(Circulation. 1996;94:966-972.)
© 1996 American Heart Association, Inc.
Articles |
Significance of Automated Stenosis Detection During Quantitative Angiography
Insights Gained From Intracoronary Ultrasound Imaging
the Cardiac Catheterisation and Intracoronary Imaging Laboratories, Thoraxcenter, Rotterdam, the Netherlands.
Correspondence to Patrick W. Serruys, MD, PhD, Catheterisation Laboratory, Thoraxcenter, Erasmus University, Postbus 1738, 3000 DR Rotterdam, Netherlands.
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Abstract |
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Background Automated stenosis analysis is a common feature of commercially available quantitative coronary angiography (QCA) systems, allowing automatic detection of the boundaries of the stenosis, interpolation of the expected dimensions of the coronary vessel at the point of obstruction, and angiographically derived estimation of atheromatous plaque size. However, the ultimate meaning of this type of analysis in terms of the degree of underlying atherosclerotic disease remains unclear. We investigated the relationship between stenosis analysis performed with QCA and the underlying degree of atherosclerotic disease judged by intracoronary ultrasound (ICUS) imaging.
Methods and Results In 40 coronary stenoses, automated identification of the sites of maximal luminal obstruction and the start of the stenosis was performed with QCA by use of curvature analysis of the obtained diameter function. Plaque size at these locations also was estimated with ICUS, with an additional ICUS measurement immediately proximal to the start of the stenosis. Crescentlike distribution of plaque, indicating an atheroma-free arc of the arterial wall, was recorded. At the site of the obstruction, total vessel area measured with ICUS was 16.65±4.04 mm2, whereas an equivalent measurement obtained from QCA-interpolated reference dimensions was 7.48±3.30 mm2 (P=.0001). Plaque area derived from QCA data was significantly less than that calculated from ICUS (6.32±3.21 and 13.29±4.22 mm2, respectively; mean difference, 6.92±4.43 mm2; P=.0001). At the start of the stenosis identified by automated analysis, ICUS plaque area was 9.38±3.17 mm2, and total vessel area was 18.77±5.19 mm2 (50±11% total vessel area stenosis). The arterial wall presented a disease-free segment in 28 proximal locations (70%) but in only 5 sites (12%) corresponding to the start of the stenosis and none at the obstruction (P=.0001). At the site of obstruction, all vessels showed a complete absence of a disease-free segment, and the atheroma presented a cufflike or all-around distribution with a variable degree of eccentricity.
Conclusions At the site of maximal obstruction, QCA underestimated plaque size as measured with ICUS. Atherosclerotic disease was consistently present at the start of the stenosis and was used as a reference site by automated stenosis analysis. At the start of the stenosis, ICUS demonstrated a mean 50±11% total vessel area stenosis, with a characteristic loss of disease-free arcs of arterial wall present in proximal locations. Thus, the site identified by automated stenosis analysis as the start of the stenosis does not represent a disease-free site but rather the place where compensatory vessel enlargement fails to preserve luminal dimensions, a phenomenon that seems related to the observed loss of a remnant arc of normal arterial wall.
Key Words: angiography • ultrasonics • coronary disease • vessels
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Introduction |
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During its relatively short history, the role of coronary angiography as a standard in the assessment of coronary artery disease has been challenged by two types of limitations. First, visual assessment of stenosis severity from the cineangiogram is associated with high intraobserver and interobserver variabilities.1 2 3 4 Second, major discrepancies between the appearance of the opacified vascular lumen and the actual degree of underlying atherosclerosis have been reported.5 6 7 8 9 These can be due to the presence of extensive diffuse disease that affects the whole length of the opacified coronary tree, without a remnant "healthy'' reference segment. More importantly, underestimation of the extent of atherosclerotic disease may occur because during the development of both diffuse and focal atherosclerotic lesions coronary arteries undergo compensatory enlargement.10 11
The advent of quantitative coronary angiography (QCA) has significantly reduced the first limitation. Several quantitative angiography systems, including the Cardiovascular Angiography Analysis System (CAAS), can perform automated stenosis detection in a given coronary segment.12 13 With the use of information obtained from computerized analysis of the entire segment, automated analysis not only detects the proximal and distal boundaries of the stenosis but also interpolates the expected dimensions of the coronary vessel at the point of obstruction (a so-called interpolated reference). The angiographic estimation of the amount of atheromatous plaque derived from this data also is a common feature of commercially available QCA packages, which are likely to become more widely used because they are now built-in features of many modern digital angiographic systems. However, whether the data calculated from automated stenosis analysis can provide reliable information on the degree or presence of underlying atherosclerotic disease remains unknown.
