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Ann Thorac Surg 2008;85:525-529. doi:10.1016/j.athoracsur.2007.09.040
© 2008 The Society of Thoracic Surgeons
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Original Articles: Cardiovascular

Serial Quantitative Coronary Analyses for the Evaluation of One-Year Change in Saphenous Vein Grafts

Nobuaki Suzuki, MDa,*, Ken Kozuma, MD, PhDa, Yasunari Ueno, MDa, Kensuke Nagaoka, MDa, Hiroyuki Kyono, MDa, Shuichi Ishikawa, MDa, Hidenori Watanabe, MD, PhDa, Naoyuki Yokoyama, MD, PhDa, Satoshi Takeshita, MD, PhDb, Takaaki Isshiki, MD, PhDa

a Department of Medicine, Teikyo University School of Medicine, Tokyo, Japan
b Department of Medicine, National Cardiovascular Center, Osaka, Japan

Accepted for publication September 20, 2007.

* Address correspondence to Dr Suzuki, Department of Medicine, Teikyo University School of Medicine, 2-11-1 Kaga Itabashi-ku, Tokyo, 173-8605, Japan (Email: nsuzu{at}bronze.ocn.ne.jp).


   Abstract
Top
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 References
 
Background: A paucity of data exists with respect to changes in whole saphenous vein grafts (SVGs) despite accelerated atherosclerosis within grafted saphenous vein conduits. In the present study, we evaluated the one-year change in SVGs by means of quantitative coronary analysis.

Methods: This study enrolled consecutive 52 patients with 109 SVGs, who underwent coronary artery bypass graft surgery successfully. A follow-up study was performed in 33 patients with 65 SVGs after one year because 16 SVGs were obstructed (baseline, 8; follow-up period, 8), and 15 patients with 28 SVGs dropped out within one year.

Results: Both minimal and mean lumen diameters decreased significantly (3.17 ± 0.64 mm vs 2.41 ± 0.57 mm, p < 0.001; 3.70 ± 0.69 mm vs 2.92 ± 0.70 mm, p < 0.001; respectively). Graft length also decreased significantly (107.1 ± 25.8 vs 100.6 ± 25.2 mm, p < 0.001). The graft shortening rate (graft shortening length/baseline graft length x 100) was greater than 5% in 33 vessels (51%) and greater than 10% in 23 vessels (35%). Coronary risk factors (smoking, diabetes mellitus, hypertension, dyslipidemia) did not reveal significant relationship with late loss of minimal and mean lumen diameters.

Conclusions: The present study showed a considerable and uniform lumen loss of SVGs after one year, irrespective of coronary risk factors. Graft length shortening was seen more than elongation.


   Introduction
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 Abstract
 Introduction
Material and Methods
 Results
 Comment
 References
 
Saphenous vein grafts (SVGs) continue to be used as conduits for aortocoronary bypass surgery. However, due to more accelerated atherosclerosis within the grafted saphenous vein conduits, long-term patency of SVGs has been an issue post-coronary artery bypass graft (CABG) surgery [1–7]. An earlier study [8] demonstrated that 15% to 20% of SVGs become occluded within the first year, which usually results in percutaneous coronary intervention. Generally, atherosclerotic change is defined as plaque proliferation, positive and negative remodeling, plaque calcification, and subsequent decrement of lumen area. Nevertheless, there is a paucity of the data with respect to changes in the whole SVG. In the present study, we evaluated the one-year change in SVGs by means of quantitative coronary analysis (QCA).


   Material and Methods
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 Abstract
 Introduction
 Material and Methods
Results
 Comment
 References
 
The protocol of this study was approved by the Institutional Review Board and the necessity for patient consent regarding this study was waived. This study enrolled 52 consecutive patients with 109 SVGs who underwent CABG surgery successfully using cardiopulmonary bypass and cardioplegic arrest. For all patients, coronary angiography and bypass angiography were performed within two months to obtain baseline measurements, and follow-up studies were planned for one year after CABG. All patients gave written informed consent for CABG and coronary angiography. Aspirin (100 mg) was prescribed indefinitely for all patients except one, who was allergic to it. Warfarin was prescribed for at least six months. Risk factors included diabetes mellitus (diet controlled, oral agent treated, or insulin treated), dyslipidemia (total cholesterol ≥ 240 mg/dL, high-density lipoprotein < 40 mg/dL, low-density lipoprotein ≥ 140 mg/dL, or oral agent treated), hypertension (systolic blood pressure ≥ 140 mm Hg, diastolic blood pressure ≥ 90 mm Hg, or oral agent treated), and smoking history.

