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Ann Thorac Surg 2009;88:1440-1444. doi:10.1016/j.athoracsur.2009.06.009
© 2009 The Society of Thoracic Surgeons
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Original Articles: Adult Cardiac

Efficacy of Aggressive Lipid Controlling Therapy for Preventing Saphenous Vein Graft Disease

Mitsumasa Hata, MD, PhDa,*, Tadateru Takayama, MDb, Akira Sezai, MDa, Isamu Yoshitake, MDa, Atsushi Hirayama, MDb, Kazutomo Minami, MDa

a Department of Cardiovascular Surgery, Nihon University School of Medicine, Tokyo, Japan
b Department of Cardiology, Nihon University School of Medicine, Tokyo, Japan

Accepted for publication June 1, 2009.

* Address correspondence to Dr Hata, Department of Cardiovascular Surgery, Nihon University School of Medicine, 30-1 Ooyaguchi Kamimachi Itabashi-ku, Tokyo, 173-8610, Japan (Email: mihata{at}med.nihon-u.ac.jp).


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Comment
 References
 
Background: We assessed the efficacy of aggressive lipid controlling therapy (ALCT), which maintains low-density lipoprotein cholesterol (LDL-C) below to 80 mg/dL and LDL/high-density lipoprotein cholesterol (HDL-C) ratio less than 1.5 for preventing postcoronary bypass (CABG) saphenous vein graft (SVG) diseases by using intracoronary angioscopy.

Methods: Twenty-one patients after CABG were divided into two groups: group I consisted of 10 patients whose serum LDL-C level and LDL/HDL could be controlled less than 80 mg/dL and 1.5, respectively, by rosuvastatin for about one year; group II consisted of 11 patients whose LDL-C level and LDL/HDL have been higher than 100 mg/dL and 2.5, respectively, regardless of having medication of pravastatin. Twenty-seven SVGs were assessed by intravascular ultrasound (IVUS) and angioscopy on postoperative 12 to 16 months.

Results: The serum LDL-C level (I: 64.1 vs II: 130.2 mg/dL) and LDL/HDL (I: 1.36 vs II: 2.64), and high sensitive C-reactive protein (I: 0.045 ± 0.100 vs II: 0.116 ± 0.020 mg/dL) were significantly lower in group I. In group II, IVUS detected eccentric plaques in 11 (78.6%) of 14 SVGs. Furthermore the angioscope showed yellow plaque in all 14 SVGs (100%) and 11 (78.6%) of them had thrombi. On the other hand, in group I, all 13 SVGs had no eccentric, yellow plaques or thrombi and the intima was entirely clear white.

Conclusions: Prophylactic treatment for yellow plaque and thrombus formation are extremely important in the development of early and late SVG disease. Aggressive lipid controlling therapy is quite attractive to avoid post CABG SVG disease and may be effective to maintain the long-term graft patency.


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Results
 Comment
 References
 
Despite the advances in the relevant technologies and techniques, nearly 25% of saphenous vein grafts (SVG) become occluded within 1 year after surgery, and 50% of SVGs fail within 10 years [1, 2]. Gansera and colleagues [3] reported that the incidence of SVG occlusion was twofold higher than that of the internal thoracic artery in symptomatic patients [3]. Even though the patient has no coronary events, more than 20% of SVG have been occluded for 10 years after surgery [4]. However, the ready availability of SVGs still accounts for their use in over 70% of coronary artery bypass graft (CABG) surgery, particularly for the emergency or multiple vessel disease patients. Recently, several investigators reported that aggressive risk factor control, together with appropriate secondary preventive medication, has shown to slow progression of SVG atherosclerosis and the long-term patency of SVG was not very different than other arterial conduits except for the internal thoracic artery [5, 6]. Furthermore, Souza and colleagues [7] showed the long-term SVG patency was 90% by harvesting with minimum trauma. Because of the need of the cardiac surgeon to perform complete revascularization for multivessel diseases, it is increasingly important to maximize the long-term SVG patency in order to optimize long-term surgical outcome.

