Author + information
- Received October 16, 1995
- Revision received May 8, 1996
- Accepted May 14, 1996
- Published online October 1, 1996.
- GASTON R. DUSSAILLANT,
- GARY S. MINTZ,
- AUGUSTO D. PICHARD,
- KENNETH M. KENT,
- LOWELL F. SATLER,
- JEFFREY J. POPMA and
- MARTIN B. LEON*
- ↵*Address for correspondence: Dr. Martin B. Leon, Director of Research, Washington Cardiology Center, 110 Irving Street, NW-4B-1, Washington, D.C. 20010.
Objectives. This study used pre-rotational and post-rotational atherectomy volumetric intravascular ultrasound analysis to determine whether rotational atherectomy causes ablation of noncalcified atherosclerotic plaque.
Background. Rotational atherectomy is currently the preferred treatment for heavily calcified coronary lesions. However, the mechanism of lumen enlargement in noncalcified lesions has not been studied in detail. Intravascular ultrasound allows detailed, cross-sectional imaging of the coronary arteries in vivo. The normal coronary artery wall, the major components of the atherosclerotic plaque and the quantitative changes in vessel, lumen and plaque cross-sectional areas and volumes that occur as a result of the atherosclerotic disease process and during transcatheter therapy can be studied in a manner otherwise not possible.
Methods. Eighteen noncalcified native vessel lesions in 18 patients were imaged before and after rotational atherectomy using intravascular ultrasound systems incorporating motorized transducer pullback through a stationary imaging sheath. External elastic membrane, lumen and plaque plus media cross-sectional areas were measured every 1 mm of lesion length (for a total of 10 image slices), and external elastic membrane, lumen and plaque plus media volumes were calculated using Simpson's rule.
Results. After rotational atherectomy, the minimal lumen cross-sectional area increased from 1.37 ± 0.50 to 2.99 ± 0.60 mm2 (mean value ± 1 SD, p < 0.0001). Lumen volume increased from 23.2 ± 9.0 to 38.0 ± 8.0 mm3 (p < 0.0001) as a result of a decrease in plaque plus media volume (from 102.2 ± 50.9 to 85.8 ± 47.7 mm3, p < 0.0001), with no change in total vessel (external elastic membrane) volume (125.3 ± 54.2 to 123.8 ± 52.9 mm3, p = 0.119).
Conclusions. Rotational atherectomy effectively ablates noncalcified plaque in non-calcium-containing lesions.
Rotational atherectomy is currently the preferred treatment for heavily calcified coronary lesions [1–5]. Experimental data in animals and human cadaver specimens have shown that the diamond-coated burr preferentially ablates calcified plaque and deflects the more elastic vessel elements [6–8]. In addition, intravascular ultrasound studies have shown that rotational atherectomy effectively ablates calcified atherosclerotic plaque in humans in vivo [9, 10]. Although angiographically noncalcified lesions can be effectively treated with rotational atherectomy and adjunctive balloon dilation , the mechanism of lumen improvement in noncalcified lesions has not been studied in detail in vivo.
Intravascular ultrasound allows detailed cross-sectional imaging of the coronary arteries in vivo. The normal coronary arterial wall, the major components of the atherosclerotic plaque and the quantitative changes in vessel, lumen, and plaque cross-sectional areas and volumes that occur as a result of the atherosclerotic disease process and during transcatheter therapy can be studied in a manner otherwise not possible.
The purpose of this study was to use planar and volumetric intravascular ultrasound analysis of noncalcified target lesions before and after rotational atherectomy to determine whether rotational atherectomy ablates noncalcified atherosclerotic plaque in vivo.
Lesions and patients. Using intravascular ultrasound, one target lesion in each of 18 patients was studied before and after primary rotational atherectomy (before adjunct device therapy). The lesion location was the left anterior descending coronary artery in six patients, the left circumflex artery in seven and the right coronary artery in five. No lesion had fluoroscopic evidence of calcification. All intravascular ultrasound studies met the following criteria: a single target lesion in a native coronary artery, nonostial in location and high quality images using motorized transducer pullback through a stationary imaging sheath. Images with excessive nonuniform rotational distortion, significant sheath and catheter artifact, any amount of superficial calcium or >30° of circumferential or 1 mm of axial deep target lesion calcium were excluded from analysis.
Rotational atherectomy procedure. With 8F to 9F guiding catheters the respective coronary ostium was engaged and the dedicated 0.02 cm (0.009 in.) guide wire (Heart Technology) was advanced across the stenosis. Then, one or two diamond-tipped Rotablator catheters (Heart Technology) were gently advanced one to three times across the stenosis at 160,000 to 200,000 rpm, using great care to avoid rpm drops >5,000 rpm during each imaging run. Intracoronary nitroglycerin was given liberally in 100- to 200-μg boluses before and after each pass of the burr. Eleven lesions were treated with a single burr, and nine lesions were treated with two burrs. The final burr size ranged from 1.5 to 2.25 mm (mean 1.95 ± 0.24) with a final burr/artery ratio of 0.65 ± 0.10. In all lesions, rotational atherectomy was followed by adjunct balloon angioplasty.