The patients received nitroglycerin and heparin (2,000 IU) before the catheterization procedure. All the angiographic images for the analyses were documented using the anteroposterior view and zoomed out to include the whole graft, as in the representative case shown in Figure 1. The QCA was performed using an offline, computer-assisted, automated edge-detection algorithm (QCA-CMS ver 6.0; Medis, Leiden, The Netherlands) independent of clinical information. Using the outer diameter of the filled catheter as the calibration standard, the reference diameter, minimum lumen diameter, diameter stenosis, lesion length, mean lumen diameter, and graft length were measured at the baseline and one-year follow-up evaluations.


Figure 1
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  		Fig 1. Representative case. (A) Baseline period. (B) One-year follow-up period. At baseline, minimal lumen diameter was 3.36 mm and graft length was 135.4 mm. However, after one year, these decreased to 2.15 mm and 120.2 mm, respectively.

 
Statistical analysis was performed using the SPSS statistical package (SPSS Inc, Chicago, IL). Continuous variables are presented as the mean value ± standard deviation (SD). Data from the baseline and follow-up studies were compared using the paired t test. The impact of coronary risk factors on lumen diameter was evaluated using the unpaired t test. Categoric variables were compared using the Pearson {chi}2 test. The Pearson product-moment correlation was used to evaluate the statistical correlation between late loss of graft length and minimal or mean lumen diameter. Differences were considered significant when p was less than 0.05.


   Results
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 Abstract
 Introduction
 Material and Methods
 Results
Comment
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Among all the enrolled patients, eight SVGs were obstructed at baseline and 15 patients with 28 SVGs dropped out within one year because of the patients’ desire. After one year, angiography could not be performed for eight SVGs (to right coronary artery, two; to left anterior descending coronary artery, three; to left circumflex coronary artery, two; to left anterior descending/circumflex coronary artery [sequential graft], one) and in six patients because of obstruction. Out of these six patients, two patients with analyzable SVGs, in addition to the obstructed ones, were enrolled. As a result, bypass angiography was performed in 33 patients with 65 SVGs, both at the baseline and the one-year follow-up evaluations. Baseline clinical demographics are shown in Table 1. In 14 patients (39%) the clinical diagnosis was unstable angina pectoris or acute myocardial infarction. All patients had multivessel disease (two-vessel disease, 36%; three-vessel disease, 64%). Neither myocardial infarction nor death was documented within one year in this cohort. Target vessel revascularization was performed in 24 vessels (22%) because of obstruction. Angiographic data are shown in Table 2. Minimal lumen diameter degreased significantly (baseline versus follow up: mean ± SD, 3.17 ± 0.64 mm vs 2.41 ± 0.57 mm [p < 0.001]; median, 3.07 mm vs 2.40 mm; range, 1.55 to 4.47 mm vs 1.11 to 3.61 mm; 95% confidential interval [CI] 3.01 to 3.33 mm vs 2.27 to 2.55 mm). Also mean lumen diameter decreased significantly (baseline versus follow up: mean ± SD, 3.70 ± 0.69 mm vs 2.92 ± 0.70 mm [p < 0.001]; median, 4.05 mm vs 3.40 mm; range, 2.83 to 5.53 mm vs 1.03 to 4.80 mm; 95% confidential interval 3.74 to 4.17 mm vs 3.26 to 3.66 mm). There was no significant difference in late loss between minimal and mean lumen diameter (0.76 ± 0.66 mm vs 0.78 ± 0.58 mm, p = 0.710). Reference diameter increased significantly (4.12 ± 0.74 mm vs 3.39 ± 0.77 mm, p < 0.001), as did diameter stenosis (22.6 ± 9.9% vs 28.0 ± 12.9%, p = 0.012). Graft length decreased significantly (107.1 ± 25.8 vs 100.6 ± 25.2 mm, p < 0.001). The graft shortening length (baseline minus follow-up value) was 6.5 ± 9.9 mm, and the graft shortening rate, calculated as graft shortening length/baseline graft length x 100, was 5.9 ± 8.8%. The graft shortening rate was greater than 5% in 33 vessels (51%) and greater than 10% in 23 vessels (35%) (Fig 2). The graft shortening rate showed no correlation with late loss of minimal and mean lumen diameters (graft shortening rate versus late loss of minimal lumen diameter: r = 0.220, p = 0.078; graft shortening rate versus late loss of mean lumen diameter: r = 0.194, p = 0.122), as shown in Figure 3. Coronary risk factors (smoking, diabetes mellitus, hypertension, dyslipidemia) did not show significant influence on late loss of minimal and mean lumen diameters (Table 3).


