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Impact of Restenosis After Optimal Directional Coronary Atherectomy on Regional Left Ventricular Function
Impact of Restenosis After Optimal Directional Coronary Atherectomy on Regional Left Ventricular Function Pierre Coste, MD, Serge Sempe´, MD, Pierre Dos Santos, MD, Catherine Jaı¨s, MD, Abdallah Moussari, MD, Franc¸ois Duclos, MD, Simone Bonoron Adele, PhD, and Pierre Besse, MD, FESC To assess the effect of optimal directional coronary atherectomy (DCA) on restenosis and left ventricular (LV) function, 95 patients who underwent DCA and adjunctive balloon angioplasty for de novo lesions were prospectively followed for 6 months. Absolute and relative coronary lumen measurements were analyzed with online quantitative coronary angiography. LV volumes, ejection fraction, and segmental wall motion were measured off-line according to the radial method for LV cineangiograms acquired in a right anterior oblique projection. Target vessels were the left anterior descending artery in 63 patients and right coronary artery in 32. Mean ({ SD) reference diameter was 3.58 { 0.65 mm. Mean lumen diameter improved significantly after DCA from 1.19 { 0.44 to 3.03 { 0.45 mm, yielding a 14 { 10% residual stenosis. Overall angiographic restenosis
rate (ú50% stenosis in diameter) at control was 23%. In patients without restenosis, there were no significant changes in LV volumes or in LV pressures. In this subgroup, ejection fraction improved significantly in the left anterior descending group (mean difference 3 { 10%, p õ0.04). Moreover, there was an increase in fractional shortening of all anterior segments (mean difference 11 { 16%, p õ0.005). Improvement in fractional shortening was less marked in the right coronary artery group even without restenosis. We conclude that: (1) optimal DCA can achieve a low restenosis rate in selected large vessels, (2) long-term beneficial effects on regional LV function are possible, particularly in patients with left anterior descending disease and in the absence of coronary restenosis. Q1997 by Excerpta Medica, Inc. (Am J Cardiol 1997;79:545–552)
irectional coronary atherectomy (DCA) was first proposed in order to reduce the incidence of reD stenosis after balloon angioplasty but controlled
tions (3.3%). Three patients (2.5%) developed myocardial infarction defined as new Q waves in the electrocardiogram and/or creatine kinase myocardial isoform more than twofold normal values. All these patients completed clinical follow-up, and 95 underwent angiography at 6 months, giving a 81% angiographic control rate in successful procedures. Thirteen of the controlled patients (12%) initially had a slight elevation in creatine kinase above the upper limits of normal. The remaining patients were either symptom-free or had Canadian Cardiac Society class 1 or 2 angina with medical treatment. None required cardiac revascularization either by coronary bypass surgery or repeat coronary angioplasty. Eligible patients who all had symptomatic ischemic heart disease were selected if the reference diameter of the selected vessel was ú3.0 mm. Otherwise, indication for DCA was determined according to the anatomic condition of the targeted vessel and morphologic criteria of the lesion to be treated.1 – 5 Patients who presented with restenosis after previous angioplasty were not included in this study. Atherectomy procedure: DCA was performed with large catheters (size 7Fr in 87% of cases) according to the usual procedure to eliminate as much residual stenosis as possible.6,9 Enlargement of the vascular lumen was obtained through a stepwise approach that comprised multiple cuts at low (10 to 20 psi) and then at high pressure (40 to 60 psi). Additional angioplasty using high-pressure inflation with a noncompliant balloon was almost systematically used to complete the atherectomy. Mean ratio of balloon size over reference diameter never exceeded 1.1. A pre-
1–3
trials have failed to confirm a clear superiority of atherectomy.4,5 However, a renewal of interest for DCA has been generated by the Optimal Atherectomy Restenosis Study which has shown lower rates of restenosis (angiographic 29.6% and clinical 18%).6 Consequently, such techniques should bring about midterm improvement in coronary flow and therefore restore ventricular function within the myocardial segments chronically exposed to ischemia.7 – 12 This study prospectively evaluated the utility of optimal DCA in 95 consecutive patients who systematically underwent 6-month follow-up angiography after a successful procedure. To investigate the hypothesis that reducing the restenosis rate would improve regional left ventricular (LV) function, we compared the coronary angiogram course of the treated narrowing with that of cardiac function estimated from segmental wall motion.