Intracoronary ultrasound (ICUS) can provide in vivo information on the characteristics of the arterial wall.14 15 This characteristic justifies its growing application in the study of atherosclerotic coronary artery disease15 16 17 18 19 20 21 22 and its proposal as an alternative to coronary angiography.14 However, comparisons between ICUS and QCA have been confined only to its ability to measure luminal dimensions and have never been used to investigate the significance of other findings obtained during automated stenosis analysis.14
The objective of this study was twofold. First, we wanted to investigate with ICUS the characteristics of the arterial wall at the site identified by automated stenosis analysis as the proximal boundary of the stenosis because previous studies with QCA assumed the absence of atherosclerotic disease at this location for the calculation of interpolated reference dimensions.23 Second, we were interested in assessing with ICUS whether, at the site of maximal luminal obstruction, the amount of atheroma derived from automated stenosis analysis reflects the degree of atherosclerotic involvement.
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Methods |
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Patient Population
The study population consisted of 40 patients (31 men, 9 women) with de novo coronary stenosis undergoing cardiac catheterization immediately before percutaneous revascularization. Mean age was 61±10 years. All investigations were approved by the Institutional Review Board of the Thoraxcenter, and patients were studied after giving informed consent.
Quantitative Angiography
In this study, both on-line and off-line QCAs were performed. After administration of intracoronary nitrates to control vasomotor tone and before ICUS examination, on-line angiographic measurements were performed by use of a Philips DCI angiography system in conjunction with a commercially available quantitative angiography package (ACA, Philips). The results of the analysis, including the location of the beginning and end of the stenosis and the point of maximal luminal obstruction identified by the computerized analysis, were permanently displayed on a video monitor, serving as a guide for the operator during the ultrasound study. Coronary cineangiograms also were obtained and later analyzed off-line with an edge detection quantitative angiography system (CAAS II, Pie Data)24 25 that uses an algorithm similar to the ACA package for stenosis identification and reference diameter interpolation.26 A description of the consecutive steps followed during the analysis of the cineangiogram is given below.
Image Acquisition
End-diastolic angiographic frames showing the stenosed vessel were selected. By use of a CCD camera, a region of interest of 512x512 pixels encompassing a wide vascular segment proximal to the stenosis was selected in the cineframe and digitized for subsequent analysis (Fig 1A
).
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Identification of Luminal Edges
After the vessel centerline was identified by the computer algorithm, a number of scan lines perpendicular to it were obtained. Luminal edges were detected on the basis of a weighted sum of the first and second derivative functions of the brightness profile of each scan line (Fig 1B
).
Diameter Function
Vessel diameters were determined by computing the shortest distance between the left- and right-edge positions. These measurements were converted to absolute values with the coronary guiding catheter used as a scaling device. When all consecutive diameter values obtained at 
0.2-mm intervals were plotted over the analyzed vessel length, a so-called diameter function was created (Fig 1C). The catheter tip was filmed empty of contrast and used as a scaling device during the calculation of absolute diameter values.
Identification of the Start of the Stenosis
Application of specific algorithms to the diameter function made possible the identification of the vessel site in which critical changes in diameter values occurred. In any coronary segment analysis, it is possible to observe dips in the diameter function resulting from changes in luminal diameter or image noise. To discriminate between these artifactual changes and the actual change in luminal diameter associated with the start of a stenosis, the diameter function was analyzed with the CAAS II by use of a curvature detection algorithm that identifies maxima in curvature through variable degrees of smoothing. The algorithm is nearly identical to that described by Rosenfeld and Johnston.27 The proximal and distal boundaries of the obstruction are defined by the positions featuring the first local maximum in curvature in the proximal and distal directions, respectively, with respect to the minimal diameter position. The extent of the stenosis is indicated in the diameter function by two dotted lines as represented by a shaded area superimposed on the artery (Fig 1C).