Plaque rupture with thrombus formation is the major cause of long-term SVG disease [8, 9]. Lowering of low density lipoprotein cholesterol (LDL-C) below 100 mg/dL has been shown to be effective for reducing the progression of atherosclerosis in SVG [10]. High density lipoprotein cholesterol (HDL-C) has also been associated with a protective effect on atherosclerosis in carotid arteries [11]. No studies to date have investigated the efficacy of aggressive statin therapy on angioscopic progression after CABG, SVG disease. The aim of this study was to identify the morphologic changes in SVG by intracoronary ultrasound and angioscopy, and to assess the efficacy of aggressive lipid controlling therapy with rosuvastatin versus moderate therapy with pravastatin.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Comment
 References
 
Twenty-one patients who have been followed-up more than 12 months after CABG were angiographically assessed. All procedures were carried out with traditional on-pump CABG using the left internal thoracic artery, one radial artery, and SVGs. In CABG, we usually used the left internal thoracic artery for the left anterior descending artery or big diagonal branch, and one radial artery for the proximal right coronary artery or first obtuse marginal branch of circumflex territory because the radial artery length is limited. The SVG is used for the distal part of the right coronary artery, second obtuse marginal branch, or distal part of the left anterior descending artery. The SVG was harvested by standard technique with scissors and clips. An endoscope was never used for graft harvesting. Furthermore, we tried to distend the harvested SVG with just a little pressure and minimize the intimal damage of SVG. All the patients underwent CABG during 2007 in our Institution. This study was a case-controlled observational study and Institutional Review Board approval was provided before publication of this manuscript and reporting of the information. The matched criteria between the groups were as follows; noninsulin user, age less than 80 years old, receiving both aspirin 100 mg and ticlopidine 200 mg daily, and receiving some calcium antagonists. Seventeen patients (81.0%) were male, and the average age was 65.6 ± 10.4 years, ranging from 31 to 78. Written informed consent was given to all patients to receive the graft assessment by coronary angiography, intravascular ultrasound (IVUS), and angioscopy. The coronary angioscopic catheter (Fibertech Co, Tokyo, Japan) used in the present study is 0.73 mm in outer diameter with a fiber containing 6,000 pixels. After the SVG angiography, we carefully put the angioscope into the distal anastomosis site of SVG. We then observed the entire SVG intima by pulling back the angioscope to the proximal anastomosis site.

We divided them into two groups. Group I consisted of 10 patients whose LDL-C level and LDL/HDL ratio have been strictly maintained lower than 80 mg/dL and 1.5, respectively, after surgery by aggressive lipid control with rosuvastatin (5 mg) at an outpatient clinic. Group II consisted of 11 matched patients whose LDL-C level and LDL/HDL ratio have exceeded 100 mg/dL and 2.5, respectively, for one year after surgery treated with pravastatin 10 mg at general practitioners. Both doses of statins were the usual starting dose of medication for Japanese patients. In this series, all patients had started taking statins approximately 14 days after the surgery when they first visited the outpatient clinic. Statins were never discontinued until angioscopic assessment. The serum level of LDL-C, HDL-C, and the LDL/HDL ratio was assessed at every month. No patients in either group received beta-blockers. We compared the two groups in terms of serum level of cholesterols, triglyceride, hemoglobin A1c, hypersensitive C-reactive protein (hsCRP), and the incidence of SVG diseases such as graft stenosis, eccentric plaque, unstable yellow plaque, and thrombi by angiography, IVUS, and angioscopy, respectively. We assessed 13 and 14 SVGs from groups I and II, respectively.

Statistical Examination
Results were expressed as the mean ± SD. Statistical calculations were conducted using StatView (SAS Inc, Cary, NC). Using parametric and nonparametric data, statistically significant differences were determined using the Student t test and Fisher exact test, respectively. A p value of less than 0.05 was considered statistically significant.