METHODS Patients: Between August 1992 and June 1995, 122 DCA procedures were performed in our center. Four were unsuccessful or gave way to complicaFrom the Catheterization Laboratory and Intensive Care Unit, IFR Coeur-Vaisseaux-Thrombose, University of Bordeaux II, Bordeaux-Pessac, France. Manuscript received May 31, 1996; revised manuscript received and accepted October 7, 1996. Address for reprints: Pierre Coste, MD, Hoˆpital Cardiologique, IFR Coeur-Vaisseaux-Thrombose, Avenue Magellan, 33604 Bordeaux-Pessac, France. Q1997 by Excerpta Medica, Inc.
0002-9149/97/$17.00 PII S0002-9149(96)00813-2
All rights reserved.
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FIGURE 1. Evaluation of regional wall motion according to the radial method percent shortening are expressed as mean { 1 SD. EF Å ejection fraction; S Å segment.
were manually traced by an independent observer. Contours were digitized and calibrated according to a computer program that takes into account distortion due to the image intensifier. LV end-diastolic volume index, LV end-systolic volume index, and LV ejection fraction were calculated according to Simpson’s rule.12 Regional wall motion was analyzed using a radial method developed by Ingels et al.12,14,15 Schematically, an index of wall displacement was measured for 10 angular sectors using a center of contraction located at 69% of the axis distance that joins the upper edge of the base of the aorta to the LV apex at end-systole. Then, segmental wall motion was expressed as a percentage of the end-diastolic value of the radius of each sector (see Figure 1). Normal values of ejection fraction and fractional shortening were calculated in a control group of 25 patients without cardiac disease or significant coronary lesions.14 Normal range values (mean { SD) were 70 { 6% for LV ejection fraction. The segments of the anterior wall, segments 6 to 10, showed the following percent shortening: S6, 35 { 5%; S7, 52 { 6%; S8, 57 { 7%; S9, 59 { 7%; and S10, 52 { 5%. For inferior and basal zones, percent shortening of segments 2 to 5 were: S2, 20 { 7%; S3, 34 { 9%; S4, 38 { 8%; and S5, 31 { 5%. To insure better reproducible measurement conditions, patients were kept under the same pharmacologic regimen between the 2 examinations, and catheterization was repeated according to the same protocol. Whenever feasible, patients had a programmed control at 6 months (average 6 { 1.9). A few of them underwent coronary angiography earlier than expected because of recurrence of unstable angina, suggesting a rapid restenosis process. Statistical analysis: Quantitative data are expressed as mean { 1 SD. Comparisons between groups were tested globally using analysis of variance for repeated measurements. When significant differences were found, comparisons within groups for continuous variables were made using Student’s paired t test. Between-group comparisons were undertaken with Student’s unpaired t test for unmatched series. Categorical variables were compared using chi-
dilation of the stenosis was necessary for 1 patient only. All patients were given aspirin (250 mg/day) and intravenous heparin (10,000 IU bolus dose) before DCA. Patients selected for follow-up had to fulfill criteria for technical success defined by: (1) residual stenosis õ50% in diameter in at least 2 different radiologic projections; (2) absence of procedural complications (vessel occlusion, myocardial infarction, emergency coronary bypass surgery, repeat angioplasty) during the hospitalization stay; and (3) no elevation in creatine kinase myocardial isoform more than twofold normal values. Quantitative analysis of angiograms: Coronary angiograms were quantified using ACA software included in Philips Digital Cardiac Imaging system (Eindhoven, The Netherlands). The reproducibility of measurements for this system has already been reported.13 Two independent observers (P.C. and S.S.) performed these quantitative analyses without knowledge of LV function data. Coronary lesions were assessed on end-diastolic images by analyzing the same segment length after systematic intracoronary injection of vasodilator (Sin1; 0.5 mg). Conditions of centering, magnification, and radiologic projections were carefully repeated during follow-up study. The guiding catheter was used as a calibration device to express measurements in absolute values. Restenosis at the site of the preceding coronary atherectomy was defined by a renarrowing of the vessel lumen ú50% in diameter on the control angiogram. Hemodynamic data and quantitative evaluation of ventricular function: Baseline values of intraventricu-
lar systolic and end-diastolic pressures, and aortic pressures were recorded with an external fluid-filled manometer by averaging values from 10 cardiac cycles with a computerized system that processed the pressure curve signal.12 LV angiograms were filmed at 50 images/s, 15 minutes before atherectomy. The LV cavity was opacified in the right oblique anterior projection (307) with 0.5 ml/kg of contrast medium using an automatic injector. Ventricular contours without ventricular premature beats only were taken into account to evaluate segmental wall motion. LV contours on end-diastolic and end-systolic frames 546