Identification of the Site of Obstruction
From the diameter function, the site of obstruction was identified as that corresponding to the lowest diameter value in the segment encompassed between the start and end of the stenosis.
Interpolated Reference Diameter
The third parameter derived from the analysis of the diameter curve is the interpolated reference diameter. After the creation of a first-degree polynomial computed through the diameter values of the proximal and distal portions of the arterial segment, a translation to the 80th percentile level was performed. Combining this information with the location of the obstruction yielded the expected vessel diameter at the site of minimal luminal diameter. In this way, a correction for the expected changes in vessel diameter between the start and end of the stenosis, such as those resulting from the origin of side branches, is introduced.
Angiographically Derived Plaque Area
On the basis of the premises discussed above, plaque area was defined as the difference between the interpolated and luminal dimensions at the obstruction site (Fig 2). This is a variation of the calculation of plaque area performed in the CAAS and other commercially available systems12 13 in the longitudinal axis (Fig 1B) and was chosen to facilitate its comparison with cross-sectional areas measured with ICUS (Fig 2).
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Intracoronary Ultrasound
ICUS was performed with a 30-MHz ICUS system (Cardiovascular Imaging Systems, Inc). Data collection was restricted to the preangioplasty stage according to the following protocol, which was designed to minimize examination time and to reduce potential risks associated with ICUS examination. Once the stenosis was crossed with the guide wire, the operator was free to perform any contrast injection and maneuver with the guiding and ICUS catheters required to advance the ultrasound catheter safely to a location distal to or wedged in the stenosis. This location was documented by contrast injection. Acquisition of ICUS and fluoroscopy images was then begun. The observer was free to adjust gain, magnification, and other settings of the ultrasound system to obtain optimal visualization of the plaque and luminal borders. Then a slow pullback of the ICUS catheter was performed, documenting its angiographic location with frequent contrast injections. Particular attention was paid to documentation of the location of the ICUS catheter in three specific locations identified by QCA: the site of maximal obstruction, the start of the stenosis as identified by QCA analysis, and a more proximal location that was adjacent to the start of the stenosis but was not identified as part of a lesion by QCA analysis (Fig 3). If satisfactory images were recorded during the pullback, the ICUS catheter was withdrawn and coronary angioplasty was continued. After the procedure, off-line analysis of ICUS images obtained at the three locations was performed with the videotaped images. The analysis was performed independently in two separate sessions by two observers with expertise in ICUS. A digital planimeter, which is a built-in feature of the described ICUS system, was used to obtain area measurements. The following variables were recorded. First, luminal cross-sectional area was obtained by planimetry after identification of the luminal borders, which was facilitated by frequent injections of contrast medium intended also for angiographic documentation. Second, cross-sectional area of artery or total arterial area also was obtained by planimetry after the area contained within the inner border of the echo-lucent media was traced. Third, plaque area was calculated from ultrasound as the difference between total arterial area and luminal area. The degree of obstruction caused by atheroma in the potential luminal area, or percent area stenosis, was calculated according to the following formula: (Plaque Area/Total Arterial Area)x100, assuming that total arterial area equals that within the internal elastic lamina. Fourth, two patterns of atheromatous involvement as judged by ICUS were used to classify coronary segments in those with or without a remnant arc of vascular wall free of atheroma (crescentlike and cufflike distributions, respectively).
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Correlation Between ICUS and QCA Data
A number of measures were taken to ensure that ICUS images matched the angiographically defined locations described above. First, on-line quantitative analysis was performed and displayed on one of the monitors to be used as a reference during the entire procedure. Second, simultaneous recording of fluoroscopic and echocardiographic images was performed with a digital video mixer to facilitate the subsequent correlation between ultrasound images and specific angiographic locations. Finally, additional information on the course of the ICUS examination, such as the position of the echo probe at different locations within the coronary artery, was recorded throughout the procedure in predesigned logbook forms with the time counter of the ICUS system (which is included in all images recorded) used as a reference.
