Ann Thorac Surg 2004;78:1066-1068
© 2004 The Society of Thoracic Surgeons
Case report
Bidirectional cavopulmonary shunt for acute right ventricular failure in an adult patient
Takashi Kunihara, MDa,
Vakhtang Dzindzibadze, MDa,
Diana Aicher, MDa,
Hans-Joachim Schäfers, MDa,*
a Department of Thoracic and Cardiovascular Surgery, University Hospital Homburg, Homburg, Germany
Accepted for publication June 25, 2003.
* Address reprint requests to Dr Schäfers, Department of Thoracic and Cardiovascular Surgery, University Hospital Homburg, Kirrberger Strasse 1, Homburg/Saar D-66421, Germany
chhjsc{at}uniklinik-saarland.de
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Abstract
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Right ventricular failure due to right coronary occlusion is an uncommon but serious complication of acute aortic dissection. We report a patient with right coronary occlusion from acute type A aortic dissection who developed right ventricular failure that persisted after proximal aortic repair, rendering weaning from extracorporeal circulation unsuccessful. With a bidirectional cavopulmonary shunt and the use of an intraaortic balloon, the patient could be weaned successfully from cardiopulmonary bypass. This procedure may be an alternative to a right ventricular assist device in selected candidates.
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Introduction
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As acute aortic dissection frequently involves aortic branch vessels, coronary artery malperfusion is not uncommon and greatly influences the patient's prognosis [1, 2]. Right ventricular (RV) failure is a possible consequence of right coronary artery (RCA) ischemia, and is difficult to treat [3]. We report on a patient with acute inferior myocardial infarction (MI) due to acute aortic dissection type A (AADA) who underwent proximal aortic repair. Because of extreme difficulty in weaning from cardiopulmonary bypass (CPB) in spite of an additional coronary arterial bypass grafting (CABG), we performed a bidirectional cavopulmonary shunt (BCPS). Weaning from CPB was then successful.
A 36-year-old man with a past history of coarctation repair was admitted to another hospital with acute chest pain. An acute inferior MI was diagnosed and treated by thrombolysis (maximal creatine kinase, 760 U/L; MB fraction, 55 U/L). Electrocardiogram showed ST segment elevation in leads II and III, and aVF that subsequently changed to inverted T wave with Q wave. Four days later, persistent pain and increasing dyspnea led to computed tomography examination, which revealed AADA. He was then transferred to our hospital and underwent emergency surgery.
During induction, the patient became hypotensive and required increasing vasopressor support. Central venous pressure (CVP) was 27 mm Hg. The chest was opened through a median sternotomy. Right ventricular function appeared markedly impaired and there was minimal pericardial effusion. Cardiopulmonary was established using right axillary artery and right atrium for cannulation. During core cooling, the ascending aorta was cross-clamped and cardioplegia was given directly into the coronary ostia. The aortic valve was found bicuspid and the RCA ostium compressed by the false lumen. Partial aortic arch replacement was performed using hypothermic circulatory arrest (21°C, 12 minutes). Circulation was resumed, and the aortic root was remodeled. The ostium of the RCA was reconstructed and anastomosed to the Dacron graft. Coronary circulation was resumed after a cross-clamp time of 106 minutes. After sufficient reperfusion, RV contractility was still severely impaired. Using a segment of the saphenous vein, a CABG was anastomosed to the RCA and two RV coronary branches. An intraaortic balloon pump (IABP) was inserted to minimize left atrial pressure. Nevertheless, it was impossible to conclude CPB due to persistent RV failure despite preserved left ventricular (LV) function. At 50% of CPB flow, CVP increased to 14 mm Hg with pulmonary arterial (PA) pressure at similar level and left atrial pressure of 5 mm Hg. Systemic output did not improve with inhalation of iloprost. With diffuse bleeding and normal PA pressure, the patient did not appear to be a good candidate for RV assist device (RVAD). Instead, we performed a bidirectional cardiopulmonary shunt between the superior vena cava and the right pulmonary artery, and vasopressors as well as inhalative treatment with iloprost were continued. The patient could be weaned from CPB after 251 minutes. Immediately after the procedure, RV contractility, as determined by inspection and transesophageal echocardiography, was almost absent. Nevertheless, the dosage of vasopressors could be reduced to 0.5 µg/kg/min, with a CVP (superior cava tributary) of 20 mm Hg.
