Mechanisms of Lumen Enlargement After Excimer Laser Coronary Angioplasty
An Intravascular Ultrasound Study
Background The mechanisms of excimer laser coronary angioplasty (ELCA) have never been studied in human coronary arteries in vivo.
Methods and Results ELCA was used to treat 202 lesions in 190 patients. Forty-nine lesions in 48 patients were studied by use of sequential (before and after ELCA and after adjunctive device therapy) intravascular ultrasound (IVUS). External elastic membrane (EEM), lumen, and plaque+media (P+M=EEM−lumen) cross-sectional areas (CSAs) and lesion arcs of calcium were measured before and after ELCA and after adjunct device use. Lumen improvement after ELCA (1.4±0.5 to 2.7±0.8 mm2) was the result of both tissue ablation (decrease in P+M CSA from 16.8±7.1 to 15.9±6.7 mm2, P<.0001) and vessel expansion (increase in EEM CSA from 18.2±7.1 to 18.6±6.8 mm2, P=.0245), with no change in calcium. The decrease in P+M CSA was 39% of the CSA of the laser catheter used. Dissections were present in 39% of lesions, 84% within superficial calcium; fibrocalcific deposits developed a “fragmented” appearance.
Conclusions ELCA increased lumen CSA by both atheroablation and vessel expansion without calcium ablation. Superficial fibrocalcific deposits developed a characteristic fragmented appearance. These findings support both photoablation and forced vessel expansion as mechanisms of lumen enlargement and plaque dissection after ELCA.
The use of ELCA in transcatheter cardiovascular interventions has been described in numerous reports.1 2 3 In particular, ELCA finds its greatest use in tubular, diffuse, calcified, total, subtotal, and ostial lesions. Advocates of laser angioplasty claim that the photoablative properties of excimer lasers result in precise atheroablation, including calcium, without harmful thermal injury.4 5 6 7 Although this has been demonstrated in vitro, it has never been proved in humans in vivo.
IVUS allows transmural imaging of coronary arteries in humans in vivo, providing unique insight into the pathology of coronary artery disease by defining vessel wall geometry and the major components of the atherosclerotic plaque. Serial IVUS studies have been used to investigate the mechanisms of transcatheter therapy in humans in vivo.8 9 10 11 For example, several studies have delineated the mechanisms of balloon angioplasty,8 9 12 including the reasons for postangioplasty dissections.13 Other studies have used sequential (preintervention and postintervention) IVUS imaging to assess the contribution of tissue removal to lumen improvement after both DCA and rotational atherectomy.10 11
The purpose of this study was to use sequential (preintervention and postintervention) IVUS imaging to assess the mechanisms of lumen improvement after ELCA of coronary artery disease in humans in vivo.
Patient and Lesion Characteristics
From July 1991 to May 1994, IVUS imaging was performed as part of 202 ELCA procedures in 190 patients. Forty-nine lesions in 48 patients were imaged before intervention and after ELCA; 41 lesions were also imaged after adjunct device use. Analysis of this subset constitutes the basis of this report.
The 37 men and 11 women had a mean age of 63±11 years. Twelve patients presented with stable angina pectoris; the rest had unstable angina, of whom 4 had postinfarction angina. The imaged and treated vessels were left main in 2, left anterior descending in 20, left circumflex in 9, and right coronary artery in 9 and saphenous vein grafts in 9 patients. Nine lesions were aortoostial in location.
All patients were treated and studied after giving informed consent. ELCA and IVUS imaging protocols have the ongoing approval of the Washington Hospital Center Institutional Review Board.
The ELCA procedure (Spectranetics/Advanced Interventional Systems) was performed as described elsewhere.1 2 3 14 15 The largest laser fiber catheter used was a 1.3-mm catheter in 6, 1.6-mm catheter in 6, 1.8-mm directional laser catheter in 32, 2.0-mm catheter in 3, and 2.2-mm catheter in 2 lesions. Energy densities ranged from 25 to 65 mJ/mm2 (mean, 57.9±5.4 mJ/mm2), and the number of pulses ranged from 30 to 1880 (mean, 339±352). A single laser pass technique was used in 69% of the lesions. Adjunct devices were used in all lesions: PTCA in 31 and DCA in 18.
Angiograms were reviewed by a core angiographic laboratory that was blinded to the ultrasound results. Standard qualitative morphological criteria were recorded on the basis of their identification in any unforeshortened view.16 Calcification was identified as readily apparent radiopacities within the vascular wall at the site of the stenosis and was classified as none to mild, moderate (radiopacities noted only during the cardiac cycle before contrast injection), or severe (radiopacities noted without cardiac motion before contrast injection, generally compromising both sides of the arterial lumen). An eccentric target lesion had one lumen edge in the outer one quarter of the apparently normal lumen.
