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European Heart Journal Advance Access originally published online on May 22, 2006
European Heart Journal 2006 27(15):1778-1784; doi:10.1093/eurheartj/ehl034
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© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Relation between baseline plaque burden and subsequent remodelling of atherosclerotic left main coronary arteries: a serial intravascular ultrasound study with long-term (≥12 months) follow-up

Marc Hartmann1, Clemens von Birgelen1,*, Gary S. Mintz2, Patrick M.J. Verhorst1 and Raimund Erbel3

1 Department of Cardiology, Medisch Spectrum Twente, Thoraxcentrum Twente, Haaksbergerstraat 55, 7513 ER Enschede, The Netherlands
2 Cardiovascular Research Foundation, New York, NY, USA
3 Department of Cardiology, Essen University, Essen, Germany

Received 2 March 2006; revised 27 March 2006; accepted 27 April 2006; online publish-ahead-of-print 22 May 2006.

* Corresponding author. Tel: +31 53 487 2490; fax: +31 53 487 2152. E-mail address: von.birgelen{at}12move.nl

See page 1761 for the editorial comment on this article (doi:10.1093/eurheartj/ehl129)


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Conclusions
 Acknowledgements
 References
 
Aims Glagov's histopathological observation and non-serial intravascular ultrasound studies (IVUS) concluded that compensatory coronary remodelling diminishes as 40% atherosclerotic plaque burden is reached. We tested this hypothesis with serial IVUS.

Methods and results Serial IVUS examinations of 46 atherosclerotic non-stenotic left main stems (18±8 months apart) were analysed to assess the relation between baseline plaque burden (=plaque+media area/vessel area) vs. serial remodelling (=vessel area at baseline–at follow-up). There were 25 plaques with baseline plaque burden <40% (30.1±6.6%, group A) and 21 plaques with baseline plaque burden ≥40% (46.1±5.8%, group B). There was no relation between baseline plaque burden vs. subsequent changes in vessel area overall (r=0.07, P=0.7), for group A (r=0.03, P=0.6), and group B (r=0.01, P=0.8). The frequency of positive serial remodelling (vessel area increase) vs. negative or intermediate serial remodelling (no change or decrease) were similar in group A [17 (68%) vs. 8 (32%)] and group B lesions [18 (86%) vs. 3 (14%)] (P=0.2).

Conclusion IVUS demonstrates that serial coronary remodelling is not related to baseline plaque burden. Lesions with baseline plaque burden <40% may subsequently show a lack of compensation or frank arterial shrinkage, whereas lesions with baseline plaque burden >40% may continue to develop compensatory enlargement.

Key Words: Coronary artery disease • Intravascular ultrasound • Remodelling


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Conclusions
 Acknowledgements
 References
 
The concept of positive remodelling—human coronary artery enlargement with increasing atherosclerotic plaque burden to maintain lumen dimensions—was introduced by Glagov et al.1 based on their histopathological data. Using regression analysis, they concluded that compensatory remodelling diminished when plaque burden reached a level of 40% and that plaque progression beyond this threshold lead to lumen narrowing.1 Early cross-sectional in vivo intravascular ultrasound studies (IVUS) at a single point in time confirmed these findings.2–5 However, all observations at a single point in time have shortcomings in analysing a dynamic process.6–15 In fact, direct evidence of remodelling requires serial measurements of total vessel dimensions obtained at two (or more) time-points.16–18

In the present study, we retrospectively analysed serial IVUS data in non-stenotic left main (LM) lesions to evaluate the relation between baseline atherosclerotic plaque burden and serial remodelling (i.e. subsequent changes in lesion site total vessel area).


