| | Anemia is associated with abdominal aortic aneurysm (AAA) size and decreased long-term survival after endovascular AAA repairReceived 24 April 2007; accepted 10 June 2007. published online 31 August 2007. ObjectiveAnemia is a common comorbid condition in various inflammatory states and an established predictor of mortality in patients with chronic heart failure, ischemic heart disease, and end-stage renal disease. The present study of patients with abdominal aortic aneurysm (AAA) undergoing endovascular repair (EVAR) assessed the relationships between baseline hemoglobin concentration and AAA size, as well as anemia and long-term survival. MethodsBetween March 1994 and November 2006, 711 patients (65 women, mean age 75.8 ± 7.8 years) underwent elective EVAR. Anemia was defined as a hemoglobin level <13 g/dL in men and <12 g/dL in women. Post-EVAR mean follow-up was 48.3 ± 32.0 months. Association of hemoglobin level with AAA size was assessed with multiple linear regression. Mortality was determined with use of the internet-based Social Security Death Index and the electronic hospital record. Kaplan-Meier survival curves of anemic and nonanemic patient groups were compared by the log-rank method. Multivariable logistic regression models were used to determine the influence of anemia on vital status after EVAR. ResultsA total of 218/711 (30.7%) of AAA patients undergoing EVAR had anemia at baseline. After adjustment for various risk factors, hemoglobin level was inversely related to maximum AAA diameter (β: − .144, 95%-CI: −1.482 − .322, P = .002). Post-EVAR survival was 65.5% at 5 years and 44.4% at 10 years. In long-term follow-up, survival was significantly lower in patients with anemia as compared to patients without anemia (P < .0001 by log-rank). Baseline hemoglobin levels were independently related to long-term mortality in multivariable Cox regression analysis adjusted for various risk factors (adjusted HR: 0.866, 95% CI: .783 to .958, P = .005). Within this model, statin use (adjusted HR: .517, 95% CI: .308 to .868, P = .013) was independently related to long-term survival, whereas baseline AAA diameter (adjusted HR: 1.022, 95% CI: 1.009 to 1.036, P = .001) was an independently associated with increased mortality. ConclusionsBaseline hemoglobin concentration is independently associated with AAA size and reduced long-term survival following EVAR. Thus, the presence or absence of anemia offers a potential refinement of existing risk stratification instruments. Abdominal aortic aneurysm (AAA) is a potentially fatal condition as its propensity to rupture increases as maximum AAA diameter increases.1 Aneurysm formation and progression is associated with chronic transmural aortic wall inflammation.2, 3 Endovascular AAA repair (EVAR), a minimally-invasive treatment option, has proven advantages over open surgical AAA repair in the perioperative period.4, 5 Protection from AAA-related death, a crucial end-point after EVAR,6 has been shown to be as high as in 96% at 5 years and 93% at 9 years.7, 8, 9 However, the cumulative 5-year survival of 49% highlights the increased mid-term mortality risk of these often medically frail patients.7, 8 Besides the devastating consequences of AAA rupture, the systemic implications of aneurysmal disease have recently increasingly been acknowledged.7, 8, 10, 11, 12, 13 In particular, AAA patients were shown to be at significant risk for cardiovascular complications5, 7, 8, 14, 15 and AAA is now considered a coronary heart disease risk equivalent.16 Furthermore, AAA size is independently associated with inflammatory markers10, 11, 12, 13 as well as with an increased risk of perioperative complications17 and cardiovascular mid-term mortality after open surgical18 and endovascular19, 20 AAA repair. Anemia is an important predictor of mortality in hemodialysis patients and in those with chronic heart failure and ischemic heart disease.21, 22, 23, 24, 25, 26 Anemia of chronic disease (ACD) is second most prevalent after anemia of iron deficiency.23, 27, 28, 29 The prevalence of