Impact of Local Atherosclerotic Remodeling on the Calculation of Percent Luminal Narrowing

doi:10.1016/S0002-9149(96)00775-8

The American Journal of Cardiology

Volume 79, Issue 4, 15 February 1997, Pages 402-405

https://doi.org/10.1016/S0002-9149(96)00775-8 Get rights and content

Abstract

The choice of the reference site in order to calculate percent luminal narrowing mainly depends on which diagnostic tool is used for examination. In intravascular ultrasound or histology, the local area encompassed by the internal elastic lamina (IEL) area is used as a reference. However, the local IEL area, and thereby the reference value, may have been altered by atherosclerotic remodeling. In the present study we examined the impact of local arterial remodeling on the calculation of luminal narrowing. Forty-five human femoral arteries were analyzed, 32 postmortem and 20 in vivo, by intravascular ultrasound. Cross sections were examined every 0.5 cm over an arterial segment length of 10 to 15 cm. In each cross section we measured the lumen area and the IEL area. Two reference areas were used to calculate percent luminal narrowing: (1) the lumen area in the cross section that contained the least amount of plaque (distant reference); and (2) the local IEL area (local reference). In each cross section, the IEL area was expressed as percent of the IEL area in the cross section that contained the least amount of plaque (relative IEL area). Using the distant reference, we found that less luminal narrowing was observed for cross sections with a relative IEL area >100% (indicating compensatory enlargement) than for those with a relative IEL area <100% (indicating shrinkage), whereas percent luminal narrowing calculated using the local reference hardly differed between cross section with a relative IEL area >100% and <100%. Thus, arterial wall remodeling makes the local IEL area an unreliable reference for calculation of percent luminal narrowing. The calculated percent luminal narrowing using a distant, nondiseased reference site reflects the actual change of the luminal area more accurately.

Section snippets

Histopathology

Thirty-two femoral arteries were taken from donated corpses (13 men and 19 women, mean age [± SD] 80.9 ± 8.6 years). Four arteries were obtained within 24 hours after postmortem examination and filled with glycol methacrylate technovit 7001 under a physiologic pressure of 90 mm Hg, and fixed in formalin 4%, pH 7.4. Twenty-eight femoral arteries were taken from corpses that had been fixed in formalin 4%, pH 7.4. The latter corpses had been fixed by pressure infusion (100 + age mm Hg) of formalin

Results

A total of 695 histologic and 444 intravascular ultrasound cross sections obtained from 32 and 26 arterial segments, respectively, were examined. Table 1 lists the number of cross sections found in each of the categories of relative IEL area together with the corresponding lumen area, IEL area, and plaque area.

Fig. 1 shows the relation between the calculated percent luminal narrowing using the reference that contained the least amount of plaque (distant reference) and the local IEL area (local

Discussion

The principal finding of this study was that a decrease in the luminal area (compared with a reference at the location with the least amount of plaque) was not reflected by the calculated percent luminal narrowing using the local area encompassed by the IEL area in the same transversal plane as a reference. Even when the lumen was found to be enlarged, due to overcompensation,5, 7a significant percent luminal narrowing was calculated if the local vessel size was used as a reference. The local

Acknowledgements

This study was supported by Grant 94-115 from the Dutch Heart Foundation.