Intravascular ultrasound imaging protocol. Patients were studied after giving written informed consent. Intravascular ultrasound imaging was performed as part of ongoing protocols approved by the Institutional Review Board of the Washington Hospital Center. Pre-rotational and post-rotational atherectomy ultrasound imaging studies were performed after administration of 200 μg of intracoronary nitroglycerin (in addition to the nitroglycerin used during the rotational atherectomy procedure).
To perform volumetric analysis, only imaging systems incorporating motorized transducer pullback through a stationary imaging sheath were used in this study. Motorized transducer pullback through a stationary imaging sheath allows the transducer to move at the same speed as the proximal end of the catheter. The first system (Cardiovascular Imaging Systems/InterTherapy) incorporated a single-element, 25-MHz transducer coupled to an angled mirror mounted on the tip of a flexible shaft and rotated at 1,800 rpm within a 3.9F, short monorail polyethylene imaging sheath to form planar cross-sectional images in real time. The second system (Cardiovascular Imaging Systems Inc), which incorporated a 30-MHz, beveled transducer, rotated at 1,800 rpm within a 3.2F, short monorail imaging sheath. All studies were recorded only during transducer pullback onto high quality s-VHS tape for off-line analysis.
Validation of normal coronary artery anatomy; plaque composition and morphology; and measurements of external elastic membrane cross-sectional area, lumen cross-sectional area and plaque plus media cross-sectional area by intravascular ultrasound have been reported previously [12–18]. The external elastic membrane is shorthand for the border between the hypoechoic media and the hyperechoic adventitia. Because media thickness cannot be measured accurately, plaque plus media cross-sectional area was used as a measurement of the amount of atherosclerotic plaque . Furthermore, because acoustic shadowing by target lesion calcium makes measurement of the external elastic membrane cross-sectional area difficult, and because the purpose of the study was to study rotational atherectomy in noncalcified lesions, lesions containing any amount of superficial calcium or >30° of circumferential or 1 mm of axial deep calcium were excluded. Calcium produced bright echoes (brighter than the reference adventitia) with acoustic shadowing of deeper arterial structures. The circumferential arc of calcium was measured using a protractor centered on the lumen; the axial length of calcium was measured by counting the number of seconds of videotape on which lesion calcium was present (2 s videotape = 1 mm axial arterial length). Deep calcium was located adjacent to the media-adventitia border, whereas superficial calcium was located closer to the tissue-lumen border .
By using a reproducible axial landmark (usually the aortoostial junction or a large proximal side branch) and a known pullback speed, identical cross-sectional image slices could be identified on serial studies, and measurements before and after intervention could be compared. The image slice selected for planar analysis was at the smallest postintervention lumen cross-sectional area. In noncalcified lesions, this cross section typically also contains the largest postintervention plaque burden. Measurements made using computerized planimetry included (Fig. 1): 1) lesion site external elastic membrane cross-sectional area (mm2); 2) lesion site lumen cross-sectional area (mm2); 3) Plaque plus media cross-sectional area (mm2) = External elastic membrane cross-sectional area - Lumen cross-sectional area. Maximal and minimal plaque plus media thicknesses were used to measure total plaque thickness. If the plaque appeared to be packed around the ultrasound imaging catheter, the lumen was assumed to be the size of the catheter.
Each target lesion was normalized for a reference segment. The reference segment selected was the most visually normal cross-section within 10 mm of the lesion proximally, but distal to a major side branch. Reference segment cross-sectional measurements made were similar to the lesion site cross-sectional measurements.
Volumetric intravascular ultrasound analysis. Similarly, histologic validation of the method of measuring arterial, lumen and plaque plus media volumes has also been reported previously . The volumetric intravascular ultrasound measurements of lumen and plaque plus media volumes correlated significantly with histologic findings (r = 0.95, p < 0.001 and r = 0.96, p < 0.01, respectively).