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Comment
 References
 
There was no difference between the groups in terms of average age, sex, prevalence of hypertension, diabetes, smoking, and target vessels of SVGs (Table 1). Average postoperative study duration was approximately 14 months in both groups (Table 2). The serum LDL-C level was significantly lower in group I (64.1 ± 11.9 mg/dL) compared with group II (130.2 ± 66.1 mg/dL) (p = 0.0038; Table 2). The LDL/HDL ratio was significantly lower in group I (1.36 ± 0.34) than that of group II (2.64 ± 1.25) (p = 0.0036; Table 2). The Hs-CRP was significantly lower in group I (0.045 ± 0.100 mg/dL) than that of group II (0.116 ± 0.020 mg/dL) (p = 0.0125; Table 2). There was no difference between the groups in terms of the level of HDL, triglyceride, and hemoglobin A1c levels (Table 2). All SVGs and other arterial grafts in both groups were patent on graft angiography. In group II, however, IVUS detected one or two large amounts of eccentric plaques in a low-density echoic lesion, which length was more than 2 cm at around the mid portion of SVG intima in 11 (78.6%) out of 14 SVGs. Angioscopy demonstrated the yellow plaques (Fig 1) on the same points of SVG intima. Even though IVUS did not detect the plaques, the angioscopy showed some yellow plaques on the mid portion of SVG intima and finally, yellow plaques were indicated in all 14 SVGs (100%). Furthermore, angioscope also revealed white thrombi on the yellow plaques in 11 (78.6%) of 14 SVGs (Fig 2). Graft angiography revealed 50% to 75% stenosis in five of these SVGs with thrombi. On the other hand, in group I, all 13 SVGs had no eccentric, yellow plaques or thrombi, and the intima was entirely clear white (Figs 3 and 4). Go The incidence of SVG diseases such as yellow plaque and thrombi was significantly higher in group II than in group I (p < 0.0001; Table 3). During follow-up periods, there was no coronary event in either group.


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  		Table 1 Patient Profiles
 

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  		Table 2 Laboratory Data
 

Figure 1
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  		Fig 1. Yellow plaque in saphenous vein grafts detected by angioscopy.

 

Figure 2
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  		Fig 2. Massive thrombus formation on the yellow plaque detected by angioscopy.

 

Figure 3
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  		Fig 3. Entire clear white intima without any yellow plaque and thrombi detected by angioscopy. Around the distal anastomosis site.

 

Figure 4
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  		Fig 4. Around the proximal anastomosis site.

 

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  		Table 3 Findings of CAG, IVUS, and Angioscopy
 

   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
References
 
It is evident from this angioscopic study that the major features of SVG diseases are the presence of unstable atherosclerotic plaques and thrombi. Especially, SVG atherosclerosis predisposes to thrombosis because of the high content of lipids and tissue factor, chronic flow disturbances, and associated impairment of vasodilatation. The SVG atheromas are more diffuse and vulnerable to rupture, and the major consequences of plaque rupture in SVGs seem to be rapid platelet aggregation and certain thrombotic occlusion [12]. Therefore, antiplatelet agents and cholesterol lowering therapy are theoretically attractive options for the prevention of such consequences.

In the present study, all patients received ticlopidine as well as aspirin. Our previous study [9] showed that ticlopidine reduced the development of SVG thrombi caused by nonlaminar or sluggish flow within the SVG. Several investigators have also reported that the addition of ticlopidine to aspirin significantly inhibited high shear stress which induced platelet aggregation [13]. In the present study, although the patients in both groups have received the same antiplatelet therapy, more than 70% of SVGs in group II still had thrombi; no thrombi, on the other hand, was detected in all group I SVGs. It should be demonstrated that thrombi on the yellow plaques were not only caused by platelet aggregation due to sluggish blood flow, but also by multiple plaque rupture of vulnerable plaques [14, 15]. The predominant mechanisms for SVG disease are intimal hyperplasia appearing from postoperative early phase and accelerated atherosclerosis. Saphenous vein graft atherosclerosis is especially prone to thrombi because of the high content of lipids and tissue factor, chronic flow disturbance, and impaired vasodilation. These SVG atheroma are more diffuse and vulnerable to rupture, and the consequences of plaque rupture in SVGs seem to be associated with almost certain thrombotic occlusion [12]. Therefore, regular antiplatelet therapy is not enough to avoid SVG thrombi; it may be more important and essential to interrupt the development of vulnerable yellow plaques.

A post-CABG trial with angiographic assessment has shown that aggressive lowering and maintenance of the LDL-C level below 100 mg/dL was more effective than moderate lowering of LDL-C in reducing the progression of atherosclerosis in SVGs. It defined the prognostic factors for risk of atherosclerotic progression in SVGs in the large and well-characterized post-CABG patient population [10]. In the present study, the LDL-C level of group I was maintained below 80 mg/dL. However, the National Cholesterol Education Program (NCEP) Adult Treatment Panel III guidelines now recommend achieving more aggressive target levels (an LDL-C level <70 mg/dL) in certain very high-risk secondary prevention patients [14]. O'Keefe and colleagues (15) also proposed, based on accumulating data from multiple populations that do not develop atherosclerosis or coronary events, that normal LDL-C levels are approximately 50 to 70 mg/dL. Von Birgelen and colleagues [16] further suggested that an LDL-C level of 75 mg/dL is, on average, associated with plaque regression. Moreover, many investigators have recommended "aggressive lipid-lowering therapy" as a recent international consensus to keep serum LDL-C level between 70 and 80 mg/dL in order to avoid the development of atherosclerotic plaques [17, 18].