Calculation of luminal area from QCA was obtained off-line as an average of measurements obtained in two different angiographic views. The spatial correlation between ICUS images and QCA data was performed in the angiographic projection used during the procedure and later during off-line analysis, which was chosen as the best for the purposes of this study.
Exclusion Criteria
Vessels with anatomic features that interfere with computerized stenosis analysis, including ostial lesions in which a proximal segment of the vessel was not present and total or functional occlusions with incomplete opacification of the coronary segment distal to the stenosis, were excluded from the study. Likewise, vessels in which ICUS examination was deemed infeasible were excluded. These included stenoses with heavy calcification resulting in complete shadowing during ICUS, which precluded the visualization of the echo-lucent media and other structures used in ICUS measurements, and vessels with extreme tortuosity in which difficult negotiation of the device was anticipated.
Statistical Analysis
Mean±SD was calculated for all continuous variables. Least-squares linear regression analysis was performed, and correlation coefficients were calculated. Interobserver variability was expressed as the mean difference±SD of the measurements obtained by the two ICUS observers. Likewise, mean difference±SD was used to express the disagreement between ICUS and QCA measurements. Continuous variables were compared by use of two-tailed paired and unpaired Student's t tests (with Bonferroni's correction when more than two groups were compared) and one-factor ANOVA as required. A value of P<.05 was considered statistically significant.
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Results |
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Examination of the vessel with ICUS was successful in 40 patients. There were no complications associated with ICUS, although transient myocardial ischemia was frequent at the time when the stenosis was crossed with the ultrasound catheter. Wedging of the ICUS catheter in the stenosis was observed in 24 cases (60%). The mean difference in ICUS measurements obtained by the two observers was 0.12±1.31 mm2 for luminal area, 0.30±2.46 mm2 for total vessel area, and 0.40±2.53 mm2 for plaque area.
Findings at the Site of Maximal Obstruction
QCA revealed a minimal luminal cross-sectional area of 1.24±1.12 mm2. At the site of obstruction, ICUS yielded a luminal area of 2.80±1.64 mm2. In the 16 cases in which the ultrasound catheter was not wedged, a good correlation between angiographic and ICUS luminal measurements was observed (QCA luminal area=0.45xICUS luminal area-0.40; r=.78; P=.0002).
At the site of the obstruction, ICUS revealed a total vessel area of 16.65±4.04 mm2 (83±10% total vessel area stenosis; Fig 4). This was significantly larger than that calculated from interpolated reference dimensions obtained with QCA (7.48±3.30 mm2, P=.0001). Thus, QCA underestimated the dimensions of the original vessel as assessed with ICUS. As a result of this difference, plaque area derived from angiographic data was significantly less than that calculated from ICUS data (6.32±3.21 and 13.29±4.22 mm2, respectively; mean difference, 6.92±4.43 mm2; P=.0001). Regression analysis yielded a poor correlation between both estimates of plaque size, with severe underestimation of ICUS plaque by QCA (QCA plaque area=0.23xICUS plaque area+3.25; r=.31; P=.05; Fig 5).
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Findings at the Start of the Stenosis and in the Proximal Vessel
At the site identified as the start of the stenosis by QCA analysis, ICUS plaque area was 9.38±3.17 mm2, and total vessel area was 18.77±5.19 mm2 (50±11% total vessel area stenosis). Proximal to that location, the vessel presented a similar total vessel area (19.67±5.00 mm2). Although this location was not included in the stenosis by QCA analysis, atheromatous involvement was demonstrated in all cases, although with smaller plaques (7.79±2.91 mm2; total vessel area stenosis, 40±14%; Fig 4).
Qualitative Aspects of Atheromatous Involvement at the Site of Obstruction, Start of the Stenosis, and Angiographically Normal Locations
Significant differences were found in the distribution of the atheromatous plaque around the lumen in the three locations studied. Thus, the arterial wall presented a disease-free segment in 28 proximal locations (70%) but in only 5 sites (12%) corresponding to the start of the stenosis and none at the obstruction (P=.0001; Fig 6). At the site of obstruction, all vessels showed complete absence of a disease-free segment, and the atheroma presented a cufflike or all-around distribution with a variable degree of eccentricity.
