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Ann Thorac Surg 2002;73:652-653
© 2002 The Society of Thoracic Surgeons
a Department of Cardiothoracic Surgery, The Prince of Wales Hospital, The University of New South Wales, Sydney, New South Wales, Australia
Accepted for publication May 14, 2001.
* Address reprint requests to Dr Iliopoulos, Department of Cardiothoracic Surgery, Prince of Wales Hospital, Barker St, Randwick, N.S.W., Australia, 2031
e-mail: jimiliopoulos{at}hotmail.com
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Introduction |
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A 29-year-old man was admitted to a hospital after experiencing an episode of collapse in association with chest pain at rest. There was a 4-month history of exertional chest pain and palpitations. There was a known history of PXE, which was diagnosed in childhood by skin biopsy. There were no risk factors for arteriosclerosis, and the family history was unremarkable.
On examination the patient appeared well, and the vital signs were unremarkable. The heart sounds were normal, and there were no cardiac murmurs. The radial and ulnar pulses were weak bilaterally, as were the dorsalis pedis and posterior tibial pulses.
Full blood count, erythrocyte sedimentation rate, serum biochemistry, and thyroid function tests returned normal results. Fasting glucose and lipid studies had normal results, as did coagulation studies. There was no rise in cardiac enzymes.
The resting electrocardiogram showed ST-segment elevations in lead V3. There were no further ischemic changes in serial electrocardiograms. Two-dimensional echocardiography revealed mild concentric left ventricular hypertrophy, but results were otherwise normal. Chest radiography was unremarkable.
Coronary angiography demonstrated the presence of severe triple-vessel disease with a tight proximal lesion in a large left anterior descending artery. There was total occlusion of a small marginal circumflex branch, and there was total occlusion of the right coronary artery, which filled retrogradely. Left ventriculography returned normal results, with a calculated ejection fraction of 0.59. The LIMA was not studied angiographically.
In August 1997, using standard cardiopulmonary bypass with topical and systemic hypothermia and cold anterograde cardioplegic arrest, double coronary artery bypass grafting was performed. Segments of reversed long saphenous vein were anastomosed end-to-side to the right coronary artery and to the left anterior descending artery.
The postoperative course was unremarkable, and the patient was discharged home on day 5 postoperatively. The patient has remained asymptomatic postoperatively.
Coronary angiography performed at 36 months postoperatively showed patent grafts, which were disease free, with good run-off. There were no significant changes in the native circulation. Angiography of the LIMA showed a patent vessel that was macroscopically free of disease.
Informed consent was obtained from the patient for all investigations and surgical interventions.
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Cardiovascular complications are common and result from elastic fiber degeneration and calcification of the internal elastic lamina of medium-sized arteries. Cardiovascular complications include premature coronary artery disease, cerebrovascular disease, peripheral vascular disease, renovascular hypertension, and, less commonly, restrictive cardiomyopathy, fibrous thickening of the endocardium, and mitral valve disease [7, 8].
There are seven reports in the literature of patients with PXE who have undergone coronary artery revascularization [1–6].
In view of the patient’s history of PXE, its predilection for medium-sized arteries, and the uncertainty regarding progression of LIMA disease with grafting, we decided not to use the LIMA as a conduit. However, angiographic examination of this vessel at 36 months postoperatively showed a patent in situ vessel with no stenosis, suggesting it may safely have been used as a conduit in the initial procedure.
The use of the LIMA as a conduit has been criticized by a number of authors because some form of disease has been found in the LIMA in the 4 PXE patients who have undergone coronary artery bypass grafting when the LIMA has been considered for use as a conduit [2, 4–6]. Two specimens were not stenosed but showed calcification of the internal elastic lamina and media on histologic examination, and the LIMA was used as a conduit in these patients [2, 4]. The foci of calcification in these nonstenosed vessels were small (50 µm to 100 µm in diameter). In the two other cases, the LIMA was found to be stenosed at operation and was not used as a conduit [5, 6].
The natural history of LIMA disease in PXE is unknown, as are the effects of harvesting and anastomosis on the progression of the disease in the LIMA. Furthermore, there is no angiographic evidence of early occlusion of LIMA grafts in PXE patients who have undergone coronary artery revascularization [2, 4]. Whether to use the LIMA as a conduit in patients with PXE is therefore unclear.
We believe that a diagnosis of PXE does not preclude the use of LIMA grafts for coronary artery revascularization provided that angiographic evaluation of the LIMA is undertaken at the time of coronary angiography. Surgical revascularization may be feasible using a LIMA that has been shown to be patent on angiography. However, careful follow-up of the patient will be required, because the effect of surgical intervention on the disease process in the LIMA is unknown. Any angiographic stenosis of the LIMA precludes its use as a conduit.
PXE patients undergoing coronary artery bypass grafting at a young age may represent for reoperation. The use of saphenous vein graft at the initial operation allows a longitudinal study of the LIMA in situ, such that if reoperation is required, a patent LIMA may be used as a conduit.
In conclusion, coronary artery revascularization remains a feasible and beneficial treatment for coronary artery disease in patients with PXE. Careful angiographic evaluation of the LIMA and coronary arteries is required in patients with PXE with suspected coronary artery disease. A nonstenosed LIMA at angiography may be used as a conduit for coronary artery revascularization; however, both the effect of harvest and anastomosis on the disease process in the LIMA and the long-term patency of LIMA grafts remain unknown.
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