ACD increases with age.23, 27, 28, 29 ACD is typically normochromic, normocytic, and hypoproliferative, and it is particularly encountered in the setting of chronic inflammatory conditions.21, 23, 27, 29 Thus, the pathophysiology of both AAA and ACD has recently been linked to chronic inflammation.10, 11, 13, 21, 23, 29, 30 The purposes of this study were to evaluate the relationship between hemoglobin concentration and AAA size and between baseline anemia and long-term survival after EVAR. Patients and methods  Between March 1994 and November 2006, 711 consecutive patients underwent elective EVAR for infrarenal AAA at a single center and were entered in a prospectively maintained database. EVAR was carried out by a dedicated interdisciplinary team consisting of interventional radiologists, vascular surgeons, and anesthesiologists as described previously.31, 32 Definitions Anemia was defined according to the World Health Organization as a hemoglobin level <13 g/dL in men and <12 g/dL in women.33 General definitions34 as well as classification of cardiovascular risk factors35 followed the standards proposed by the Society of Vascular Surgery/International Society for Cardiovascular Surgery (SVS/ISCVS). Patient treatment A total of 326/711 (45.9%) patients were treated within five multicenter clinical trials of specific endografts. The results of several of these trials have recently been published.36, 37, 38, 39 The study protocols were in accordance with the Declaration of Helsinki and approved by the local ethics committee. Each patient gave written informed consent prior to participating in the trial. Furthermore, 385/711 (54.1%) patients were treated with use of commercially available endografts. Ethics committee approval was not obtained for these patients, since they were treated on a regular clinical basis using FDA-approved devices. Patients with anatomically suitable AAAs were eligible for EVAR if they had an infrarenal aortic aneurysm that was 50 mm or larger in maximum transverse diameter or if they had documented imaging evidence of 1.5 times the reference aortic diameter and expansion rate >10% per year. Exclusion criteria for the present investigation were a life expectancy of <1 year, pregnancy, systemic infection, inflammatory aneurysm, AAA associated with connective tissue disease, or Marfan’s syndrome and an untreatable bleeding diathesis or hypercoagulable state. All patient baseline characteristics and laboratory data were collected preoperatively and are described in Table I. | | |  | Baseline factor | No anemia N = 493 | Anemia n = 218 | P | |
|---|
| Female gender, n (%) | 51 (10.3%) | 14(6.4%) | .1198⁎ | | | Age, mean ± SD (years) | 74.6 ± 7.5 | 78.5 ± 7.5 | <.0001† | | | Maximum AAA diameter mean ± SD (mm) | 57.0 ± 9.7 | 60.8 ± 12.2 | <.0001† | | | Height, mean ± SD (inches) | 68.9 ± 3.5 | 68.9 ± 3.1 | .9955† | | | Weight, mean ± SD (pound) | 186.4 ± 37.0 | 174.7 ± 31.2 | <.0001† | | | Baseline hemoglobin, mean ± SD (g/dl) | 14.4 ± 1.0 | 11.6 ± 1.1 | <.0001† | | | Baseline hematocrit, mean ± SD (%) | 42.8 ± 3.1 | 35.3 ± 3.2 | <.0001† | | | Postprocedural hemoglobin, mean ± SD (g/dl) | 11.8 ± 1.7 | 10.1 ± 1.3 | <.0001† | | | Postprocedural hematocrit, mean ± SD (%) | 35.2 ± 3.8 | 30.6 ± 3.6 | <.001† | | | White blood cell count, mean ± SD (cells/mcl) | 7.4 ± 6.9 | 7.4 ± 6.7 | .9550† | | | Creatinine clearance, mean ± SD (ml/min) | 56.7 ± 18.9 | 44.9 ± 17.8 | <.0001† | | | History of cancer, n (%) | 121(24.5%) | 62(28.4%) | .3062†⁎ | | | Arterial hypertension, n (%) | 388(78.7%) | 185(84.9%) | .0640⁎ | | | Hyperlipidemia, n (%) | 269(54.6%) | 96(44.0%) | .0116⁎ | | | Diabetes mellitus, n (%) | 69(14.0%) | 38(17.4%) | .2558⁎ | | | Smoking, n (%) | 388(78.7%) | 164(75.2%) | .3293⁎ | | | COPD, n (%) | 163(33.1%) | 65(29.8%) | .4331⁎ | | | History of cerebrovascular disease, n (%) | 72(14.6%) | 45(20.6%) | .0488⁎ | | | History of PAOD, n (%) | 127(25.8%) | 78(35.8%) | .0072⁎ | | | History of coronary artery disease, n (%) | 208(42.2%) | 112(51.4%) | .0272⁎ | | | History of atrial fibrillation, n (%) | 61(12.4%) | 38(17.4%) | .0785⁎ | | | Cardiac risk, n (%) | | | | | | 0 | 186(37.7%) | 56(25.7%) | .0020† | | | 1 | 61(12.4%) | 20(9.2%) | .2499† | | | 2 | 233(47.3%) | 122(55.9%) | .0346⁎ | | | 3 | 13(2.6%) | 20(9.2%) | .0003⁎ | | | Renal risk, n (%) | | | | | | 0 | 422(85.6%) | 134(61.5%) | <.0001⁎ | | | 1 | 60(12.2%) | 54(24.7%) | <.0001⁎ | | | 2 | 10(2.0%) | 24(11.0%) | <.0001⁎ | | | 3 | 1(0.02%) | 6(2.8%) | .0041 | | | Pulmonary risk, n (%) | | | | | | 0 | 279(56.6%) | 104(47.7%) | .0338⁎ | | | 1 | 124(25.2%) | 68(31.2%) | .0997⁎ | | | 2 | 60(12.1%) | 33(15.1%) | .2800⁎ | | | 3 | 30(6.1%) | 13(6.0%) | .0000⁎ | | | Betablocker, n (%) | 200(40.6%) | 107(49.1%) | .0400⁎ | | | Statin, n (%) | 217(44.0%) | 86(39.4%) | .2851⁎ | | | Antiplatelet therapy, n (%) | 211(42.8%) | 113(51.8%) | .0276⁎ | | | ACE inhibitor, n (%) | 113(22.9%) | 63(28.9%) | .0908⁎ | | | | |
| ⁎ from Fisher exact test. †from Student t-test. |
Follow-up Mean follow-up was 48.3 ± 32.0 months. The Social Security Death Index (SSDI, http://ssdi.rootsweb.com/) was used to ascertain mortality as of November 30, 2006. Statistical analysis Continuous data are presented as mean ± standard deviation (SD). Categorical data are given as absolute numbers and percentages. For univariable comparison of unpaired continuous data, the Student t test was used. For univariable comparison of paired continuous data, the paired t test was utilized. Categorical data was compared with use of the Fisher exact test. Multiple linear regression (adjusted for all baseline variables with significant difference in univariable comparison and for factors with potential impact on baseline AAA size and cause of anemia) was performed to assess the association between hemoglobin concentration and AAA size. Survival rates according to presence or absence of anemia at baseline are presented as Kaplan-Meier curves and compared by means of the log-rank test. Multivariable Cox proportional hazards analysis (adjusted for all baseline variables with significant difference in univariable comparison and for factors with potential impact and cause of anemia23 as well as for factors with impact on decreased patient survival) was applied to assess the effect of hemoglobin concentration on survival. Results of the Cox regression model were presented as the hazard ratio (HR) and the 95% confidence interval (95% CI). A P value <.05 was considered statistically significant. All calculations were performed using SPSS (Version 13.0, SPSS, Chicago, Ill). Results Anemia was present in 218/711 (30.7%) of patients undergoing EVAR. Table I outlines patient demographic data, risk factors, comorbidities, and cardiovascular medications of patients contained in the present study. Patients with anemia were significantly older, had a larger maximum AAA diameter, as well as a lower body weight and creatinine clearance compared to patients without anemia. Hyperlipidemia was less prevalent, whereas history of symptomatic atherothrombosis as well as betablocker and antiplatelet therapy was more frequent in patients with anemia compared with patients without anemia. Furthermore, patients with anemia were less likely to have favorable cardiac, renal, and pulmonary risk scores than were patients without anemia. Postprocedural hemoglobin concentration and hematocrit were significantly lower in patients diagnosed with anemia at baseline as compared to patients without anemia (P < .0001 and P < .001, Table I). Postprocedural hemoglobin concentrations as well as hematocrit were significantly lower compared with preprocedural values in both patients with and without anemia at baseline (P < .0001). With use of cell savers, transfusion was necessary in a total of 48/711 (6.8%) patients: 15/493 (3%) of patients without anemia at baseline and 30/218 (14%) of patients with anemia at baseline received blood products (P < .0001). Hemoglobin level was inversely related to maximum AAA diameter (β: −.144, 95% CI: −1.482 to −.322, P = .002) within a linear regression model adjusted for age; weight; height; creatinine