Regarding “Outcomes for symptomatic abdominal aortic aneurysms in the American College of Surgeons National Surgical Quality Improvement Program”

Regarding “Outcomes for symptomatic abdominal aortic aneurysms in the American College of Surgeons National Surgical Quality Improvement Program”

1548 Journal of Vascular Surgery Letters to the Editor May 2017 Gheorghe Doros, PhD Denis V. Rybin, PhD Department of Biostatistics Boston School ...

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1548

Journal of Vascular Surgery

Letters to the Editor

May 2017

Gheorghe Doros, PhD Denis V. Rybin, PhD Department of Biostatistics Boston School of Public Health Boston, Mass

REFERENCES 1. Eslami MH, Rybin DV, Doros G, Farber A. Description of a risk predictive model of 30-day postoperative mortality after elective abdominal aortic aneurysm repair. J Vasc Surg 2016;65:65-74.e2. 2. Harrell F. Regression modeling strategies: with applications to linear models, logistic and ordinal regression, and survival analysis. New York: Springer; 2015. 3. Ambler GK, Gohel MS, Mitchell DC, Loftus IM, Boyle JR. The Abdominal Aortic Aneurysm Statistically Corrected Operative Risk Evaluation (AAA SCORE) for predicting mortality after open and endovascular interventions. J Vasc Surg 2015;61: 35-43. 4. Eslami MH, Rybin D, Doros G, Kalish JA, Farber A; Vascular Study Group of New England. Comparison of a Vascular Study Group of New England risk prediction model with established risk prediction models of in-hospital mortality after elective abdominal aortic aneurysm repair. J Vasc Surg 2015;62:1125-33. http://dx.doi.org/10.1016/j.jvs.2016.12.091

Regarding “Outcomes for symptomatic abdominal aortic aneurysms in the American College of Surgeons National Surgical Quality Improvement Program” We have read with great interest the recently published study by Soden et al,1 where the authors have tried to evaluate and compare major postoperative outcomes among patients treated for asymptomatic, symptomatic, and ruptured abdominal aortic aneurysms (AAAs). However, some points need to be made. First, in the asymptomatic nonruptured group, the authors report that “patients with prior open repair with unsatisfactory result or prior endovascular repair with unsatisfactory result” were included, “because symptomatic and rupture groups contained some of these patients as well.” However, the authors should explain and define the term “unsatisfactory results.” After endovascular repair, a continuing aneurysm enlargement or a type I endoleak is a definite indication for new aneurysm treatment. However, in open surgery, which could be an indication for new aneurysm treatment, except if for an abdominal pseudoaneurysm? Moreover, in the case of endovascular repair, the authors declare that no case of conversion from endovascular to open repair was included. In our opinion, a more detailed report of those patients would be more informative. Secondly, the authors report very high rates of symptomatic or ruptured AAAs among patients treated for aneurysms <5 cm in diameter (11% symptomatic and

15% ruptured for diameter <4 cm), without discussing this finding. As we have underlined recently,2 pooled data indicate that for each 0.5-cm increase in the diameter of small AAAs, growth rate of the aneurysm increases also by w0.59 mm per year and the rupture rate by a factor of w1.91.3 However, Lo et al4 showed in a large study of >4000 patients that men exhibited an odds ratio of only 1.0 for rupture risk in AAAs <5.5 cm, and women also showed no correlation between AAA diameter and rupture. Therefore, careful identification of symptoms, even in patients with small AAAs, is imperative to correctly report them as symptomatic and not misinterpret research outcomes. Finally, the correct timing for treating a symptomatic AAA remains a controversial issue. The authors report that one-half of the symptomatic patientsdnot the rupturesdwere treated on the next day of the admission, almost one-third within the next 3 days, and the rest (21%) afterwards. However, providing any information concerning the number of patients that presented with a rupture during this time of delay would be useful as well. The latest guidelines on proper management of patients with AAA suggest that ruptured cases should be treated as an emergency, although symptomatic cases (not ruptures) could be delayed up to 48 hours in selected patients that could perhaps benefit from preoperative preparation and optimization.5 Therefore, research studies should focus on the identification or stratification of such patients in order to improve postoperative outcomes.

Konstantinos Filis, MD, PhD George Galyfos, MD, PhD Vascular Unit First Department of Propedeutic Surgery University of Athens Medical School Ippokration Hospital Athens, Greece

REFERENCES 1. Soden PA, Zettervall SL, Ultee KH, Darling JD, Buck DB, Hile CN, et al. Outcomes for symptomatic abdominal aortic aneurysms in the American College of Surgeons National Surgical Quality Improvement Program. J Vasc Surg 2016;64: 297-305. 2. Galyfos G, Voulalas G, Stamatatos I, Kerasidis S, Stefanidis I, Giannakakis S, et al. Small abdominal aortic aneurysms: should we wait? Vasc Dis Manage 2015;12:152-9. 3. RESCAN Collaborators; Bown MJ, Sweeting MJ, Brown LC, Powell JT, Thompson SG. Surveillance intervals for small abdominal aortic aneurysms: a meta-analysis. JAMA 2013; 309:806-13. 4. Lo RC, Lu B, Fokkema MT, Conrad M, Patel VI, Fillinger M, et al; Vascular Study Group of New England. Relative importance of aneurysm diameter and body size for predicting abdominal aortic aneurysm rupture in men and women. J Vasc Surg 2014;59:1209-16.