Target lesion location was designated as ostial, proximal, mid, and distal. Ostial lesions were those that began within 3 mm of a major coronary ostium.
Quantitative angiographic analysis was performed with a computer-assisted, automated edge detection algorithm (ImageComm).17 With the external diameter of the contrast-filled catheters used as the calibration standard, the minimal lumen diameter at end diastole before intervention was measured from multiple projections, and the results from the worst view were recorded. Lesion length was measured from shoulder to shoulder.
Intravascular Ultrasound Imaging
Intracoronary nitroglycerin (100 to 200 μg) was administered before each IVUS imaging run. IVUS studies were performed by use of one of two commercially available systems. In each case, the ultrasound transducer was advanced beyond the target lesion and withdrawn to the aortoostial junction in a single continuous run without interruption. The first (Cardiovascular Imaging Systems Inc/InterTherapy Inc) incorporated a single-element 25-MHz transducer and an angled mirror mounted on the tip of a flexible shaft that was rotated at 1800 rpm within a 3.9F short monorail polyethylene imaging sheath to form planar images in real time. The second (Cardiovascular Imaging Systems Inc) incorporated a single-element 30-MHz beveled transducer within either a 2.9F long monorail imaging catheter having a common distal lumen design (the distal lumen accommodates either the imaging core or the guide wire but not both) or a 3.2F short monorail imaging catheter. With both systems, the transducer was withdrawn automatically at 0.5 mm/s to perform the imaging sequence. IVUS studies were recorded on 1/2-in high-resolution super VHS tape for off-line analysis.
Qualitative and Quantitative IVUS Analyses
The same anatomic image slice was analyzed before intervention, after ELCA, and after adjunct device use, and the differences were compared. By use of one or more reproducible axial landmarks (eg, the aortoostial junction and/or a large proximal or distal side branch) and the known pullback speed of 0.5 mm/s, identical cross-sectional slices on serial studies could be identified for comparison. Qualitative (plaque morphology) and quantitative (cross-sectional) analyses of the ultrasound images were performed by a single individual blinded to the angiographic and clinical results.
The in vitro validation of qualitative and quantitative IVUS analysis was reported previously.18 19 20 21 22 23 24 25 Single images were digitized, and the following lesion site measurements were made with computer planimetry: EEM CSA (in square millimeters); lumen CSA (in square millimeters); P+M CSA (in square millimeters), which is EEM minus lumen area; and minimum lumen diameter (in millimeters).
The EEM is shorthand for the media-adventitia border, which has been shown to be a reproducible measurement of total vessel CSA. When the atherosclerotic plaque encompassed the catheter, the lumen was assumed to be the size of the imaging catheter. Because medial thickness could not be measured accurately, P+M CSA was used as a measurement of the atherosclerotic plaque. Each border (EEM and lumen) is routinely traced two to four times, and the results are averaged.
In practice, the postintervention images are analyzed first to determine the image slice with the smallest final lumen CSA; if multiple image slices have the same lumen CSA, then the image slice with the largest plaque CSA and the most well-defined media-adventitia border is selected for analysis. (At a pullback speed of 0.5 mm/s, there are 60 video frames per millimeter of arterial length from which to select.) Second, the axial relation of this image slice to various longitudinal landmarks is studied, and the nearest longitudinal landmarks (well-defined side branches or peculiar and unique arcs of calcium or perivascular structures) that are repeatedly identifiable on multiple imaging runs are noted. The distances from the selected image slice to these axial landmarks are measured (from seconds of videotape where 2 seconds of videotape equals 1 mm of axial length, given a motorized transducer pullback speed of 0.5 mm/s). Next, this process is reversed to identify the preintervention image slice that corresponds to the selected postintervention image slice. (The axial landmarks are identified first, and the videotape is advanced or rewound the requisite number of seconds. The preintervention study is then analyzed frame by frame to identify the preintervention image that corresponds to the postintervention image.) Finally, the preintervention and postintervention image slices are compared visually to ensure that the image slices are indeed from the same anatomic location within the lesion. When the same lesions are studied at least 3 months apart, the intraclass correlation coefficient for each of these measurements is >.90. The intraclass correlation coefficient considers between-lesion and within-lesion variabilities and is widely used as a measure of interrater variability.26 27 Specifically, the intraclass correlation coefficient for repeated preintervention measurement of the EEM CSA is .99; of the lumen CSA, .96; and of the P+M CSA, .99. The intraclass correlation coefficient for repeated postintervention measurement of the EEM CSA is .99; of the lumen CSA, .92; and of P+M CSA, .98. In our laboratory, this protocol has been used to study acute and chronic transcatheter device effects in >2500 lesions. Some of these analyses have been reported previously.8 10 11 28 29 30 31 32
Because calcium produces bright echoes (brighter than the vessel adventitia) with acoustic shadowing of deeper structures, the measurement of the EEM CSA can sometimes be difficult. To circumvent this problem, two types of extrapolation can be used. Briefly, because the cross section of the coronary artery was more or less circular, extrapolation of the circumference of the EEM was possible, provided that each calcific deposit did not shadow >60° of the adventitial circumference. Also, real-time axial movement of the transducer just distal and proximal to a calcific deposit or to find the smallest circumferential arc of calcium within a large calcific deposit unmasked and filled in contiguous parts of the adventitia that were otherwise shadowed by that deposit. In this study, lesions that required circumferential extrapolation of >30° or axial transducer movement of >1 mm (2 seconds or 60 frames of videotape) were eliminated. Over this short length of coronary artery, there is a negligible change in EEM CSA when IVUS imaging is used in vivo.33 These techniques have been described previously.11 28 The reproducibility of the above analyses included lesions with target lesion calcification in which measurement of the EEM CSA required circumferential or axial extrapolation.
