus.bwh.harvard.edu
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Abstract
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Right ventricular (RV) failure is a significant source of mortality after cardiac transplantation. The use of RV assist devices (RVAD) as a bridge to recovery has been reported. However, early changes of RV structure and anatomy after RVAD implantation have yet to be described. We report a case of RV failure after transplantation requiring RVAD implantation. After 3 weeks of gradual weaning of inotropic and RVAD support, the device was explanted successfully. Transesophageal echocardiography documents RV hypertrophy and remodeling between RVAD implantation and removal, suggesting a rapid adaptive response of the right ventricle in the presence of pulmonary hypertension.
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Introduction
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Right ventricular (RV) failure remains a leading cause of early death after orthotopic heart transplantation (OHT). Usually RV failure is related to persistent recipient pulmonary hypertension associated with a history of chronic congestive heart failure. Failure of the donor’s right ventricle to adapt to increased pulmonary vascular resistance (PVR) leads to hemodynamic collapse. Strategies to improve ventricular mechanics include reducing PVR with vasodilators and increasing RV contractility with inotropic agents [1, 2]. Use of a right ventricular assist device (RVAD) is indicated when refractory RV failure is present despite maximal pharmacological therapy. RVAD support is effective as a bridge to RV recovery, particularly if implanted before end-organ injury becomes irreversible [3]. However, echocardiographic evidence of adaptive changes of the right ventricle to elevated PVR after RVAD implantation has not been described previously. We present a patient in whom transesophageal echocardiography demonstrated anatomical and functional changes of the right ventricle associated with RVAD weaning.
A 20-year-old male presented for OHT. At age 4 he was diagnosed with a Wilms’ tumor and treated by nephrectomy and adriamycin chemotherapy. He subsequently developed adriamycin-induced cardiomyopathy. In addition he underwent wedge resection of a right pulmonary nodule followed by radiation therapy. During evaluation for cardiac transplantation he was found to have pulmonary hypertension caused by both chronic congestive heart failure and radiation-induced pulmonary fibrosis. Because intravenous vasodilator therapy resulted in only partial reversal of the elevated PVR (a decrease from 350 to 300 dynes · sec · cm-5), he was considered a high-risk transplant candidate [4].
Orthotopic heart transplantation was performed without technical difficulty (total donor ischemic time < 90 minutes) using an excellent donor organ. However, when attempting to wean the patient from cardiopulmonary bypass, he developed severe isolated RV dysfunction. Despite maximal pharmacological support, including inhaled nitric oxide, the patient could not be weaned from cardiopulmonary bypass. Intraoperative transesophageal echocardiography revealed a dilated right ventricle with a globally hypokinetic appearance and thin walls (Fig 1).
There was evidence of interventricular septal bowing towards the left ventricle during systole. An RVAD (Thoratec Corp, Pleasanton, CA) was implanted through the right atrium and main pulmonary artery, and the patient was brought to the intensive care unit with stable hemodynamics. During the next 3 weeks, the patient was extubated and the inotropic medications were weaned. In an asynchronous mode the RVAD rate was decreased sequentially from 60 to 20, followed by decreasing the vacuum. This was accompanied by a change in RVAD flow from 6 to 1.3 L/min. At this point the patient was fully anticoagulated and tolerated a hand pump trial without hemodynamic compromise. PVR remained unchanged between 270 and 300 dynes · sec · cm-5 throughout the weaning period. On postoperative day 22 the RVAD was successfully explanted. Intraoperative transesophageal echocardiography demonstrated RV hypertrophy, fractional shortening of more than 40%, and no signs of RV failure (Fig 2).
The patient was discharged home after 18 days of an unremarkable postoperative course. He subsequently resumed a normal life as a college student.
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Fig 1. Intraoperative transesophageal echocardiography (mid-esophageal four-chamber view) after orthotopic cardiac transplantation while attempting to wean the patient from cardiopulmonary bypass demonstrates severe right ventricular failure. During systole, the interventricular septum bows towards the left ventricle. The right ventricle appears hypokinetic and dilated: right ventricular free wall (a) = 7 mm; interventricular septum (b) = 10 mm. (LV = left ventricle; RV = right ventricle.)
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Fig 2. Intraoperative transesophageal echocardiographic imaging of the right ventricle during removal of the right ventricular assist device on posttransplant day 22. (A) The right ventricle appears hypertrophic without signs of failure (mid-esophageal four-chamber view): right ventricular free wall (a) = 13 mm; interventricular septum (b) = 18 mm. (B) Echocardiographic M-mode evaluation of the right ventricle (transgastric mid-short axis view) demonstrates fractional shortening of 40%: diastolic diameter (D) = 33 mm; systolic diameter (S) = 19 mm. (LV = left ventricle; RA = right atrium; RV = right ventricle.)
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Comment
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This case report presents echocardiographic evidence of the RV adaptive response to increased PVR after OHT during 3 weeks of RVAD support and subsequent sequential weaning. The fact that the PVR remained stable throughout the weaning period underlines that the adaptive process was caused by a change in right ventricular performance as opposed to a reduction in pulmonary hypertension. Echocardiographic signs of RV remodeling and recovery include an 80% increase in wall thickness and concomitant functional improvement. RV performance and adaption to induced pulmonary hypertension after OHT has been studied experimentally, suggesting that the hypertrophic response may be associated with an increase in 
1-adrenergic receptor density [5]. Chen and colleagues [6] demonstrated that in the setting of experimentally induced pulmonary hypertension, RV performance adapts after OHT by significantly increasing power and contractility. However, clinical evidence including echocardiographic images of changes in RV ejection fraction or wall thickness has not been previously published. This case report supports the utility of RVAD implantation as a bridge to recovery in the setting of acute RV failure after OHT in recipients who are high-risk candidates due to pulmonary hypertension.
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References
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- Ardehali A., Hughes K., Sadeghi A., et al. Inhaled nitric oxide for pulmonary hypertension after heart transplantation. Transplantation 2001;72(4):638-641.[Medline]
- Chen E.P., Bittner H.B., Davis R.D., Van Trigt P. Hemodynamic and inotropic effects of milrinone after heart transplantation in the setting of recipient pulmonary hypertension. J Heart Lung Transplant 1998;17:669-678.[Medline]
- Chen J.M., Levin H.R., Rose E.A., et al. Experience with right ventricular assist devices for perioperative right-sided circulatory failure. Ann Thorac Surg 1996;61:305-313.[Abstract/Free Full Text]
- Costard-Jackle A., Fowler M.B. Influence of preoperative pulmonary artery pressure on mortality after heart transplantation: testing of potential reversibility of pulmonary hypertension with nitroprusside is useful in defining a high risk group. J Am Coll Cardiol 1992;19:48-54.[Abstract]
- Chen E.P., Akhter S.A., Bittner H.B., Koch W.J., Davis R.D., Van Trigt P., 3rd Molecular and functional mechanisms of right ventricular adaptation in chronic pulmonary hypertension. Ann Thorac Surg 1999;67:1053-1058.[Abstract/Free Full Text]
- Chen E.P., Bittner H.B., Davis R.D., Van Trigt P. Right ventricular adaptation to increased afterload after orthotopic cardiac transplantation in the setting of recipient chronic pulmonary hypertension. Circulation 1997;96(Suppl 9):II141-II147.
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Abstract
Introduction