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Conclusions
 Acknowledgements
 References
 
Study population
We retrospectively analysed serial IVUS data of 46 patients who had haemodynamically non-significant de novo LM atherosclerotic lesions and reliable reference segments. These 46 patients were derived from a population of 60 lesions that has previously been reported.10,18–20 Fourteen LM lesions were excluded because there was a lack of a well-defined reference.6,10

All patients meeting the following criteria were selected for retrospective analysis from our IVUS database: (i) serial high-quality IVUS imaging of the entire LM stem ≥12 months apart; (ii) calcifications that did not limit the quantitative assessment of vessel area (shadowing ≤75° of the adventitial circumference by individual calcific deposits; (iii) non-ostial target site location; (iv) angiographic lumen diameter stenosis <30% (‘worst view’ visual assessment); (v) no intervention in the very proximal left anterior descending or circumflex coronary artery segments because these interventions could have affected the LM artery; and (vi) well-defined lesion and reference segment image slices.6

Patients were examined in the Essen University Cardiac Catheterization Laboratory with a follow-up of 18±8 months (median 15 months, IQR: 12–20 months). Follow-up IVUS studies (each patient had one follow-up IVUS examination) were performed during clinically driven follow-up catheterization because of (i) repeat interventions of a (non-LM) coronary stenosis; (ii) re-evaluation of the results of interventional procedures; and/or (iii) clinical symptoms such as progression of angina pectoris (not related to significant LM stem disease). Differences in the timing of follow-up catheterization were not related to the target of the present study—LM coronary artery disease (CAD). The IVUS study was approved by the Local Council on Human Research. All patients signed a written informed consent form as approved by the Local Medical Ethics Committee.

Demographics, medication, and lipid profile
Demographics including cardiovascular risk factors, medications, and lipid profiles were recorded including diabetes mellitus and hypertension (medication-dependent); hypercholesterolaemia [medication-dependent, total serum cholesterol >200 mg/dL, or low-density lipoprotein (LDL) cholesterol >160 mg/dL]; history of smoking, and family history of CAD. Data of laboratory tests were the mean of the baseline and follow-up values. Plasma concentrations of total cholesterol, LDL cholesterol, high-density lipoprotein (HDL) cholesterol, and triglycerides were measured by standard enzymatic methods. Medication was recorded only if drugs were taken for >50% of the follow-up interval (e.g. clopidogrel for 4 weeks was not tabulated).

IVUS imaging
IVUS was performed as previously described.10,18 In brief, IVUS studies were performed during percutaneous coronary interventions of mid or distal left anterior or left circumflex arteries after intracoronary injections of 200 µg nitroglycerin. Two commercial systems were used: a mechanical sector scanner (Boston Scientific Corporation, San Jose, CA, USA) incorporating a 30 MHz single-element bevelled transducer or a solid-state device (Endosonics, Rancho Cordova, CA, USA). Slow continuous pullbacks of the IVUS transducer were started as distal as possible in one of the left coronary arteries and were generally performed using a motorized pullback device (at 0.5 mm/s). IVUS images of the entire pullback were recorded on 0.5 in. high-resolution s-VHS tape for off-line analysis. In addition, a dedicated image-in image system (Echo-Map, Siemens, Erlangen, Germany)21 was used to record the ‘angiographic’ position of the IVUS probe together with the corresponding IVUS image—especially, at sites of characteristic landmarks (i.e. calcifications or unusual plaque shapes) and/or the target site. Importantly, at Essen University, if a patient undergoes imaging with one IVUS system during an index procedure, the same IVUS system is used at follow-up.

IVUS analysis
The target lesion site image slice was the slice with the smallest baseline lumen area.18 If there were several slices with equal lumen size, the one with the largest total vessel and plaque+media (=total vessel minus lumen area) area was analysed.18 A LM stem reference image slice was selected as the most normal-looking cross-section (largest lumen with smallest plaque+media area) distal or proximal to the target lesion.10 Exact matching of the initial and follow-up IVUS studies was ensured using side-by-side comparison of the serial IVUS video sequences along with information of the pullback speed;6 the operators' recorded comments (on video tape); and characteristic calcifications, vascular and perivascular landmarks, and plaque shapes. If required, the angiographic sequences of the dedicated image-in-image system (Echo-Map) were revisited to optimize matching.21