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tribution of patients treated in the days after myocardial infarction was not different with respect to the target vessel. All patients conserved contractility within the infarcted area and all had normal coronary flow (Thrombolysis In Myocardial Infarction trial grade 3) in the infarct-related vessel. The DCA procedure was performed after a period of clinical stabilization, ú5 days after an ischemic episode at rest and ¢8 days after myocardial infarction. Angiographic restenosis at six months: Figure 2 illustrates the immediate postprocedure and 6-month outcome of our population in terms of the degree of stenosis measured by quantitative angiography. Twenty-two patients (23%) had angiographic restenosis. During follow-up, none of them experienced a new myocardial infarction. Ten of these 22 patients were rehospitalized for recurrence of angina pectoris and underwent a new intervention for myocardial revascularization, either repeat balloon angioplasty (n Å 7) or coronary bypass surgery (n Å 3). Therefore, only 11% of the entire population underwent a target vessel revascularization in the territory concerned with atherectomy. No other clinical cardiac event was noted during the follow-up period. If one applies the commonly accepted criterion of ú50% stenosis in diameter at control, the restenosis rate in the right coronary artery group appeared higher than that of the left anterior descending group, but the small number of patients with restenosis limits the statistical power of this comparison. This
square analysis, or Fisher’s exact test when appropriate. Statistical analyses were performed with SAS software (SAS Institute, version 6.04, Cary, North Carolina). A p level of probability õ0.05 was retained as significant.
RESULTS Population characteristics: The population was divided into 2 subgroups according to the myocardial area to be revascularized, and therefore according to the targeted coronary vessel (i.e., right coronary or left anterior descending artery). Baseline clinical characteristics and angiographic data of the overall population and subgroup analysis are detailed in Table I. These characteristics were similar to those found in studies dealing with DCA1 – 6 and, in addition, they were similar in the 2 coronary territory subgroups. Most patients presented with unstable angina, and 46 (48%) had experienced a recent myocardial infarction in the vascular territory of the target vessel. This recruitment feature may be explained by an anatomic selection based on the morphologic characteristics of the lesions, foremost of which was intraluminal thrombus. Among the 46 patients with prior myocardial infarction, 41 had myocardial infarction õ2 months before the procedure. Among these patients, 56% were initially treated with a thrombolytic agent and coronary recanalization was angiographically documented õ6 hours after the onset of chest pain (average 3.1 { 2.3 hours). The disTABLE I Clinical and Angiographic Data of Study Population Variables Clinical data Age (yr) Male gender Hypercholesterolemia Systemic hypertension History of smoking Diabetes mellitus Family history of CAD Prior myocardial infarction Delay from myocardial infarction to DCA (d) Unstable angina 1-vessel disease Multivessel disease 7Fr atherectomy device Quantitative angiography Minimum lumen diameter (mm) Before procedure After procedure Control Reference diameter (mm) Before procedure After procedure Control % Diameter stenosis Before procedure After procedure Control Restenosis ú50%
Right Coronary Artery Group (n Å 32)
Left Anterior Descending Artery Group (n Å 63)
Total Population (n Å 95)
54 { 12 26 (81%) 25 (78%) 11 (34%) 23 (72%) 4 (12%) 14 (44%) 16 (50%) 36 { 56 22 (69%) 16 (50%) 16 (50%) 28 (87%)
56 { 12 53 (84%) 45 (71%) 31 (49%) 45 (71%) 13 (21%) 31 (49%) 30 (48%) 29 { 32 50 (79%) 39 (62%) 24 (38%) 52 (83%)
55 { 12 79 (83%) 70 (74%) 42 (44%) 68 (72%) 17 (18%) 45 (47%) 46 (48%) 31 { 41 71 (75%) 55 (58%) 40 (42%) 80 (84%)
1.29 { 0.50 3.14 { 0.50* 2.21 { 0.86‡
1.14 { 0.40 2.97 { 0.42* 2.15 { 0.72‡
1.19 { 0.44 3.03 { 0.45* 2.17 { 0.61‡
3.67 { 0.69 3.69 { 0.70 3.52 { 0.66†
3.53 { 0.63 3.49 { 0.53 3.44 { 0.58
3.58 { 0.65 3.56 { 0.60 3.47 { 0.61†
64.2 { 11.3 14.0 { 12.4* 37.1 { 20‡ 9 (28%)
67.3 { 8.45 14.8 { 9.5* 37.4 { 18.6‡ 13 (21%)
66.2 { 9.6 14.5 { 10.5* 37.3 { 18.9‡ 22 (23%)
*p õ0.001 before versus after procedure; †p õ0.02; ‡p õ0.001 control versus after procedure. Numeric values are expressed as mean { SD, categorical values are numbers and percentage of the total number in each group. CAD Å coronary artery disease; DCA Å directional coronary atherectomy.