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Relationship between carotid artery remodeling and plaque vulnerability with T1-weighted magnetic resonance imaging
2014, Journal of Stroke and Cerebrovascular Diseases
Citation Excerpt :
This is the first report to examine the relationship between histologic markers related to the carotid plaque vulnerability and carotid artery remodeling, suggesting that CRI is a useful marker of future stroke risk in significant carotid stenosis (≥50%). Because Gragov et al1 first reported expansive vessel remodeling to maintain an adequate luminal area in response to the development of atherosclerotic plaques at early stages, several studies using various imaging modalities2-8 have been published regarding outward remodeling and plaque vulnerability of the coronary artery. The Atherosclerosis Risk in the Communities study has assessed the carotid arteries of healthy individuals with B-mode ultrasound and found that, when carotid arterial enlargement accompanies increased wall thickness, there is less lumen constriction than expected, suggesting the pathogenesis of symptoms related to carotid stenosis.23
The aim of this study was to validate the relationship between carotid artery remodeling defined as the carotid remodeling index (CRI) and plaque vulnerability by comparing the degree of outward remodeling calculated using 3-dimensional inversion recovery-based T1-weighted imaging (magnetization-prepared rapid acquisition gradient echo [MPRAGE]) with the symptomatology and histology of plaques extracted during carotid endarterectomy.
Sixty-one patients with 50% stenosis or more (North American Symptomatic Carotid Endarterectomy Trial criteria) were included. The average rate of stenosis was 79.8%. The CRI was determined by measuring the external cross-sectional vessel area (CSVA) at the maximum stenosis of the internal carotid artery (ICA) and dividing it by the external CSVA at the distal ICA (unaffected by atherosclerosis) using MPRAGE imaging.
The CRI was significantly higher in symptomatic patients compared with asymptomatic patients (1.98 ± .26 versus 1.68 ± .24, P < .0001). A higher CRI positively correlated with the necrotic core area (r = .57, P < .0001) and negatively correlated with the fibrous cap thickness (r = −.33, P = .01). It was also significantly associated with severe intraplaque hemorrhage (P < .0001) and the prevalence of cap inflammation with macrophage (P = .03) and lymphocyte (P = .01) infiltration.
The larger outward remodeling of the carotid artery on MPRAGE imaging had symptomatic carotid plaques and histologically vulnerable plaques. This study indicates that MPRAGE imaging is useful for the assessment of carotid artery remodeling.
Positive remodeling is associated with more plaque vulnerability and higher frequency of plaque prolapse accompanied with post-procedural cardiac enzyme elevation compared with intermediate/negative remodeling in patients with acute myocardial infarction
2009, Journal of Cardiology
We assessed the impact of remodeling patterns on pre- and post-procedural intravascular ultrasound (IVUS) findings and cardiac enzyme elevation after stenting in 310 acute myocardial infarction (AMI) patients.
The positive remodeling (PR) (PR group, n = 113) was defined as remodeling index (lesion/reference external elastic membrane cross-sectional area) >1.05, intermediate remodeling (IR) as between 0.95 and 1.05, and negative remodeling (NR) as < 0.95 (IR/NR group, n = 197). IVUS findings included ruptured plaque (a cavity that communicated with the lumen with an overlying residual fibrous cap fragment), multiple ruptured plaques (different plaque ruptures separated by a >5-mm length of artery containing smooth lumen contours), thrombus (discrete intraluminal filling defects), and plaque prolapse (tissue extrusion through the stent strut at post-stenting). We compared pre- and post-procedural IVUS findings and cardiac-specific troponin I (cTnI) elevation after stenting according to the remodeling pattern.
The plaque rupture (60% vs. 42%, p = 0.004), multiple plaque ruptures (22% vs. 14%, p = 0.014), and IVUS-detected thrombus (42% vs. 28%, p = 0.012) were more common in the PR group compared with the IR/NR group. Post-stenting plaque prolapse was observed more frequently (36% vs. 22%, p = 0.008), and cTnI was elevated more significantly after stenting in the PR group compared with the IR/NR group (ΔcTnI; +7.8 ± 51.1 ng/ml vs. +0.9 ± 41.1 ng/ml, p = 0.008). Multivariate analysis showed that PR [odds ratio (OR) = 1.92; 95% CI 1.04–2.98, p = 0.028], plaque rupture (OR 1.98; 95% CI 1.16–3.45, p = 0.025), IVUS-detected thrombus (OR 2.30; 95% CI 1.22–3.98, p = 0.008), and plaque prolapse (OR 8.40; 95% CI 4.19–16.84, p < 0.001) were independently associated with post-stenting cTnI elevation.