The lumen area was measured by tracing the leading edge of the intima. The total vessel area was measured by tracing the leading edge of the adventitia. As in many previous IVUS studies, plaque+ media was used as a measure of atherosclerotic plaque because IVUS cannot measure media thickness accurately.6 Plaque burden (%) was calculated as (plaque+media divided by total vessel area)x100%. In our laboratory, the intraclass correlation coefficient is 0.99 for repeated measurements of total vessel, 0.96 for lumen, and 0.99 for plaque+media area. We used a cut-off value of 40% to compare the baseline and serial remodelling of lesions with a baseline plaque burden <40% (group A) vs. ≥40% (group B). Rationale for using this cut-off value, as introduced by Glagov et al. based on their regression analyses of histopathological data, was the fact that this value was considered to be a threshold above which no compensatory coronary remodelling occurs.1

Plaque composition was assessed visually as previously described.6 The arc of calcium was measured with a protractor centred on the lumen; if necessary, the total arc of calcium was obtained by adding arcs of individual deposits. As in previous IVUS studies,18,19,22 plaques were classified as calcified if the total arc of lesion calcium was >180°. Extrapolation of the total vessel area boundary behind calcium was possible, if each individual calcific deposit did not shadow >75° of the adventitial border.18

We calculated the changes between the initial and follow-up IVUS measurements. To compensate for the variation in follow-up interval and to obtain comparable data, measurements were normalized for the length of the follow-up period; and annual changes (i.e. changes per year) were calculated (normalized area changes=individual area changes divided by the individual follow-up period in months multiplied by 12), reported and compared.

The baseline remodelling index (RI) was calculated as lesion site divided by reference total vessel area.6,10 As in previous studies, a remodelling index >1 defined positive baseline remodelling and a remodelling index ≤1 intermediate/negative baseline remodelling.6,8–10 The change in lesion site total vessel area during follow-up was the measure of serial arterial remodelling. As in previous studies, changes in total vessel area >0 defined positive serial remodelling and changes in total vessel area ≤0 defined intermediate/negative serial remodelling.6,10,16–18

Statistical analysis
Analyses were performed with SPSS 13.0 (SPSS Inc., Chicago, IL, USA). Dichotomous data are presented as frequencies and compared using {chi}2 statistics or Fisher's exact test when at least 25% of values showed an expected frequency less than 5. Quantitative data are presented as mean±1 SD and compared using Student's t-test and linear regression analysis. Two-sided P-values of less than 0.05 were considered significant. The alpha-level was not adjusted for multiple testing, as we did not perform multiple testing.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Conclusions
 Acknowledgements
 References
 
Demographics, medications, and lipid profile
There were 25 plaques with a baseline plaque burden <40% (group A) and 21 plaques with a baseline plaque burden ≥40% (group B). Comparing these two groups, there were no differences in demographics, medications, and lipid profiles with the exception of more ACE-inhibitor use in group B (Table 1).


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  		Table 1 Demographics, medication, and lipid profile

 
Baseline IVUS data and Glagovian analysis
Baseline IVUS data are presented in Table 2. In keeping with the definitions, group B plaques had a greater baseline plaque burden than group A (P<0.0001). Because there is no difference in total vessel area, lumen area was significantly smaller in group B plaques when compared with group A plaques (P<0.0004). Plaque composition including the total arc of calcium did not differ between the two groups (Table 2). Using baseline IVUS measurements, it was possible to reproduce the linear relationship between plaque and vessel size as well as between plaque burden and lumen size that was first shown by Glagov et al.1 (Figure 1). There was a significant positive relation between plaque+media vs. total vessel area suggesting compensatory enlargement to accommodate for an increase in plaque size. There was a significant negative correlation between lumen area vs. plaque burden in lesions with plaque burden ≥40% (group B), but no relationship between lumen area vs. plaque burden in lesions with plaque burden <40% (group A) or in the entire study population (r=–0.18, P=0.4; data not shown) (Figure 1) suggesting a stop of compensatory enlargement beyond a plaque burden of 40%.


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  		Table 2 Baseline intravascular ultrasound data

 

Figure 0341
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  		Figure 1 Regression analyses following Glagov et al.1 with baseline IVUS data. Upper panel: There was a positive linear relation between plaque+ media and total vessel area (‘compensatory enlargement hypothesis’). Lower panel: There was a negative linear relation between baseline plaque burden and lumen area only in plaques with plaque burden >40% (‘compensatory cut-off hypothesis’).