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FIGURE 2. Cumulative percentage of patients as a function of percent diameter stenosis as estimated with quantitative coronary angiography. Pre DCA Å before directional coronary atherectomy; Post DCA after directional coronary atherectomy; Control Å control angiogram.
TABLE II Hemodynamic Data and Segmental Wall Motion in Patients Without Restenosis Before Atherectomy Right Coronary Artery (n Å 23) Ejection fraction (%) Fractional shortening (%) Segment 2 Segment 3 Segment 4 Segment 5 Segment 6 Segment 7 Segment 8 Segment 9 Segment 10 Heart rate (beats/min) LV pressure (mm Hg) End-diastolic Systolic Mean aortic pressure (mm Hg) LV volume index (ml/m2) End-diastolic End-systolic
Follow-Up Angiography
Left Anterior Descending Artery (n Å 50)
Total Population (n Å 73)
Right Coronary Artery (n Å 23)
Left Anterior Descending Artery (n Å 50)
Total Population (n Å 73)
67 { 11
59 { 15§
61 { 14
73 { 8‡
62 { 17*
65 { 15‡
23 41 45 39 37 49 53 56 47 70
29 41 38 26 19 28 32 35 35 70
27 41 41 30 25 35 39 42 39 70
26 48 51 43 42 58 62 61 51 71
25 43 42 30 27 39 44 46 39 68
25 44 45 34 32 45 50 50 43 69
{ 12 { 19 { 18 { 16 { 22 { 26 { 22 { 21 { 20 {9
{ 18 { 16 { 19 { 19\ { 19Ø { 27\ { 27Ø { 26\ { 21§ { 12
{ 16 { 17 { 19 { 19 { 22 { 28 { 28 { 26 { 21 { 11
13 { 7 126 { 21 93 { 14
17 { 8 129 { 24 94 { 16
16 { 8 128 { 23 94 { 16
89 { 24 30 { 12
103 { 38 45 { 31
99 { 35 40 { 27
{9 { 16* { 14 { 13 { 19 { 18* { 17† { 19 { 15 { 10
{ 11 { 17 { 19 { 18† { 22‡ { 27‡ { 28‡ { 28‡ { 23 { 13
{ 11 { 17 { 18* { 17‡ { 22‡ { 26‡ { 26‡ { 27‡ { 22 { 12
13 { 6 139 { 25* 95 { 14
16 { 8 141 { 29† 99 { 18
15 { 7 141 { 28‡ 98 { 17
86 { 34 27 { 20
106 { 41 45 { 39
99 { 40 39 { 34
*p õ0.05; †p õ0.01; ‡p õ0.001 before atherectomy versus at control in the same group; §p õ0.05; \p õ0.01; Øp õ0.001 right coronary artery group versus left anterior descending artery group. Values are expressed as mean { SD. LV Å left ventricular.