Journal of Vascular Surgery

Letters to the Editor

1549

Volume 65, Number 5 5. Moll FL, Powell JT, Fraedrich G, Verzini F, Haulon S, Waltham M, et al; European Society for Vascular Surgery. Management of abdominal aortic aneurysms clinical practice guidelines of the European Society for Vascular Surgery. Eur J Vasc Endovasc Surg 2011;41(Suppl 1):S1-58. http://dx.doi.org/10.1016/j.jvs.2016.11.051

Reply We appreciate the opportunity to respond to comments made by Filis and Galyfos. Regarding their first point, that “unsatisfactory results” should be further explained, we are, unfortunately, limited by the constraints of using a clinical registry without being able to further define each preset collected data measure from contributing hospitals nationally. Only one indication for each procedure is captured within the National Surgical Quality Improvement Program (NSQIP), and clinical reviewers take this directly from the operative note of the treating physician. Therefore, determining what consisted of an unsatisfactory result of prior repair, whether by endovascular aneurysm repair (EVAR) or open repair, is left to the discretion of the treating physician. Inclusion of this group in patients undergoing repair of asymptomatic aneurysms would only increase the 30-day mortality and morbidity, making the difference between asymptomatic and symptomatic aneurysms that much more striking. We also did not want to include acute conversions from EVAR to open repair because there were too few cases of this for a meaningful analysis, we did not have enough data to describe what led to the conversion, and it was outside of the scope of our manuscript. For the second point, we agree that symptomatic aneurysms could potentially be misdiagnosed; however, all patients identified as having symptomatic aneurysms in the NSQIP were diagnosed by the treating physician, and therefore, we believe the diagnosis was as accurate as possible. The NSQIP defines symptomatic as an aneurysm causing abdominal or back pain or causing local compressive symptoms and that is not ruptured. Furthermore, we believe the strength and utility of clinical registries is demonstrated in our manuscript, which allowed for the analysis of a much greater number of symptomatic aneurysms than was previously possible.1 In the analysis by Lo et al,2 only patients undergoing surgery #24 hours of symptom onset were included in the intact aneurysm group, and there was a much lower use of EVAR for repair of intact and ruptured aneurysms (53% EVAR for intact aneurysms in Lo et al2 vs 80% for intact aneurysms in our analysis), making a direct comparison difficult. However, we agree that aneurysm diameter is not the perfect measure of risk for rupture

and that additional measures, such as aortic size index and sac contour and growth rate, are also important predictors of rupture. Finally, we agree that timing is important and that certain symptomatic aneurysms are more likely to rupture than others, especially when taking into account the inclusion of aneurysms causing pain and also those causing locally compressive symptoms, as mentioned in our manuscript. Unfortunately we are unable to identify within the NSQIP the exact time of admission and operation because these are recorded by hospital day and not hours. We do agree that it is important for future research to identify potential radiographic and laboratory markers that could help stratify risk of rupture among patients with symptomatic aneurysms. Currently, NSQIP data are unable to answer these questions.

Peter A. Soden, MD Marc L. Schermerhorn, MD Beth Israel Deaconess Medical Center Boston, Mass

REFERENCES 1. De Martino RR, Nolan BW, Goodney PP, Chang CK, Schanzer A, Cambria R, et al. Outcomes of symptomatic abdominal aortic aneurysm repair. J Vasc Surg 2010;52:5-12.e1. 2. Lo RC, Lu B, Fokkema MT, Conrad M, Patel VI, Fillinger M, et al; Vascular Study Group of New England. Relative importance of aneurysm diameter and body size for predicting abdominal aortic aneurysm rupture in men and women. J Vasc Surg 2014;59:1209-16. http://dx.doi.org/10.1016/j.jvs.2016.12.093

Regarding “Perioperative and long-term impact of chronic kidney disease on carotid artery interventions” We read with great interest the article by Klarin et al,1 recently published in the Journal of Vascular Surgery, on the 30-day and long-term effect of chronic kidney disease (CKD) after carotid endarterectomy or carotid artery stenting. The authors concluded that worsening renal function, assessed by estimated glomerular filtration rate (eGFR) and classified according to National Kidney Foundation guidelines,2 affected the 30-day death rate and the risk of postoperative myocardial infarction. Although statistically significant, a lower eGFR did not increase the risk of the 30-day stroke. Multivariable logistic regression analysis showed that moderate or severe CKD were not significant predictors of 1-year neurologic events. Preoperative eGFR calculation remains a useful tool to predict the survival rate at 1, 5, and 10 years,