 
Baseline remodelling index
There was no difference in baseline remodelling index or in the categorization of lesions as baseline positive vs. baseline intermediate/negative remodelling when comparing lesions with a plaque burden ≥40% vs. lesions with a plaque burden <40% (Table 2). For all 46 patients (Figure 2) as well as for group A or group B lesions separately (r=0.03, P=0.6, and r=0.01, P=0.8, respectively; data not shown), there was no relation between baseline remodelling index vs. baseline plaque burden, which disagrees with the hypothesis of Glagov et al.1 References of group B plaques showed a greater plaque burden (P<0.01), but total vessel and lumen area did not differ significantly between both groups (Table 2).


Figure 0342
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  		Figure 2 Relation between baseline plaque burden vs. baseline remodelling index and changes in total vessel area (serial remodelling). There was no relation between plaque burden vs. baseline remodelling index (upper panel) and changes in total vessel area (lower panel).

 
Serial IVUS data
Between groups A and B, there were no significant differences in the magnitude or the direction (increase or decrease) of the annual changes in total vessel or lumen area; in other words, there were no differences in serial remodelling between the two groups (Table 3). There was also no correlation between the change in total vessel area (i.e. serial remodelling) vs. the baseline plaque burden for all 46 patients (Figure 2) or for group A and group B plaques, separately (r=0.03, P=0.6, and r=0.01, P=0.8, respectively; data not shown). In fact, changes in total vessel area were flat across the entire range of values of baseline plaque burden, indicating no relation between baseline plaque burden and serial remodelling, which also contradicts the hypothesis of Glagov et al.1 In addition, there was no relation between the change in lumen area vs. the baseline plaque burden for all 46 patients (r=0.19, P=0.7; data not shown) and for group A and group B separately (r=0.25, P=0.2, and r=–0.13, P=0.6, respectively; data not shown).


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  		Table 3 Serial intravascular ultrasound data

 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Conclusions
 Acknowledgements
 References
 
Our serial IVUS data showed that serial coronary arterial remodelling (changes in total vessel area) was not related to baseline plaque burden in moderately diseased LM coronary arteries. Serial changes in vessel area were flat across the entire range of baseline plaque burden values (17.4–64.7%). Between lesions with a baseline plaque burden <40 vs. ≥40%, there was no difference in the frequency of positive and negative serial remodelling—i.e. the increase or decrease in vessel area.

Glagov et al.1 observed a positive correlation between total vessel area and plaque area in a histopathological study of 136 LM coronary arteries; he concluded that this indicated a compensatory enlargement of the vessel during atherogenesis. There was a negative correlation between plaque burden and lumen area in lesions with ≥40% plaque burden, but not in lesions with <40% plaque burden.1 Thus, a biphasic course of lesion formation was postulated: (i) early preservation of lumen dimensions up to a plaque burden of 40% and (ii) luminal narrowing as plaque burden exceeded 40%. In the present analysis, we reproduced these relationships using linear regression analysis of baseline IVUS data. However, as baseline lumen area is arithmetically related to baseline plaque burden (plaque burden=total vessel minus lumen divided by total vessel), the use of regression analysis of related variables to analyse different coronary remodelling patterns has theoretical limitations, as has previously been discussed.2,23 Furthermore, previous studies have reported a baseline remodelling index <1.0 (evidence of intermediate or negative baseline remodelling) in lesions with plaque burden <40%.9 In the present analysis, the baseline remodelling index was not related to baseline plaque burden, and the frequencies of positive vs. intermediate or negative baseline remodelling did not differ between plaques with a baseline plaque burden <40 vs. ≥40%.