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Discussion |
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From a historical viewpoint, the reason for the development of computerized analysis of the stenosis was to provide objective, automated selection of a coronary reference segment because atherosclerotic involvement has been demonstrated at coronary locations with normal angiographic appearance.28 29 Coronary angiography represents a "luminogram" or "shadowgram" of the vessel, and its visual interpretation conveys little or no information about the extent of atherosclerotic disease in the arterial wall. Studies comparing angiographic and pathological data have demonstrated that visual interpretation of the angiogram underestimates the degree of underlying disease both at the site of the obstruction and in segments that are apparently free of disease.5 6 7 8 9 Thus, although the advent of QCA systems had facilitated a more accurate assessment of luminal obstruction, selection of a reference coronary segment for clinical and research purposes remained hampered by these limitations.
In an attempt to find a solution to this problem, several automated methods of analysis of the luminal dimensions have been developed12 13 to provide objective identification of the boundaries and lengths of the stenosis and identify a segment apparently free of atherosclerotic disease to be used as a reference during the calculation of relative measurements and for the application of interpolated reference techniques. As described above, the approach followed by the CAAS consists of applying specific algorithms to a so-called diameter function, obtained by plotting all consecutive luminal diameters in the vascular segment encompassing the stenosis. However, the relationship between computerized analysis of the luminal dimensions in a segment that encompasses a stenosis and the underlying degree of atherosclerosis has not been studied previously. The possibility of inferring information about the degree of underlying atherosclerotic disease from such computerized analysis of luminal dimensions would be supported by the concept that atherosclerosis is a focal30 rather than a diffuse31 32 process. In this regard, Baroldi33 found in a pathological study of 565 atherosclerotic coronary vessels that the length of coronary lesions was <5 mm in 13%, between 5 and 20 mm in 38%, and >20 mm in 49% of cases. Thus, a substantial number of coronary lesions have a length covered by conventional computerized angiographic analysis of a vascular segment.
Intravascular ultrasound is a novel technique that allows the visualization of the vessel wall and has been validated in pathological specimens in vitro.15 17 The technique may not be the ideal "gold standard'' in the assessment of coronary artery disease because of a number of factors that may interfere with plaque characterization and the performance of measurements. However, it offers the unique advantage of obtaining information on the structure and dimensions of the coronary artery under in vivo conditions,21 free of multiple pitfalls related to the processing of histological material in postmortem studies, and allowing comparison with other information, such as coronary angiography, obtained simultaneously in the same patient.
Our observations with ICUS indicate that atherosclerotic involvement at the site identified by QCA as the start of the lesion is common. Therefore, the site identified by the curvature detection algorithm in the diameter function does not correspond, as first thought, to a coronary location free of atherosclerotic disease. Interestingly, we found that at this level, total vessel area stenosis is quite similar to that found by Glagov et al10 to be related to the failure of compensatory mechanisms of vessel enlargement, which is observed during the early phases of atherosclerosis progression (Fig 4).10 The observations reported by other authors in coronary segments with minimal or no luminal narrowing as assessed by angiography support our findings.16 17 18 In such segments, total vessel area was occupied by atheroma in 35±23% and 45±15% in the work of Tobis et al17 and Hodgson et al,18 respectively. Although these observations were performed with different aims and therefore the collection of data was not matched with computer analysis of the stenosis, it is fair to conclude that protrusion of atheroma into the lumen probably does not occur below an atherosclerotic involvement causing 50% reduction in total vessel area, which is located at the start of the angiographic stenosis. On the basis of these observations, we can formulate the first conclusion of our study: The proximal boundary of the stenosis identified during automated stenosis analysis with the CAAS does not correspond to a location free of atherosclerotic disease but presumably to the site where the compensatory mechanisms of vessel enlargement fail to preserve luminal dimensions.