AMI patients with PR have more plaque vulnerability and higher frequency of plaque prolapse accompanied by post-procedural cardiac enzyme elevation compared with AMI patients with IR/NR.
Arterial Remodeling Patterns before Intervention Predict Diffuse In-Stent Restenosis: An Intravascular Ultrasound Study
2003, Journal of the American College of Cardiology
Citation Excerpt :
There is evidence that positive remodeling may be initially advantageous in that it prevents luminal stenosis but disadvantageous in that significant expansive remodeling may make the plaque more vulnerable (18,19). Inversely, lesions with negative remodeling may be related to higher grade stenoses (20,21), but may appear more stable. Schoenhagen et al. (18)revealed that larger plaque and vessel areas and positive remodeling were associated with unstable angina pectoris, whereas negative remodeling was more common in patients with stable angina pectoris.
The aim of this retrospective study was to determine the predictors of diffuse in-stent restenosis (ISR) among the lesions causing the first ISR by intravascular ultrasound (IVUS) studies.
Although some predictors of diffuse ISR have been reported, parameters on IVUS relating to diffuse ISR are not well characterized.
We classified 52 ISR lesions that had undergone successful stent implantation and led to restenosis into two types—focal and diffuse ISR—using quantitative coronary angiography. Restenosis was defined as ≥50% diameter stenosis, and diffuse ISR as lesion length ≥10 mm at follow-up. The remodeling index (RI) was defined as the vessel area at the target lesion divided by that of averaged reference segments.
There were no significant differences in patient, angiographic, and procedural characteristics between the focal (n = 25) and diffuse (n = 27) ISR groups. Baseline RI was significantly greater in the diffuse ISR group (1.03 ± 0.18 vs. 0.88 ± 0.24, p = 0.0159). Negative remodeling, defined as RI <0.9, was detected in 60% of the focal ISR group and in only 26% of the diffuse ISR group. By logistic regression analysis, baseline RI was the only independent predictor of diffuse ISR (p = 0.0341). Moreover, volumetric analyses revealed that lesions developing into diffuse ISR had less capacity to compensate for further plaque growth.
Among the first ISR lesions, baseline positive remodeling was the most powerful predictor of diffuse ISR. Measuring pre-interventional arterial remodeling patterns by IVUS may be helpful to stratify lesions at higher risk.
The contribution of plaque and arterial remodeling to de novo atherosclerotic luminal narrowing in the femoral artery
2002, Journal of Vascular Surgery
Background: Atherosclerotic luminal narrowing is caused by plaque growth and arterial remodeling. In peripheral arteries, a role for constrictive remodeling in luminal narrowing has been recognized, but the impact on lumen decrease has not yet been assessed. We studied to what extent arterial remodeling and plaque formation contribute to luminal narrowing in the superficial femoral artery. Methods: Elderly subjects (n = 79) were studied. Post mortem, pressure-fixed femoral arteries (n = 125) were dissected and divided into 0.5-cm segments (n = 3266). In each cross section, we measured lumen area, plaque area, and the area encompassed by the internal elastic lamina (IEL area). For each artery, the cross section with the least amount of plaque was considered the reference segment. In cross sections with a decrease in lumen area compared with the reference, we determined the contributions of both plaque increase and IEL area change. Results: A decrease in lumen area was found in 2193 cross sections. In cross sections with >50% lumen stenosis, plaque increase (accompanied by IEL area increase) fully explained lumen decrease in 80 of 280 cross sections (29%). In the remaining 200 of 280 cross sections (71%), both plaque increase and IEL area decrease contributed to lumen stenosis. In 57 of 280 cross sections (20%), IEL area decrease was the major determinant of lumen decrease, dominating over plaque increase. In 143 of 280 cross sections (51%), plaque increase was the major determinant, dominating over IEL area decrease. Conclusion: The results of this post mortem study suggest that in a substantial part (20%) of severely stenotic lesions in the femoral artery, constrictive remodeling, not plaque size, is the major determinant of lumen decrease. Further serial studies are needed to confirm these results. (J Vasc Surg 2002;36:1194-7.)