In brief, on playback of the recorded studies, an end-diastolic frame was selected every 1 mm of axial lesion length over a lesion length of 10 mm centered on the smallest preintervention lumen cross-sectional area; given a pullback speed of 0.5 mm/s, each 2 s of video playback corresponded to 1 mm of axial lesion length, resulting in 10 images slices analyzed. Because the ultrasound images were not gated, end-diastole was determined when the vessel lumen was at its largest during the cardiac cycle. To ensure that the same axial segment was analyzed in the preintervention and postintervention studies, reproducible axial landmarks (usually the aortoostial junction, a large proximal side branch, reference segment calcific deposits, alone or in combination) were used as axial reference points. In practice, the preintervention imaging run was studied first 1) to identify the center of the lesion, 2) to identify a reproducible axial landmark, and 3) to determine the distance between the center of the lesion and the axial landmark. A complete set of preintervention measurements was then made. Subsequently, the postintervention imaging run was studied to identify the reproducible axial landmark. Next, using the previously measured distance from the reproducible axial landmark to the center of the lesion, the image slice on the postintervention imaging run corresponding to the center of the lesion on the preintervention imaging run was identified. The videotape was then advanced or rewound to identify all 10 image slices, and a complete set of postintervention measurements was made. This approach permitted axial alignment and a careful comparison of the preintervention and postintervention imaging runs.
Using computerized planimetry, the external elastic membrane and lumen cross-sectional areas were manually traced, and the plaque plus media cross-sectional area was calculated as described earlier. These 10 numbered image slices were tabulated separately and were then used to calculate external elastic membrane and lumen volumes (in mm3) according to Simpson's rule. Then the plaque plus media volume (also in mm3) was calculated as External elastic membrane volume - Lumen volume. This is illustrated in Fig. 1. Furthermore, the 10 numbered image slices were compared to determine whether there was uniform plaque ablation over the length of the lesion.
In the lesions with short, focal and limited deep target lesion calcium (≤30° in circumference and ≤1 mm in axial length), extrapolation of the external elastic membrane was performed by assuming that the arterial cross-sectional geometry was circular. When the atherosclerotic plaque abutted against the catheter, the lumen was assumed to be the size of the imaging catheter.
Statistics. Statistical analysis was performed using Statview 4.02. Continuous data were presented as mean value ± SD, and categoric data were presented as frequencies. Continuous variables were compared using the paired Student t test or factorial analysis of variance (with post hoc analysis using the Fisher protected least significant difference), as appropriate. Linear regression analysis was performed to assess the relation of the change in plaque plus media volume with other variables. A value p < 0.05 was considered statistically significant.
Planar intravascular ultrasound results. Reference lumen cross-sectional areas measured 6.9 ± 2.4 mm2. The final burr cross-sectional area was 3.1 ± 0.7 mm2; the calculated burr/artery cross-sectional area ratio was 0.46 ± 0.11.
After rotational atherectomy the minimal lumen cross-sectional area increased from 1.37 ± 0.50 to 2.99 ± 0.60 mm2 (p < 0.0001). The ratio of postrotational atherectomy minimal lumen cross-sectional area to burr cross-sectional area was 1.01 ± 0.26 (range 0.55 to 1.74). The average maximal plaque thickness decreased from 1.78 ± 0.60 to 1.47 ± 0.54 mm (p < 0.0001), and the average minimal plaque thickness decreased from 0.58 ± 0.29 to 0.31 ± 0.19 mm (p < 0.0001).
Volumetric intravascular ultrasound results. After rotational atherectomy, lumen volume increased from 23.2 ± 9.0 to 38.0 ± 8.0 mm3 (p < 0.0001) as a result of a decrease in plaque plus media volume (from 102.2 ± 50.9 to 85.8 ± 47.7 mm3, p < 0.0001), with no change in total vessel (external elastic membrane) volume (125.3 ± 54.2 to 123.8 ± 52.9 mm3, p = 0.119). The measured decrease in plaque plus media volume (16.4 ± 7.2 mm3) correlated with the burr/artery cross-sectional area ratio (r = 0.501, p < 0.05) and with the preintervention plaque volume (r = 0.502, p < 0.05).
As shown in Table 1, individual responses to rotational atherectomy were variable. There was measurable plaque ablation in all patients; however, the amount of plaque ablation varied greatly, from as little as 6.1 mm3 in Patient 6 to as much as 35.9 mm2 in Patient 14. In addition, there was a wide range of responses to vessel volume. Some patients reacted with spasm with a decrease in vessel volume by as much as 14.8 mm3, while others experienced dilation with an increase in vessel volume of 7.6 mm3.
Finally, Table 2 shows the axial distribution of the changes in lumen, external elastic membrane and plaque plus media cross-sectional areas over the length of the lesions. There was a greater decrease in plaque plus media in the center of the lesion than at either end; however, this was related to the size of the preintervention lumen (p < 0.0001) and to the size of the artery (p < 0.0001), and not to the axial location of the individual cross-sectional image slice.