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  		Table 1 Patient Demographics
 

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  		Table 2 Quantitative Coronary Analysis Data
 

Figure 2
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  		Fig 2. Cumulative frequency curves of graft shortening rate. Graft shortening rate was greater than 5% in 33 SVGs (51%) and greater than 10% in 23 SVGs (35%). (SVGs = saphenous vein grafts.)

 

Figure 3
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  		Fig 3. Correlation between graft shortening rate and late loss of diameter. The late loss of neither minimal nor mean lumen diameters showed significant correlation with graft shortening rate.

 

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  		Table 3 Relationship Between Coronary Risk Factors and Late Loss
 

   Comment
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
References
 
In the present study, serial data from QCA of whole SVGs were demonstrated. The SVGs have been considered to have innate pathological mechanisms for facilitating lumen reduction. The obstruction of SVGs in the early phase occurs by thrombosis, whereas late occlusion is due to fibromuscular intimal hyperplasia or atherosclerosis, or both, with some mural thrombosis [9–13]. The increase in intimal hyperplasia, especially within one year, results from growth of fibrocollagenous tissue [12, 14–16]. Consequently, it has been reported that the long-term patency of SVGs is approximately 40% to 60% ten years after CABG [2]. Furthermore, with regard to percutaneous coronary interventions, SVGs show poor clinical outcomes when compared with native coronary arteries despite the use of drug-eluting stents. Nevertheless, to the best of our knowledge, little is known about the serial QCA data related to changes in SVGs. The present study showed that both minimal and mean lumen diameters of SVGs decreased considerably within one year after CABG. These results highlight the implications and clinical impact of progressive lumen reduction in SVGs. Although it is well known that old SVGs usually show the degeneration, there might be a paucity of the recognition in terms of changes in one-year-old SVGs. Even when the percutaneous intervention is considered for the relatively young and apparently nondegenerated SVG, one should not ignore the homogeneous atherosclerotic change or shrinkage around the target lesion. The evaluation of SVGs by means of QCA had been validated in a previous study, which demonstrated that a change of 0.4 mm in QCA of SVGs represents true progression or regression of mean lumen diameter [17]. Indeed, the QCA software of the present study has been fully validated with phantom models in the previous investigation [18]. In the present study, the mean lumen diameter of the total vessel decreased substantially from 3.70 to 2.92 mm; this contrasts with another study, which reported a reduction in mean lumen diameter of nondilated segments in a native coronary artery of only 0.03 mm within two years [19]. Moreover, in this study, minimal lumen diameter was similarly decreased, as there was no difference in late loss between minimal and mean lumen diameters. This finding indicates that one-year neointimal hyperplasia of SVGs is diffuse and uniform. In the present study, coronary risk factors did not significantly correlate with late loss of minimal and mean lumen diameters. This result supports a previously published report, which indicated that traditional cardiovascular risk factors do not predict occlusion or stenosis of SVGs five years after CABG by means of QCA [20].

The present study also reports seminal data with respect to change in SVG length. Graft shortening was considered to be a significant finding, even if the intraobserver or interobserver variability of QCA measurements was taken into account [21, 22]. It is known that tortuosity of the thoracic aorta on chest radiographs is characteristic of atherosclerotic disease [23]. Previous papers have indicated that vessel shortening or elongation may appear concurrently with constriction or dilatation [24]. We speculated that remodeling of the graft caused not only a cross-sectional change, but also a longitudinal one. Indeed, a previous investigation using computed tomography showed that negative remodeling in SVGs between postoperative months 1 and 12 was common and related to lumen loss [25], although such results should be interpreted with caution because of the lower spatial resolution of the computed tomography angiogram. The results of the present study may indicate that the one-year longitudinal remodeling of SVGs is commonly ineffective, reflecting differences in the atherosclerotic process between native arteries and SVGs. It has been known that too short a length might cause tension on the SVGs [26], which may lead to compromise in the blood flow in the SVGs [27]. We speculated that the SVGs without the sufficient length to adopt the shortening might cause the tension of whole graft and the following chronic graft failure, despite the lack of significant correlation between graft shortening rate and lumen loss in the present data. Further investigation is required for the interpretation of graft length shortening.

This study does not include any data in relation to arterial grafts, although such data also should contribute to the relevant clinical practice. Although no significant relationship of late lumen loss with coronary risk factors was observed, their severity was not taken into account in the present study.


   References
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 

  1. Lawrie GM, Lie JT, Morris Jr. GC, Beazley HL. Vein graft patency and intimal proliferation after aortocoronary bypass: early and long-term angiopathologic correlations Am J Cardiol 1976;38:856-862.[Medline]
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