clearance; hyperlipidemia; diabetes mellitus; smoking; antiplatelet and beta blocker use; cerebrovascular disease; PAOD; coronary artery disease; cardiac, pulmonary and renal risk score. Conversely, maximum AAA diameter was inversely related to hemoglobin concentration (β = −.172, 95% CI: −1.947 to −.214, P = .015) in this model. Post-EVAR 30-day rates of surgical conversion, AAA rupture, and death did not differ between both groups (P > .05, Table II). Survival was 65.5% after 5 years and 44.4% after 10 years (Fig 1). Long-term survival was significantly lower in patients with anemia as compared to patients without anemia (P < .0001, Fig 1). | | | | 30-day outcomes | All patients n = 711 | No anemia n = 493 | Anemia n = 218 | P⁎ | |
|---|
| Procedural conversion | 7(0.09%) | 5(1.0%) | 2(0.09%) | 1.0000 | | | Procedural death | 0(0.0%) | 0(0%) | 0(0%) | N/A | | | Procedural rupture | 0(0%) | 0(0%) | 0(0%) | N/A | | | 30-day conversion | 10(1.4%) | 8(1.6%) | 2(0.09%) | .7316 | | | 30-day death | 10(1.4%) | 6(1.2%) | 4(1.8%) | N/A | | | 30-day rupture | 0(0%) | 0(0%) | 0(%) | N/A | | | | |
Multivariable Cox proportional hazards analysis adjusted for age; maximum AAA diameter; weight; creatinine clearance; history of cancer; hyperlipidemia; diabetes mellitus; smoking; COPD; cerebrovascular disease; PAOD; coronary artery disease; cardiac, pulmonary and renal risk score; beta blocker, statin, antiplatelet, and ACE inhibitor use confirmed baseline hemoglobin levels to be independently associated with long-term mortality post-EVAR (adjusted HR: .866, 95% CI: .783 to .958, P = .005; Table III). Additionally, patient age (adjusted HR: 1.040, 95% CI: 1.015 to 1.065, P = .002), maximum AAA diameter (adjusted HR: 1.022, 95% CI: 1.009 to 1.036, P = .001), diabetes mellitus (adjusted HR: 1.819, 95% CI: 1.216 to 2.720, P = .004) as well as pulmonary (adjusted HR: 1.398, 95% CI: 1.157 to 1.689, P = .001) and renal risk score (adjusted HR: 1.595, 95% CI: 1.234 to 2.062, P < .001) were independently associated with reduced survival, whereas statin use was associated with greater survival (adjusted HR: .517, 95% CI: .308 to .868, P = .013) in this model (Table III). Discussion Mediation by elevated pro-inflammatory cytokines is common to the pathophysiology of both AAA and ACD.40, 41, 42 In the present study, decreased hemoglobin concentration, as a marker of chronic disease, was shown to be independently associated with AAA size and reduced long-term survival after EVAR. In the present series, 30-day mortality after EVAR was 1.4%, whereas 5-year and 10-year survival were 65.5% and 44.4%, respectively. As more long-term follow-up data on patients undergoing treatment for AAA becomes available,7, 8 the systemic implications of abdominal aortic aneurysmal disease are becoming more apparent. Still, long-term survival of AAA patients compares well with patients with symptomatic cerebrovascular disease43, 44 and various types of malignancies such as colon cancer45 and is substantially higher as compared to patients with intermittent claudication.46 Considering the fact that AAA patients are at significant risk for cardiovascular complications,7, 8, 17, 18, 20 AAA is now considered a CHD risk equivalent.16 Maximum AAA diameter as a potential marker of systemic inflammatory burden has been shown to directly correlate with inflammatory markers such as interleukin-6 and C-reactive protein.10, 11, 12, 13 Furthermore, maximum AAA diameter as an expression of AAA size was shown to influence on rates of perioperative cardiovascular complications,17 and cardiovascular midterm mortality after open surgical AAA repair18 and after EVAR.7, 8, 20 The present study confirms the highly significant inverse relationship between AAA size and long-term survival, underlining previous observations regarding mid-term survival after EVAR.7, 8, 20 Anemia has traditionally been viewed as an “innocent bystander” and accepted as an abnormality associated with chronic diseases.22 However, the presence of anemia has recently been identified as an important predictor of