Many reports have documented that rotational atherectomy was highly effective in treating angiographically calcified coronary stenoses [1–5]. Similarly, a multicenter study showed that rotational atherectomy was also effective in treating angiographically noncalcified lesions . In that study, there was no difference in procedural success (94.3% vs. 95.2%), residual diameter stenosis (21.6% vs. 23.3%) or major complications when angiographically calcified lesions were compared with angiographically noncalcified lesions. However, angiography is known to be insensitive in the detection and localization of target lesion calcium, and the absence of fluoroscopic calcification does not exclude significant lesion-associated calcium . Furthermore, a preliminary intravascular ultrasound study showed that the lumen/burr ratio after rotational atherectomy is smaller in noncalcified (0.63) than in calcified lesions (0.89) .
We have previously reported the intravascular ultrasound results of heavily calcified lesions before and after rotational atherectomy (mean arc of calcium 227 ± 107°); planar analysis showed that rotational atherectomy effectively ablated calcified plaque . Using volumetric intravascular ultrasound analysis, the current study demonstrated that rotational atherectomy was equally effective in ablating noncalcified atherosclerotic plaque; all of the lumen improvement after rotational atherectomy was accounted for by the decrease in plaque mass.
Lesion characteristics. The current study was intended as a mechanistic study of noncalcified lesions. However, based on previous intravascular ultrasound studies, these lesions represented an unusual group. Most lesions (70% to 75%) treated with new device angioplasty contain target lesion calcium; the average arc of target lesion calcium has been shown to be 115° . Even in the absence of angiographic calcium, this intravascular ultrasound analysis showed that 61% of target lesions contain calcified elements (with a mean arc of 71 ± 83°), and that 37% contained superficial calcified elements (with a mean arc of superficial calcium of 44 ± 74°) .
Intravascular ultrasound results. Volumetric intravascular ultrasound analysis showed than, on average, all of the lumen improvement after rotational atherectomy of noncalcified lesions could be accounted for by plaque ablation. Analysis of each of the 10 individual image slices measured showed that this was true throughout the length of the lesion. Thus, the mechanism of lumen enlargement in these lesions was plaque ablation and not spontaneous or forced (Dotter effect) vessel expansion.
Because the current study measured quantitative changes in plaque cross-sectional area and volume, we were able to exclude the confounding effects on lumen dimensions of arterial spasm or nitroglycerin-induced, spontaneous or forced vessel expansion/dilation. It has been suggested that spasm may be more prevalent in noncalcified lesions ; spasm would have resulted in a relatively smaller postintervention lumen for any given burr size, as well as a significant decrease in total arterial (external elastic membrane) area or volume. Spontaneous or nitroglycerin-induced vasodilation may be more common after ablation of superficial, constricting fibrocalcific plaque elements; it would have resulted in both a relatively larger postintervention lumen and a significant increase in total arterial area or volume (for any given burr size). Forced vessel expansion would also have produced an increase in external elastic membrane area or volume. In most of the lesions in the current study, the change in vessel volume was minimal and nonsignificant.
We did not attempt to compare the volumetric intravascular ultrasound results in noncalcified lesions with a comparable cohort of calcified lesions. Because calcium shadows deeper arterial structures, it would have been difficult to use volumetric methods in a similar group of heavily calcified lesions. However, it is usually possible to identify single cross sections within heavily calcified target lesions that can be analyzed using intravascular ultrasound planar methods. Thus, previously reported planar analysis of rotational atherectomy in calcified coronary lesions showed a minimal change in vessel cross-sectional area (17.3 to 16.7 mm2) and a significant decrease in plaque plus media cross-sectional area (15.7 to 13.0 mm2) after rotational atherectomy alone . In addition, the 116% increase in lumen cross-sectional area (1.8 to 3.9 mm2) was similar to the 118% increase in lumen cross-sectional area (1.37 to 2.99 mm2) found in the present study .
Two other volumetric intravascular ultrasound analyses before and after intervention have been published. Directional atherectomy increased lumen volume (32 mm3) owing to a combination of plaque removal (25 mm3) and some degree of vessel expansion (7 mm3) . Conversely, after balloon angioplasty, all of the increase in lumen volume was explained by vessel expansion with no decrease in plaque volume . In that study, analysis of the individual image slices obtained throughout the length of the lesion showed evidence of axial redistribution of atherosclerotic plaque .
Conclusions. The current study proved that rotational atherectomy effectively ablated noncalcified plaque in noncalcium-containing lesions. This explained the mechanism of lumen enlargement and suggested a role for rotational atherectomy in treating noncalcified stenoses.
↵1 This study was supported in part by the Cardiology Research Foundation, Washington, D.C., and by Heart Technology, Inc., Redmond, Washington.
- Received October 16, 1995.
- Revision received May 8, 1996.
- Accepted May 14, 1996.
- THE AMERICAN COLLEGE OF CARDIOLOGY
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