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J Thorac Cardiovasc Surg 2008;135:690-691
© 2008 The American Association for Thoracic Surgery
Brief Communication |
a Department of Cardiothoracic Surgery, National Heart Centre, Singapore
b Department of Cardiology, National Heart Centre, Singapore
Received for publication August 30, 2007; accepted for publication October 19, 2007. * Address for reprints: Masakazu Nakao, National Heart Center, Department of Cardiothoracic Surgery, Mistri Wing, 17 Third Hospital Ave, Singapore 168752. (Email: masakazu.nakao{at}nhc.com.sg).
Atrial septal perforation (ASP) is a known complication after percutaneous transvenous mitral commissurotomy (PTMC), although it usually spontaneously heals. In cases in which ASP persists, the shunting is predominantly left to right, and rarely does the shunting reverse to cause clinical cyanosis.
A 49-year-old woman with a history of longstanding rheumatic heart disease presented with breathlessness and cyanosis, as well as bilateral lower limb swelling, for 2 weeks. She had undergone closed mitral valvotomy 26 years ago and subsequent PTMC twice 14 and 4 years ago, respectively. Other significant medical histories are atrial fibrillation and diabetes mellitus. Recent transthoracic echocardiography (TTE) 1 year ago showed moderate mitral stenosis (MS) with a mitral valve area of 1.3 cm2, mild mitral regurgitation (MR), severe tricuspid regurgitation (TR) with a pulmonary artery systolic pressure of 38 mm Hg, and a small atrial septal defect with left-to-right shunt, which was already shown on TTE 4 years ago after the second PTMC. Ejection fraction was 55%. She had mild congestive cardiac failure (CCF) with multiple hospital admissions within the last few months.
She presented this admission with exacerbation of breathlessness and was found to be in CCF. She was centrally cyanosed, and oxygen saturation on room air was 80% to 86%. TTE revealed right-to-left shunt through an ASP of 0.7 cm in diameter, severe MS, trivial MR, and severe TR with a dilated annulus (
Figure 1).
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The patient improved with diuresis and subsequently agreed to surgical intervention.
Atrial septal repair with mitral valve replacement and tricuspid valve repair was performed with median sternotomy. On sternotomy, the right atrium was found to be enlarged and tense. Central venous pressure was 33 mm Hg. Cardiopulmonary bypass was instituted routinely, with aortic and bicaval cannulation. An ASP was confirmed in the central part of the interatrial septum. The mitral valve was exposed through a transseptal approach by enlarging the ASP; the valve and annulus were noted to be heavily calcified, with severe subvalvar involvement. The mitral valve was then replaced with a 29-mm Mosaic porcine bioprosthetic valve (Medtronic, Inc, Minneapolis, Minn). The interatrial septum was repaired. The tricuspid valve was then repaired with a 26-mm Edwards MC3 annuloplasty ring (Edwards LifeSciences, Irvine, Calif).
Postoperative TTE showed no residual shunt between the right and left atria. There was satisfactory bioprosthetic valve function with no MR, a pressure gradient of 4 mm Hg, and mild-to-moderate TR. Postoperative recovery was uncomplicated, and the patient was discharged on the 11th postoperative day.
Inoue and colleagues1 reported PTMC in 1984 using an interatrial septal puncture. ASP is a well-known but rare complication of PTMC. Ishikura and associates2 reported that 15.2% of patients after PTMC were found to have an ASP 1 day after the procedure on TTE, and 4.3% of these persisted more than 1 year. However, none of these shunts were clinically significant. They were also normally left-to-right shunts and did not cause cyanosis. On rare occasions, however, the combination of MS, TR, and PHT can result in an right-to-left shunt, leading to cyanosis.3
Prior admissions for CCF showed a constant left-to-right shunt, which was noted on serial echocardiographic analysis for the past 4 years. The patient had cyanosis on this admission in conjunction with recurrent CCF. TTE then revealed shunt reversal, explaining the onset of cyanosis.
One possible cause of shunt reversal was that the severe TR was directing the flow into the ASP, causing shunting to the left atrium as the severity increased. Another possibility was the change in the pressure gradient between the left and right atria: the pressure in the right atrium was 5 mm Hg higher than the pulmonary capillary wedge pressure at the time of the right heart study. This might be due to the combination of worsening pulmonary hypertension and TR.
A reversal of shunt needs to be considered when there is a sudden onset of cyanosis during the follow-up after PTMC for MS. In such cases surgical correction should be considered in the treatment options, especially in the setting of significant valve disease.
References
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