Some qualitative observations performed in the present study with ICUS may provide new insights into the mechanisms underlying compensatory vessel enlargement. We found that at the level of the proximal boundary of the stenosis, there was a significant change in the distribution of the atheroma around the coronary lumen compared with more proximal locations. This consisted of a change from a crescentlike pattern of atheroma, which was the dominant pattern in a proximal location, to a cufflike pattern at the start of the stenosis (Fig 6). At the point of maximal luminal obstruction, only the latter pattern of atheroma distribution was observed, an observation that agrees with the findings of Hangartner et al34 in a pathological study. The loss of an arc of disease-free wall, characteristic of the crescentlike distribution of atheroma, may, as first proposed by Glagov et al,10 be critical in the loss of compensatory vessel enlargement, a phenomenon that, as the present study suggests, can be observed at the start of the stenosis defined by computerized analysis of the angiogram. Previous work has demonstrated that in the presence of a normal arterial wall, vessel enlargement occurs in circumstances of increased shear rate, a phenomenon that appears to be endothelium mediated.35 During the progression of coronary artery disease, reactive expansion to the increased shear stress may constitute the basis of compensatory vessel enlargement, but it would be expected to disappear when a complete loss of normal reactive wall occurs.36 The abolishment of such a compensatory response might be due to complete encroachment of the lumen by atheroma, leading to a rapid decrease in luminal dimensions caused by inward growth of the atheromatous plaque. This phenomenon might explain the disproportionately larger degree of progression in the reference diameter found in a major study on atherosclerosis regression37 because a relatively small progression in the disease process enhanced by disturbances in flow caused by the narrowing of a neighbor36 may have led to the critical loss of a remnant arc of reactive vessel wall. These findings complement previous intravascular ultrasound16 38 and pathological34 observations on the presence of multiple crescents of atheroma in angiographically normal coronary segments, representing foci of atheroma progression that have not caused luminal obliteration owing to ongoing compensatory enlargement.
Finally, we also observed that interpolated techniques are of no use in obtaining a reliable estimate of the underlying plaque area. The basic premise of this principle is that at the point of minimal luminal narrowing, the interpolated reference area should be representative of that within the internal elastic lamina. However, we found that the interpolated reference area calculated by QCA was significantly smaller than the total vessel area observed with ICUS. This may be due in part to the initial failure of the curvature detection algorithm to identify a segment in which no disease was present on which the interpolation could be based. A second source of error could be the occurrence of focal compensatory vessel enlargement, as recently demonstrated with intravascular ultrasound by Losordo et al39 in peripheral arteries.
Study Limitations
Our study is not free of limitations. Because wedging of the ultrasound catheter was required in a number of cases to visualize the vessel wall at the site of maximal obstruction, distortion of the vessel (Dotter effect) at that site may have occurred.40 However, because atheroma is not compressible, we believe that this would not substantially influence the measurement of plaque size or the distribution of atheroma (which, as stated above, was always distributed circumferentially around the lumen at the level at which dottering might occur). Although the correlation between the angiographic and ICUS location was optimized by use of simultaneous recording of both imaging modalities and record forms as described above, some degree of spatial mismatch remains possible. In this regard, no reproducibility data on the measurements obtained can be offered because, as discussed in the "Methods" section, a single passage of the ICUS catheter through the stenosis was performed whenever possible for the sake of patient safety. Attenuation of the ultrasonic beam may interfere with identification of plaque boundaries, even when, as in our study, heavy calcification constituted an exclusion criterion. Likewise, angulation of the catheter and variations in the angle of incidence of the ultrasonic beam may affect the quality of the images and measurements obtained. Tracing of luminal and medial boundaries was performed manually and therefore was subjective. Finally, plaque area from angiographic dimensions was calculated with the assumption of circular morphology for both the lumen and the internal elastic lamina.
Conclusions
Despite these limitations, we believe that the observations performed during this study introduce a change in the concepts that are routinely used in quantitative coronary angiography with regard to automated stenosis analysis and reinforce the limitations inherent in the use of angiography in estimating the degree of atherosclerotic involvement in the coronary arteries. Automated stenosis analysis and other QCA features provide information on the hemodynamic relevance of a stenosis, and their application has been shown to have prognostic importance.41 Although the latter aspect has not been demonstrated with ICUS, it is foreseeable that its use will constitute a complementary approach to QCA in assessing the location of true "normal" reference segments for clinical and research purposes.
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Footnotes |
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Presented in part at the 43rd Annual Scientific Session of the American College of Cardiology, Atlanta, Ga, March 13-17, 1994.
Received September 29, 1995; revision received February 27, 1996; accepted March 4, 1996.
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