Nissen and colleagues [19] reported that rosuvastatin had a strong effect on lowering the LDL-C level to less than 70 mg/dL. Harley and colleagues [20] also described that rosuvastatin was more effective at reducing LDL-C levels and attaining a NCEP LDL-C goal than other statins. In the present study, however, we mentioned the "aggressive lipid-controlling therapy" rather than "aggressive lipid-lowering therapy." Campeau and colleagues [21] observed that elevated plasma cholesterol and LDL-C, as well as low HDL-C, was associated with atherosclerotic progression in SVGs. Recently, it is important to control not only LDL-C but also HDL-C for preventing atherosclerosis development and coronary events. Astor and colleagues [22] suggested that a graded association exists between lower levels of HDL-C and were associated with increased risk of heart attack irrespective of the LDL-C levels. In fact, serum HDL-C levels are variable. Therefore, it is essential to examine the combined effects of higher HDL-C levels with various levels of LDL-C, and the LDL/HDL ratio was the most sensitive marker for the atherosclerosis progression [23]. Several studies proposed an LDL/HDL ratio of 2.0 or less to halt the progression of atherosclerosis [24, 25], while that of 1.5 or less produced remarkable regression of atherosclerosis [19, 26]. In the present study, aggressive lipid controlling therapy could keep the patient's LDL/HDL ratio less than 1.5. Furthermore, a serum LDL-C level was maintained at approximately 60 mg/dL, which was almost similar to the LDL-C level of that of a new born baby [15]. Therefore, SVG endoscopy shown as entire clear white intima in all SVGs by aggressive lipid control looked like "baby skin."

Study Limitation
This study has several limitations. It is a case control analysis of a single institution. Therefore, the sample size was slightly small, quantitative coronary analysis in angiography has not been conducted, and we have no data of coagulation factors in each patient. In the aggressive lipid controlling therapy, however, serum LDL-C and the LDL/HDL ratio were quite strictly controlled lower than 80 mg and 1.5, respectively. These lipid controls were much more aggressive than those of a previous report [10]. Furthermore, as far as we know, the data from SVG endoscopy in very high-intensity statin therapy is quite unique and results were obviously better than regular treatment. We have to keep observing the patients and future studies are needed to determine the effect of the observed changes on long-term outcome.

Conclusion
Prophylactic treatment for yellow plaque and thrombus formation are extremely important in the development of early and late SVG disease. Use of more effective new generation statins is vitally important to achieve a LDL/HDL ratio below 1.5. Aggressive lipid controlling therapy is quite attractive to avoid post-CABG SVG disease and the study indicated that it may be effective to maintain the long-term graft patency.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 

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  6. Shah PJ, Bui K, Blackmore S, et al. Has the in situ right internal thoracic artery been overlooked?. An angiographic study of the radial artery, internal thoracic arteries and saphenous vein graft patencies in symptomatic patients. Eur J Cardiothorac Surg 2005;27:870-875.[Abstract/Free Full Text]
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  8. Murphy GJ, Angelini GD. Insights into the pathogenesis of vein graft disease: lessons from intravascular ultrasound Cardiovasc Ultrasound 2004;2:8.[Medline]
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  15. O'Keefe Jr JH, Cordain L, Harris WH, Moe RM, Vogel R. Optimal low-density lipoprotein is 50 to 70 mg/dl lower is better and physiologically normal J Am Coll Cardiol 2004;43:2142-2147.[Abstract/Free Full Text]
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  18. Okazaki S, Yokoyama T, Miyauchi K, et al. Early statin treatment in patients with acute coronary syndrome. Demonstration of the beneficial effect on atherosclerotic lesions by serial volumetric intravascular ultrasound analysis during half a year after coronary event: The ESTABLISH Study. Circulation 2004;110:1061-1068.[Abstract/Free Full Text]
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