Atheromas that cause fatal thrombosis are usually large and frequently accompanied by vessel enlargement
2001, Cardiovascular Pathology
Several lines of clinical evidence show that AMI frequently occurs at sites with mild to moderate degree of coronary stenosis. The degree of luminal stenosis depends on plaque deposition and degree of vessel remodeling, features poorly assessed by coronary angiography. This postmortem study tested the hypothesis that the size of coronary atheroma and the type of remodeling distinguish culprit lesion responsible for fatal AMI from equi-stenotic nonculprit lesion in the same coronary tree. The main coronary branches from 36 consecutive patients with fatal AMI were studied. The culprit lesion (Group 1) and an equi-stenotic nonculprit segment (Group 2) obtained in measurements of another coronary branch from the same patient were compared. Morphometry and plaque composition was assessed in both groups. Compared to Group 2, Group 1 had larger areas of: plaque 9.6 vs. 4.7 mm², vessel 12.7 vs. 7.4 mm² and lumen 1.7 vs. 1.2 mm²; (P<.01). Positive remodeling was more frequent in Group 1 than Group 2: 21/30 (70%) vs. 8/26 (31%). Plaque area correlated positively with lipid core and macrophages and negatively with fibrosis and smooth muscle cells. Atherosclerotic plaques that cause fatal thrombosis are more frequently positively remodeled and tend to be larger than nonculprit plaques with the same degree of cross-sectional stenosis. We tested whether arterial remodeling and plaque size vary between segments containing a fatal thrombosed plaque versus an equi-stenotic nonculprit plaque. Culprit vessel segments had higher cross-sectional areas of intimal plaque and of vessel wall than equi-stenotic nonculprit plaques. The cross-sectional area of the vessel correlated positively with both the lipid core area and CD68⁺ macrophage content, and negatively with fibrosis area and smooth muscle cell content. These results add elements explaining limitations of angiography in identifying plaques and provide new insights into the role of remodeling in plaque instability.
Relation of arterial geometry to luminal narrowing and histologic markers for plaque vulnerability: The remodeling paradox
1998, Journal of the American College of Cardiology
Objective. To relate local arterial geometry with markers that are thought to be related to plaque rupture.
Background. Plaque rupture often occurs at sites with minor luminal stenosis and has retrospectively been characterized by colocalization of inflammatory cells. Recent studies have demonstrated that luminal narrowing is related with the mode of atherosclerotic arterial remodeling.
Methods. We obtained 1,521 cross section slices at regular intervals from 50 atherosclerotic femoral arteries. Per artery, the slices with the largest and smallest lumen area, vessel area and plaque area were selected for staining on the presence of macrophages (CD68), T-lymphocytes (CD45RO), smooth muscle cells (alpha-actin) and collagen.
Results. Inflammation of the cap or shoulder of the plaque was observed in 33% of all cross sections. Significantly more CD68 and CD45RO positive cells, more atheroma, less collagen and less alpha-actin positive staining was observed in cross sections with the largest plaque area and largest vessel area vs. cross sections with the smallest plaque area and smallest vessel area, respectively. No difference in the number of inflammatory cells was observed between cross sections with the largest and smallest lumen area.
Conclusion. Intraindividually, pathohistologic markers previously reported to be related to plaque vulnerability were associated with a larger plaque area and vessel area. In addition, inflammation of the cap and shoulder of the plaque was a common finding in the atherosclerotic femoral artery.

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Impact of Local Atherosclerotic Remodeling on the Calculation of Percent Luminal Narrowing

Abstract

Section snippets

Histopathology

Results

Discussion

Acknowledgements

Am J Cardiol

J Vasc Surg

Atherosclerosis

Am Heart J

The effect of balloon angioplasty on the femoral artery evaluated with intravascular ultrasound

Circulation

Focal compensatory enlargement of human arteries in response to enlarging atherosclerotic plaques

Circulation