Plaque composition was assessed for the presence and extent of calcium. Calcium was identified as plaque that was brighter than the reference adventitia with acoustic shadowing of deeper arterial structures.34 Because of acoustic shadowing, the thickness of the calcific deposit could not be measured. Therefore, calcium was quantified by its total circumference (expressed as an arc, in degrees, measured with a protractor centered on the lumen). The location of target lesion calcium was defined as superficial (calcium at the intima-lumen interface or closer to the lumen than to the adventitia), deep (calcium at the media-adventitia border or closer to the adventitia than to the lumen), or both. The largest arc of superficial calcium within the lesion was also measured as above. To assess calcium removal, ultrasound images before and after ELCA, were compared quantitatively (to detect a change in the total or superficial arc of calcium) and qualitatively (ability to visualize deeper arterial structures that could not be seen before intervention).
Dissections or tears in the plaque were abrupt, focal interruptions in the continuity of the plaque or intima that spanned normal tissue planes radially, axially, or circumferentially but did not necessarily extend to the media. Dissection planes were classified according to location: within calcium, at the junction of calcified and noncalcified plaque, and within noncalcified plaque.
Statistical analysis was performed with statview version 4.01. Quantitative data were presented as mean±SD. Qualitative data were presented as frequencies. Comparisons between groups were performed by use of paired and unpaired t tests for continuous variables or χ2 statistics and Fisher’s exact test for categorical variables. Sequential measurements were compared by use of ANOVA for repeated measures with post hoc analysis and by use of Fisher’s protected least-significant differences test. The level of significance was defined as P<.05.
Three (6%) of the lesions were totally occluded before intervention. Twenty-one (43%) of the lesions were calcified, and 35 (71%) were eccentric. Mean lesion length was 9.8±5.4 mm. Table 1⇓ shows the quantitative analysis. After ELCA, there was a significant increase in minimum lumen diameter and a significant improvement in percent diameter stenosis. Lesions treated with adjunct DCA had larger reference lumen diameters compared with lesions treated with adjunct PTCA. Minimum lumen diameters were larger and percent diameter stenosis was smaller after adjunct DCA than after adjunct PTCA.
IVUS Analysis After ELCA
By IVUS analysis, 36 (73%) of the lesions contained calcium (P<.0001 versus angiography), and 29 (59%) of the lesions contained superficial calcium.
A comparison of IVUS images in the 49 lesions studied both before and after ELCA is shown in Table 2⇓ and Fig 1⇓. The lumen improvement after ELCA (from 1.4±0.5 to 2.7±0.8 mm2) was the result of both tissue ablation (a decrease in P+M CSA from 16.8±7.1 to 15.9±6.7 mm2, P<.0001) and vessel expansion (increase in EEM CSA from 18.2±7.1 to 18.6±6.8 mm2, P=.0245). Despite these small changes, 96% of the lesions showed an increase in lumen CSA, 67% showed an increase in EEM CSA, and 78% showed a decrease in P+M CSA. There was no change in the arc of calcium or of superficial calcium, nor was there subjective evidence of calcium removal (eg, increased ultrasound penetration of deeper arterial structures).
After ELCA, the IVUS measurement of minimum lumen diameter correlated only fairly with the quantitative angiography (r=.433, P=.0059).
