Abstract

We thank the readers for their comments, and we were very interested to see that they have obtained a similar incidence of cTnI elevation in 29% of patients after elective open aortic reconstruction at a unit that did not perform endovascular abdominal aortic aneurysm repair at the time. This, in our opinion, would confirm our results that there is a statistically and almost certainly clinically significant difference in the incidence of subclinical myocardial damage after the two types of infrarenal abdominal aortic aneurysm repair. In our two groups of patients, the preoperative management did not include routine β-blockade and statin therapy. Although this was not prospectively documented, medical optimization was more likely to have taken place in the open group in view of the degree of severity of the planned procedure. It is quite unlikely that medical optimization would have contributed to the reduction in myocardial injury associated with endovascular repair. Our study protocol, as approved by the local ethics committee, dictated analysis of all samples in batches in a way that was not related to the day-to-day management of the individual patient. This was to avoid unnecessary interventions based on the results of a serum analysis that under normal circumstances would not take place according to the best current practice of that time, because troponin measurement is not a routine part of postoperative patient care. Regarding “A prospective study of subclinical myocardial damage in endovascular versus open repair of infrarenal abdominal aortic aneurysms”Journal of Vascular SurgeryVol. 42Issue 3PreviewWe read with interest the article by Abraham et al (J Vasc Surg 2005;41:377-81) reporting increased levels of cardiac troponin (cTn) T in 9% of patients after elective endovascular repair and 25% of patients after elective open repair of infrarenal abdominal aortic aneurysm. These findings are similar to our own, in which increased levels of cTnI were detected in 10 (29%) of 35 patients after elective open aortic reconstruction.1 Because our study was performed in a unit that did not perform endovascular abdominal aortic aneurysm repair at the time, it seems unlikely that the authors’ suggestion that institutional unfamiliarity with open aortic surgery, or more advanced arterial disease in patients unsuitable for endovascular repair, can adequately explain the higher incidence of myocardial injury in the open repair group. Full-Text PDF Open Archive

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