The aims of this study were to clarify the prevalence and the risk factors for unsuspected abdominal aortic aneurysm (AAA) in patients who underwent coronary artery bypass grafting for severe coronary artery disease and to identify the most at risk patients for AAA. Among 217 patients (189 men, mean age 64 ± 11 years), asymptomatic AAAs, as prospectively identified by echocardiography, were found in 15 patients (6.9%). All patients with AAAs were men and smokers or past smokers. Factors significantly associated by univariate analysis with asymptomatic AAA presence were smoking (p = 0.003), symptomatic peripheral artery disease (p = 0.006), significant carotid artery stenosis (p = 0.007), and larger femoral and popliteal diameters (p = 0.008 and p = 0.0012, respectively). The other classic demographic, clinical, and biologic features were equally distributed among patients. In conclusion, in patients who underwent coronary artery bypass grafting who were men and aged <75 years with smoking histories, the prevalence of AAA was as high as 24% when they had concomitant peripheral arterial disease and/or carotid artery stenosis (vs 4.4% in the absence of either condition, p = 0.007), justifying consideration of AAA screening in this subgroup of in-hospital patients.
The aims of this study were to examine the prevalence of abdominal aortic aneurysm (AAA) in patients who underwent coronary artery bypass grafting (CABG) and to analyze the associated risk factors in this in-hospital population.
Methods
Over a 4-year period (from June 2002 to December 2006), 217 patients with severe coronary artery disease (CAD) who underwent elective CABG were included (CORONary Aneurysm [CORONA] study). During this period, there was no significant change in AAA screening guidelines or severe CAD treatment modalities. All patients had documented CAD defined by a stenosis of >75% in ≥1 of the main coronary arteries on angiography. The local ethics committee approved the protocol. The preoperative data of all enrolled patients were prospectively collected. Data included body mass index, age, gender, smoking status (current or past smokers vs nonsmokers), diabetes mellitus (fasting glucose ≥7 mmol/L and/or the use of diet or oral hypoglycemic agents or insulin treatment), arterial hypertension (patients receiving antihypertensive medications or having known but untreated blood pressure >140/90 mm Hg), hypercholesterolemia (fasting serum total cholesterol >220 mg/dl and/or low-density lipoprotein cholesterol >140 mg/dl and/or hypercholesterolemia treatment), hypertriglyceridemia (serum triglyceride ≥150 mg/dl and/or hypertriglyceridemia treatment), and family history of cardiovascular diseases. Clinical data included history of myocardial infarction, stroke, symptomatic angina pectoris, peripheral arterial disease (PAD; patients with Fontaine claudication stage ≥IIa or and/or history of treatment for chronic limb ischemia), AAA surgery, and coronary angioplasty. The left ventricular ejection fraction, number of stenosed coronary vessels, and medications were also recorded. In all enrolled patients, the carotid arteries were analyzed by duplex ultrasound scanning ≤1 month before CABG, and carotid artery stenosis (CAS) was considered significant if >70%. All patients underwent postsurgery abdominal echocardiographic examinations focusing on the aorta and its major branches (iliac, femoral, and popliteal). The suprarenal aortic diameter was measured distal to the origin of the superior mesenteric artery, just above the level of the renal arteries. The infrarenal aortic diameter was measured at the site of maximum aortic diameter below the renal arteries. In all locations, the measurement was performed in a transverse plane; anteroposterior outside-to-outside wall dimension was reported. For the present study, patients were screened positively for the presence of an AAA if the infrarenal aortic diameter was ≥30 mm or the infrarenal/suprarenal ratio was >1.5. All other arterial aneurysms were defined as being ≥1.5 times the diameter of the proximal adjacent segment.
Venous blood samples were collected from the antecubital vein the day before surgery. After centrifugation, the supernatants were immediately stored at −80°C until further analysis. Plasma fibrinogen was measured using a clotting assay (Diagnostica Stago, Asnières, France) and serum high-sensitivity C-reactive protein (CRP) with an immunonephelometric assay (Dade Behring, Rueil-Malmaison, France). Leukocytes were quantified using an automated hematology analyzer (SYSMEX XE-2100; Sysmex, Kobe, Japan).
All data are reported as mean ± SD or as median (interquartile range) for continuous variables, and as absolute numbers and percentages of patients for categorical variables. A Mann-Whitney U test for continuous variables and Pearson’s chi-square test for dichotomous variables were used to compare the prevalence of these variables between patients with and those without AAAs. Fisher’s exact test was used when pertinent. For all analyses, a p value ≤0.05 was considered statistically significant. All statistical analyses were performed using SPSS version 13.0 for Windows (SPSS, Inc., Chicago, Illinois).