The post-ELCA lumen CSA averaged 17% larger than the CSA of the largest laser catheter used; the decrease in P+M CSA averaged only 39% of the CSA of the largest laser catheter used. However, these were extremely variable and were not predicted by any angiographic or IVUS lesion characteristic. In some lesions, lumen improvement was due entirely to plaque ablation (Fig 2⇓); in others, it was due entirely to vessel expansion (Fig 3⇓).
Dissections were present in 39% of the lesions after ELCA. Most of the dissections (84%) were within superficial calcified deposits; after ELCA, calcified deposits often developed a characteristic “fragmented” or “shattered” appearance: newly created, sharp-edged gaps within a previously solid calcium deposit (Fig 4⇓). The resulting calcium fragments often were displaced circumferentially. Conversely, dissections occurred in 14% of the lesions that contained only deep calcium and in 23% that contained no calcium (P=.0471).
IVUS Analysis After Adjunct Device Use
Table 3⇓ summarizes the quantitative IVUS analysis after adjunct device therapy. The mechanism of progressive lumen enlargement after adjunctive PTCA was vessel expansion (increase in EEM CSA); after adjunctive DCA, it was a combination of vessel expansion and additional atheroablation (decrease in P+M CSA). There was no significant change in lesion calcification.
Overall, the number of lesions with dissections increased to 30 of 41 (73%), and there was almost a threefold increase in the number of dissection planes per lesion site. New dissections were almost entirely at the junction of calcified and noncalcified plaque.
In vitro or in vivo animal models of atherosclerosis suggest that excimer lasers can precisely cut through atheroma, including calcium, without harmful thermal injury.4 5 6 7 35 However, the mechanisms of ELCA have never been studied in human coronary arteries in vivo. Moreover, animal models of atherosclerosis do not duplicate human pathology; in particular, animal atherosclerosis is lipid rich, whereas the hemodynamically significant human coronary artery lesion is the mature fibrocalcific plaque. For example, as is typical of most target lesions undergoing transcatheter therapy,34 73% of the lesions in this report contained IVUS calcium. In addition, recent studies, including in vitro studies, have focused on the incidence of postprocedure dissections, suggesting that the mechanism of ELCA may be more complicated than simple photoablation.36 37 38 39
IVUS imaging provides high-quality tomographic images of the coronary artery lumen, lumen-intima interface, atherosclerotic plaque, and vessel wall in vivo. It has proved useful for evaluating mechanisms and results of various transcatheter therapies, including PTCA, DCA, rotational atherectomy, and endovascular stent placement.8 9 10 11 12 13 (For example, all of the lumen improvement after rotational atherectomy has been shown to be the result of tissue ablation11 ; 75% of the lumen improvement after primary DCA has been shown to be the result of tissue removal.9 10 ) IVUS images acquired before intervention are essential for the accurate assessment of changes in plaque morphology that occur in direct response to intervention. We have been routinely obtaining IVUS images in our patients with angiographically severe stenoses before transcatheter interventions without adverse sequelae.38 Similarly, sequential imaging has been shown to be essential for separating primary and adjunct device effects.11 The use of the motorized pullback device assisted in comparing sequential imaging studies. The steps used to make these measurements are described in detail above. Because the transducer always was pulled back to an easily reproducible landmark (eg, the aortoostial junction, a large proximal side branch, or a characteristic proximal calcific deposit), the same tomographic image slice could be identified after each imaging run. This facilitated comparative measurements.
Baseline Lesion Characteristics
Patients treated with ELCA in this study had stenoses that were angiographically severe (minimum lumen diameter, 0.86±0.51 mm with 6% total occlusions) and moderately long (9.8±5.4 mm). The severity, length, complexity, and location of these target lesions before intervention were comparable to those reported in other studies using angiography to evaluate the effect of ELCA.1 2 3 14 15
Mechanisms of Lumen Improvement After ELCA
Comparison of the sequential IVUS images before and after ELCA showed that the contribution of tissue ablation (decrease in P+M CSA) to lumen improvement averaged 76%, and the contribution of vessel expansion (increase in vessel or EEM CSA) averaged 24%. Furthermore, the decrease in P+M CSA averaged only 39% of the CSA of the laser catheter. There were two potential mechanisms of ELCA-induced vessel expansion. The presence of dead space between the laser fibers may have contributed to inadequate tissue ablation and could have resulted in a Dotter effect.37 However, a Dotter effect would not have produced a lumen larger than the laser catheter used.
Alternatively, laser-induced shock waves and forceful expansion of vapor bubbles into tissue could have caused acute vessel expansion.37 38 39 The relative contributions of tissue ablation and vessel expansion to lumen enlargement after ELCA varied among lesions. It was not possible to relate the relative contributions of these two potential mechanisms to any qualitative or quantitative angiographic or ultrasound variable.
