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Eur J Cardiothorac Surg 2003;23:139-140
© 2003 Elsevier Science NL
Letter to the Editor |
Department of Cardiovascular Surgery, Bursa Yüksek Ihtisas Teaching and Research Hospital, Duacinari, 16330 Bursa, Turkey
Received 1 October 2002; accepted 17 October 2002.
* Corresponding author. Tel.: +90-224-360-5050; fax: +90-224-360-5055
e-mail: syavuz{at}ttnet.net.tr
Key Words: Iatrogenic left main coronary artery stenosis Aortic valve replacement Coronary artery bypass grafting
We thank Dr Demaria et al. for their valuable comments and interest in our recent publication [1], and we are honored by the attention paid to our work.
We have read their article recently published in Cardiovascular Surgery [2]. In their retrospective study, they have also observed the findings similar to our case.
Dr Demaria et al. offer an additional useful tip for the etiology of endothelial dysfunction [3]. We agree that the safest technique for morphological and functional preservation of the coronary artery endothelial and muscular layers remains to be established.
Iatrogenic stenosis of the left main coronary artery is a disastrous complication after aortic valve replacement (AVR). The true incidence of this complication is not known. However, there must be more cases that have not been reported, and the natural history of this condition leads to inevitable death.
As we state in our article, the etiology of these lesions remains unproven, but most likely they represent mechanical injury to the vessel wall because of cannulation of the coronary ostia or because of the pulsatile pressure of the perfusing balloon cannula, and fibrous proliferation in the aortic root secondary to turbulent flow around a prosthetic valve.
At an autopsy study, Trimble et al. [4] reported that histologically, at the ostia and in the areas of coronary arterial stenosis, the intima was markedly thickened by loose cellular fibromuscular connective tissue and morphologically, the intimal thickening was distinctly different from that caused by atherosclerosis.
We appreciate the opportunity to compare our agreements with Dr Demaria et al. As they describe in their letter and we state in our article, various measures to prevent the development of iatrogenic left main coronary artery stenosis during coronary arterial perfusion include using retrograde delivery as an alternative method of myocardial protection, avoiding placement of sutures around coronary ostia to secure perfusion cannula, avoidance of high pressure flow, maintenance of coronary perfusion under 100 mmHg, and no using a too-large coronary perfusion cannula.
Whatever the etiology is, coronary ostial stenosis must be suspected in patients who develop recent onset of severe angina, ventricular arrhythmias or congestive heart failure after AVR. Surgical intervention (coronary artery bypass grafting or surgical angioplasty) should be performed without delay.
References
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