Results
Characteristics of the study population are listed in Table 1 . We counted 189 male patients; the mean age was 64 ± 11 years. Twenty-three patients (11%) were aged <50 years. External aortic diameters and infrarenal/suprarenal ratios are also listed in Table 1 . For popliteal and femoral arteries, no significant difference was found between the right and left sides (data not shown), and mean diameters of the right and left sides are indicated. Fifteen patients (6.9%) had AAAs. Four patients (1.84%) had asymptomatic popliteal arterial aneurysms, 3 of them with unilateral aneurysms (popliteal diameters 12, 12.4, and 15 mm), while the fourth had a bilateral aneurysm (14.5 and 19 mm). One femoral arterial aneurysm was detected, with a diameter of 13.8 mm. The mean infrarenal aortic diameter of the 15 patients with AAAs was 35.3 ± 9.1 mm (range 26 to 53). Among them, 2 patients with aortic diameters >50 mm were referred for surgical treatment. In 2 patients with AAAs, the infrarenal aortic diameters were <30 mm (26 and 27.6 mm); nonetheless, the infrarenal/suprarenal ratios were >1.5 (1.51 and 1.56). Two patients with AAAs presented with right and left iliac extensions. Another patient with an AAA had an asymptomatic popliteal arterial aneurysm. A fourth patient with an AAA, with an infrarenal/suprarenal ratio >1.5 and an infrarenal aortic diameter of 26 mm, presented with a femoral arterial aneurysm with a diameter of 13.8 mm. All AAAs were found in men aged >54 years (median age 67, interquartile range 54 to 84). AAAs were diagnosed in 15 men aged >50 years (9%), in 8 aged >65 years (9.5%), and in 5 aged >75 years (16.1%). Interestingly, 7 AAAs were diagnosed in men aged 50 to 65 years, 1 with a diameter of 53 mm. The second patient with an aortic diameter >50 mm was 84 years old. All patients with AAAs were current or past smokers, and histories of PAD and of CAS were found in 6 and 4 patients with AAAs, respectively. Had we respected the recommendation for one-time screening in men aged 65 to 75 years who had ever smoked, only 3 AAAs of the 15 diagnosed in the total study population would have been detected.
| Characteristic | All Patients | No AAA | AAA | p Value ⁎ |
|---|---|---|---|---|
| (n = 217) | (n = 202) | (n = 15) | ||
| Age (years) | 64 (56–73) | 64 (56–73) | 67 (58–75) | 0.24 |
| Gender (% female) | 28 (13%) | 28 (14%) | 0 (0%) | 0.12 |
| Body mass index (kg/m 2 ) | 27 (25–30) | 27 (25–30) | 27 (24–30) | 0.52 |
| Arterial hypertension | 143 (66%) | 134 (66%) | 9 (60%) | 0.62 |
| Smoking | 139 (64%) | 124 (61%) | 15 (100%) | 0.003 |
| Diabetes mellitus | 63 (29%) | 57 (28%) | 6 (40%) | 0.38 |
| Hypercholesterolemia | 138 (64%) | 129 (64%) | 9 (60%) | 0.76 |
| Hypertriglyceridemia | 37 (17%) | 34 (17%) | 3 (20%) | 0.73 |
| Positive family history of cardiovascular diseases | 81 (37%) | 73 (36%) | 8 (53%) | 0.18 |
| Left ventricular ejection fraction <50% | 60 (28%) | 56 (30%) | 4 (33%) | 1.0 |
| Unstable angina pectoris | 36 (17%) | 35 (17%) | 1 (17%) | 0.35 |
| Stable angina pectoris | 82 (38%) | 79 (39%) | 3 (20%) | 0.15 |
| Previous myocardial infarction | 81 (37%) | 76 (38%) | 5 (33%) | 0.74 |
| Previous coronary angioplasty | 53 (24%) | 49 (24%) | 4 (27%) | 1.0 |
| 1- or 2-vessel disease | 74 (34%) | 70 (34.5%) | 4 (27%) | 0.4 |
| 3- or 4-vessel disease | 143 (66%) | 132 (65.5%) | 11 (73%) | 0.52 |
| Peripheral arterial disease | 28 (13%) | 22 (11%) | 6 (40%) | 0.006 |
| Carotid artery stenosis | 18 (8%) | 14 (7%) | 4 (27%) | 0.007 |
| Stroke | 19 (9%) | 17 (8%) | 2 (13%) | 0.63 |
| Aspirin | 179 (82%) | 166 (82%) | 13 (87%) | 0.48 |
| β blockers | 158 (73%) | 148 (73%) | 10 (67%) | 0.56 |
| Angiotensin-converting enzyme inhibitors | 101 (46%) | 95 (47%) | 6 (40%) | 0.79 |
| Calcium antagonists | 54 (25%) | 51 (25%) | 3 (20%) | 0.77 |
| Statins | 169 (78%) | 157 (78%) | 12 (80%) | 1.0 |
| Leukocytes (g/L) | 6.9 (5.9–8.1) | 6.9 (5.9–8.1) | 7.6 (5.7–9.0) | 0.63 |
| Fibrinogen (g/L) | 3.35 (2.9–4.0) | 3.32 (2.9–4.0) | 3.6 (3.2–4.1) | 0.20 |
| C-reactive protein (mg/L) | 1.75 (0.9–3.5) | 1.69 (0.81–3.49) | 2.75 (1.71–3.74) | 0.053 |
| Infrarenal aortic artery diameter (mm) | 18.4 ± 5.4 | 17.3 ± 2.6 | 35.3 ± 9.1 | — |
| Infrarenal/suprarenal aortic diameter ratio | 0.99 ± 0.20 | 0.96 ± 0.11 | 1.64 ± 0.42 | — |
| Suprarenal aortic artery diameter (mm) | 18.2 ± 2.7 | 18.1 ± 2.6 | 20.6 ± 4.0 | 0.038 |
| Femoral artery diameter (mm) | 8.9 ± 1.5 | 8.8 ± 1.4 | 10.4 ± 1.9 | 0.008 |
| Popliteal artery diameter (mm) | 7.2 ± 1.5 | 7.1 ± 1.5 | 8.7 ± 1.5 | 0.0012 |
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