Sequential imaging shows that the magnitude of lumen improvement after ELCA is at most modest and perhaps less than suggested by angiography. The only fair correlation between quantitative angiographic and IVUS assessment of post-ELCA minimum lumen diameter (r=.433) may explain some of this discrepancy.
Sequential IVUS analysis consistently failed to demonstrate calcium ablation either quantitatively (by a measurable decrease in the arc of calcium or of superficial calcium) or qualitatively (eg, visual evidence of reduced shadowing and increased ultrasound penetration into deeper tissue planes). This is in distinct contrast to sequential IVUS analysis before and after rotational atherectomy, which was able to demonstrate quantitative and qualitative calcium ablation.11
Dissections after ELCA almost always occurred within superficial fibrocalcific plaque. The visual appearance of these dissections (a fragmenting of superficial fibrocalcific deposits) was, in our experience, unique to ELCA. PTCA caused dissections at the junction of calcified and noncalcified plaque.13 Rotational atherectomy caused fissuring of superficial calcium in approximately 25% of lesions.11 The fissures caused by rotational atherectomy differed from the ELCA-induced fragmentation of calcific deposits in that fissures were barely perceptible hairline spaces or cracks within otherwise unbroken and displaced calcium deposits. In experimental models, it has been shown that ELCA-induced vapor bubble expansion caused significant dissections.38 39 Thus, forced lumen and vessel expansion and plaque fragmentation after ELCA in human coronary arteries may be related.40
Mechanisms of Adjunctive Device Therapy
Although it was not the main purpose of this study to evaluate and compare the mechanisms of adjunctive PTCA and DCA after ELCA, several observations are noteworthy. Angiographic minimum lumen diameters and IVUS lumen CSA were larger and angiographic percent diameter stenoses were smaller after adjunct DCA than after adjunct PTCA. The mechanism of progressive lumen improvement after adjunct PTCA was additional vessel expansion; after adjunct DCA, it was a combination of vessel expansion and tissue removal. After both adjunctive PTCA and DCA, there was an increase in frequency and number of dissections, primarily at the junction of calcified and noncalcified plaque. Thus, the mechanism of adjunctive PTCA was similar to that of primary PTCA, and the mechanism of adjunctive DCA was similar to that of primary DCA.8 9 10 11 12 13 41
This study presented a heterogeneous patient and lesion population, including both native vessel and vein graft lesion location. However, the population was similar to that of most reports using angiography to assess the effects of ELCA. The changes observed were small, perhaps smaller than the resolution of sequential IVUS analysis. Furthermore, these observations depend on the ability of IVUS imaging to sequentially study the same anatomic image slice. However, this methodology has been used to study other transcatheter devices8 10 11 28 29 30 31 32 ; extreme care was taken to analyze the same cross section on repeated studies. Furthermore, the small changes noted only served to emphasize the conclusion that lumen improvement and atheroablation after ELCA are, at most, modest. Mostly small (≤1.8 mm) laser fiber catheters were used. A greater degree of tissue ablation might have been demonstrated if 1.3-mm catheters had been consistently followed by ≥2.0-mm catheters.42 However, the treatment strategy was designed to minimize dissections and complications; the angiographic percent diameter stenosis after ELCA alone averaged 50%.
ELCA increased lumen CSA by a combination of atheroablation and vessel expansion. The amount of tissue ablation was small, variable, and averaged ≈40% of the laser catheter CSA. A concomitant increase in vessel CSA accounted for a lumen CSA larger than that of the laser catheter. Dissections occurred within superficial fibrocalcific plaque that developed a characteristic fragmented appearance. These findings support both photoablation and forced vessel expansion (mediated by either acoustic shock wave or vapor bubble) as mechanisms of lumen enlargement and plaque dissection after ELCA in humans in vivo.
Selected Abbreviations and Acronyms
|DCA||=||directional coronary atherectomy|
|EEM||=||external elastic membrane|
|ELCA||=||excimer laser coronary angioplasty|
|P+M||=||plaque plus media|
|PTCA||=||percutaneous transluminal coronary angioplasty|
This study was sponsored in part by The Cardiology Research Foundation, Washington, DC, and The Medlantic Research Institute, Washington, DC.
Reprint requests to Martin B. Leon, MD, Director, Cardiovascular Research, Washington Cardiology Center, 110 Irving St NW, Ste 4B-1, Washington, DC 20010.
- Received August 3, 1994.
- Revision received August 1, 1995.
- Accepted August 6, 1995.
- Copyright © 1995 by American Heart Association
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