increased mortality in patients with end-stage renal disease, chronic heart failure and ischemic heart disease.21, 22, 23, 24, 25, 26 In inflammatory states, increased hepcidin concentrations cause iron sequestration in macrophages, resulting in hypoferremia and anemia.21, 23, 29, 47 Furthermore, pro-inflammatory cytokines induce hypoferremia by modulating macrophage iron metabolism via induction of ferritin biosynthesis.48 In the present series, anemia was highly prevalent and was independently associated with AAA size and increased mortality during long-term follow-up after multivariable adjustment of a multitude of clinical baseline factors. Given these associations, we speculate that there may be a role for anemia as an inflammatory surrogate marker and risk stratification tool in patients with AAA, although no direct link between anemia and inflammatory markers was established in the present study. Although the effect of statins in reducing the risk of cardiovascular disease is well established, robust data on its dedicated use in patients with AAA is scarce. Statins are associated with greater long-term survival after open AAA surgery49 and after EVAR.50 Besides their well-studied lipid-lowering and anti-inflammatory properties associated with improved cardiovascular outcomes, statins reduce levels of enzymes involved in aortic wall degeneration in cell culture51, 52 and in human AAA tissue.53 The present series confirms statin use to be an independent predictor of decreased long-term mortality in AAA patients, thereby underlining important observations from the EUROSTAR registry.50 Fewer than 50% of patients in the present series were prescribed statins prior to EVAR. The fact that treatment of cardiovascular risk is currently still suboptimal in patients with AAA has recently been highlighted by others.15 Despite the fact that AAA has been recognized as a coronary heart disease risk equivalent,16 dedicated recommendations regarding drug treatment are currently lacking. Three shortcomings of the present study must be addressed. First, since ACD can nowadays not be diagnosed even with specific laboratory tests directly aimed at differentiating anemia of inflammation from anemia resulting from other causes,23, 54 we cannot entirely rule out that causes for anemia other than chronic inflammation might have contributed to the above-described results. Nevertheless, three features of our analysis render the impacts of such artefacts less likely. By including age, creatinine clearance, and history of cancer in the multivariable analysis assessing factors contributing to reduced survival, the impact of these major causes of anemia was minimized.23 Furthermore, the inverse relationship of hemoglobin levels and AAA size observed in this study further support assumptions for a link between anemia and chronic inflammation in this series. Second, the lack of available data to enable systematic and reliable determination of the causes of death in patients who underwent elective EVAR prevented an assessment of the direct relationship between anemia and cardiovascular events. Third, since anemia was diagnosed by a blood test prior to EVAR, the impact of anemia occurring during follow-up cannot be assessed utilizing this approach. In summary, in the present series baseline hemoglobin concentration, as a marker of chronic disease, was shown to be independently associated with both AAA size and reduced long-term survival following EVAR. Thus, the presence or absence of anemia offers a potential refinement of existing risk stratification instruments. Since no direct link between inflammatory markers and anemia could be established in the present series, further investigations into the molecular linkage between anemia, inflammatory changes and AAA are warranted. 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Competition of interest: none. PII: S0741-5214(07)00998-6 doi:10.1016/j.jvs.2007.06.027 © 2007 The Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved. | |
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