Recently, we demonstrated that a baseline remodelling index correlated with serial remodelling (subsequent changes in total vessel area).10 However, for various reasons (e.g. limitations of a single time-point observation, reference segment selection, vessel tapering, plaque burden, and remodelling of the reference), these baseline indices are acknowledged to be only indirect evidence of serial remodelling.6,9 Direct evidence of remodelling requires serial vessel area measurements obtained at two (or more) time-points, as progression of atherosclerosis and changes in vessel dimension are both dynamic processes.2,6,7 Few studies have assessed coronary arterial remodelling using serial IVUS measurements.16–18 Such studies permit the assessment of remodelling independent of potential changes of the reference segment.6,10,16–18 Shiran et al.16 studied 31 moderately diseased (mean plaque burden <40%) LM stems and demonstrated that lumen changes during 6 months follow-up resulted primarily from changes in total vessel dimensions—i.e. serial remodelling. In the data presented by Schartl et al.,17 serial remodelling during 12 months IVUS follow-up did not differ between lesion with a baseline plaque burden <45 and ≥45%. In the present study, we demonstrated that magnitude and direction of the changes in total vessel area (the magnitude and direction of serial remodelling) were similar in plaques with a baseline plaque burden <40 vs. ≥40%. Thus, lesions with mild baseline plaque burden can either continue to compensate for continued plaque progression to preserve lumen dimensions (i.e. there can be additional serial positive remodelling) or these lesions may develop luminal stenosis as a result of either plaque progression without serial positive remodelling or shrinkage of the total vessel area (negative serial remodelling).10,16

Induction of plaque regression is a major target of pharmacological interventions.24,25 Treatment with multiple pharmacological agents (e.g. aggressive lipid lowering) may affect serial coronary remodelling (e.g. reverse remodelling) as well as plaque progression/regression.26,27

Limitations
As with most long-term serial IVUS studies, the current report included a relatively small number of patients. We only included patients who underwent non-LM intervention and who were admitted for repeat cardiac catheterization ≥12 months later; thus, the findings of the current study may not be applicable to the general population and other vessels. We only studied mild to moderate LM disease as representatives of non-intervened coronary segments; therefore, our findings may not be applicable to all (stenotic and non-stenotic) coronary segments. The range of plaque burden was somewhat limited (mean: 37.4±10.2%, median: 38.2%, range: 17.4–64.7%), however, serial IVUS assessment of significant luminal stenoses is difficult, as such lesions are generally stented and thus not available for follow-up. Heavily calcified lesions were excluded because ultrasound cannot penetrate calcified tissue to measure total vessel area (and remodelling) accurately.6 We used two IVUS systems; although this approach may have shortcomings, every effort was taken to obtain the most reliable data possible as previously discussed.10,18 Three-dimensional (electrocardiogram-gated) IVUS analyses may be superior for the assessment of atherosclerotic coronary arteries when compared with the two-dimensional analysis used in the current study.28 Of the 60 patients that were reported previously, only 46 patients could be included in the present analysis because of a lack of a well-defined reference segment in the other 14 patients.10,18 Intensive medical treatment (e.g. statins) may influence the remodelling process.17,26,27 Our data used only one definition of the baseline remodelling index; therefore, our findings may not apply to other definitions.8 In populations of more advanced atherosclerotic lesions, a predominance of soft plaque composition in lesions with positive remodelling has been shown.29 As previously reported, we could not demonstrate a relation between plaque composition and serial remodelling in our population.18 In addition, the IVUS analysis of coronary plaque composition based on radiofrequency data (‘virtual histology’) may be superior to visual assessment of plaque composition.30


   Conclusions
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusions
Acknowledgements
 References
 
This IVUS study demonstrates that serial coronary remodelling is not related to baseline plaque burden. Subsequent changes in vessel area are flat across a wide range of baseline plaque burdens. Arterial shrinkage can occur in lesions with baseline plaque burden <40%, whereas lesions with baseline plaque burden >40% may continue to develop compensatory enlargement.


   Acknowledgements
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusions
 Acknowledgements
References
 
The authors thank Dr Job van der Palen (Medisch Spectrum Twente, Enschede, The Netherlands) for statistical advice.

Conflict of interest: none declared.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusions
 Acknowledgements
 References
 

  1. Glagov S, Weisenberg E, Zarins CK, Stankunavicius R, Kolettis GJ. (1987) Compensatory enlargement of human atherosclerotic coronary arteries. N Engl J Med 316:1371–1375.[Abstract]
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