The postoperative course was without major complications. Central venous pressure rose to a maximum of 23 mm Hg under continued administration of vasopressors and nebulized iloprost. Venous pressure decreased to 18 mm Hg until the first postoperative day. The IABP was removed on the 2nd postoperative day, and the patient was extubated on postoperative day 5 with a CVP of 13 mm Hg. Repeated TEE studies during the postoperative period showed almost absent RV contractility until day 4. Contractility then improved slowly to an estimated RV ejection fraction of 20% on day 10. He was discharged 19 days postoperatively with a medication of Cumarin (phenprocoumon), which was discontinued after 3 months. Two months after discharge, the patient underwent heart catheterization, which demonstrated a patent BCPS and CABG (Fig 1). No obstruction was seen in his coronary arteries. There was mild hypokinesia in the LV inferior wall, and RV function became normal as determined by echocardiography and angiography. Hemodynamic examination disclosed PA pressure of 24/10 mm Hg and cardiac output of 4.9 L/min. A grade I-II aortic valve insufficiency was observed; this has remained stable 18 months postoperatively.
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Comment
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Coronary artery malperfusion is not uncommon in AADA. It occurs in 10% of reported cases and frequently involves the RCA [1, 2]. In most instances, RCA flow can be rapidly restored by either ostial reconstruction or CABG. When myocardium is damaged irreversibly, however, due to delay in diagnosis or treatment, RV failure will ensue. Post-CPB RV failure is seen less frequently than LV failure, and it is important to differentiate between reduced contractility and increased afterload in its treatment [3]. The IABP may be introduced for mild reduction of left atrial and thus also PA pressures. A right ventricular assist device may be the most effective solution in this situation; it has, however, the disadvantages of bleeding and infection [4]. We have already applied RVAD to previous patients with AADA who developed RV failure with catastrophic consequences. This patient also exhibited diffuse bleeding; therefore, we hesitated to implant RVAD and performed BCPS. Our decision therefore appeared as an unconventional, but appealing solution, and indeed, it led to rapid stabilization of hemodynamic function.
A BCPS was first described clinically in 1985 and has been mainly performed as a palliative treatment in pediatric patients for cyanotic congenital heart disease [5]. Whereas it has been used only rarely in adults, it may still have a value in selected patients with more advanced age, provided there is no preexistent increase in PA resistance due to pulmonary disease [6]. It can augment pulmonary flow without increasing RV work in congenital heart disease or maintain pulmonary flow while decreasing RV work, such as in our patient. Furthermore, it requires no anticoagulation in the early postoperative period, which is a major advantage, especially for patients with diffuse bleeding tendency. Therefore, it may be justified as a last resort for patients with RV failure in the absence of pulmonary hypertension when LV function is preserved.
The question remains whether this aid in the acute period may leave young patients with an irreversible potential problem, whereas an RVAD is a reversible solution. Longer observations will be necessary to answer this question. In addition, restoration of a normal anatomic situation by reoperation is a realistic option, should it become necessary by hemodynamic alterations. It may also be debated when to introduce a procedure such as a Glenn. This, however, is similar to the common situation of ventricular failure, in which a decision for a VAD has to be made. In our patient, neither coronary revascularization nor prolonged CPB support led to any recognizable recovery of RV function. Although conceptually promising, the management of acute RV failure using a BCPS lacks the support of long-term follow-up data. Despite this limitation, we believe this procedure may be a useful alternative in selected candidates.
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References
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Abstract
Introduction