study confirms the importance of late loss when compared with the acute gain that was expressed by a significant enlargement of the coronary lumen after optimal atherectomy (on average 1.84 mm). More precisely, the loss index expressed as the late loss divided by the initial gain was 0.49 { 0.42. Evaluation of left ventricular function: The parameters of LV function were analyzed according to presence or absence of angiographic restenosis as previously defined. Main results are summarized in Tables II and III with respect to the vessel dilated and the restenosis process. Heart rate and mean aor548
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tic pressure did not change significantly between the 2 examinations. We observed only a mild to moderate elevation in LV systolic pressure in patients without restenosis at control (/12 { 23 mm Hg, p õ0.001). Globally, there was no significant variation in LV volumes, but ejection fraction increased in the group without restenosis (/4 { 9%, p õ0.005). In contrast, there was no significant variation in ejection fraction (03 { 9%, p Å NS) in patients with angiographic restenosis. Conversely, regional wall motion analysis demonstrated a highly significant improvement in segmental shortening, most of which was
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TABLE III Hemodynamic Data and Segmental Wall Motion in Patients With Restenosis Before Atherectomy
Ejection fraction (%) Fractional shortening (%) Segment 2 Segment 3 Segment 4 Segment 5 Segment 6 Segment 7 Segment 8 Segment 9 Segment 10 Heart rate (beats/min) LV pressure (mm Hg) End-diastolic Systolic Mean aortic pressure (mm Hg) LV volume index (ml/m2) End-diastolic End-systolic
Follow-Up Angiography
Right Coronary Artery (n Å 9)
Left Anterior Descending Artery (n Å 13)
Total Population (n Å 22)
Right Coronary Artery (n Å 9)
Left Anterior Descending Artery (n Å 13)
68 { 8
66 { 9
67 { 8
68 { 7
62 { 8
65 { 8
21 42 41 31 38 53 57 58 50 61
34 43 47 33 24 32 38 43 43 63
29 43 45 33 30 40 46 49 46 62
23 43 44 36 33 50 58 59 39 63
37 47 41 26 17 27 33 33 33 67
31 45 43 30 23 36 43 44 36 65
{9 { 21 { 20 { 16 { 18 { 20 { 17 { 16 { 17 {7
{ 22 { 20 { 21 { 24 { 26 { 32 { 29 { 28 { 20 { 10
{ 18 { 20 { 21 { 21 { 24 { 30 { 27 { 24 { 19 {9
{4 { 15 { 15 { 17 { 17 { 14 { 14 { 15 {8 {9
{ 22 { 22 { 22 { 21 { 17 { 21 { 21 { 18 { 10 {8
15 { 6 122 { 13 91 { 8
15 { 8 124 { 25 97 { 20
15 { 7 123 { 21 95 { 16
14 { 4 131 { 17 98 { 11
13 { 8 134 { 25 100 { 21
87 { 21 28 { 11
91 { 16 32 { 10
90 { 18 30 { 10
88 { 18 28 { 11
84 { 21 31 { 7
Total Population (n Å 22)
{ 18 { 19 { 20 { 20 { 18 { 22 { 22 { 21 { 9* {9
13 { 6 133 { 22* 99 { 18 85 { 19 30 { 9
*p õ0.05 before atherectomy versus at control in the same group. Values are expressed as mean { SD. LV Å left ventricular.
FIGURE 3. Segmental wall motion of the left ventricle in patients with left anterior descending lesion and without restenosis at control angiogram. Left ventricular segments (Seg) are plotted on the X-axis and fractional shortening on the Y-axis. Normal range values are indicated as mean { 2 SD. Note the absence of significant variation in percent shortening of basal segments. Abbreviations as in Figure 2.
accounted for by anterior zones (/10% and /11% for segments 7 and 8, respectively, p õ0.001). At baseline examination, regional shortening was significantly abnormal, corresponding to a net hypokinesia due to myocardial stunning in patients with unstable angina, or to depressed contractility linked to underlying necrosis (Figures 3 and 4). This feature was far more pronounced in anterior than in inferior segments. In the restenosis group, 9 patients (41%) had prior myocardial infarction, and 5 patients had inferior and 4 anterior infarction. The vascular distribution was not statistically different when compared with that of the 37 patients (51%) with prior
infarction in the group without restenosis: 11 patients had inferior and 26 anterior infarctions. Improvement in segmental wall motion was not influenced by previous infarction in the vascular territory concerned with atherectomy. Indeed, multivariate analysis of variance for repeated measurements did not show significant interaction between previous myocardial infarction and percent fractional shortening (for segment 7, F Å 2.02, p Å 0.15). In the absence of restenosis, the time course of the regional wall motion in patients with myocardial infarction did not exhibit differences when compared with that of the other patients. However, subgroup analysis demon-
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FIGURE 4. Segmental wall motion of the left ventricle in patients with left anterior descending lesion and restenosis at control angiogram. The left ventricular wall was considered to be hypokinetic if percent shortening of ¢2 contiguous segments (Seg) were õ2 SD values from the mean value. Abbreviations as in Figure 2.
erectomy Restenosis Study (3.15 mm).6 We must emphasize that most of the vessels treated in our experience were larger than those in previous reported studies. This may have favored a lower restenosis rate.17,18 Another explanation might involve the thrombotic material that is very frequently deposited on freshly ruptured plaques.19 Indeed, the residual thrombus that is left after angioplasty is considered as a strong predictive parameter of restenosis.20 By removing a large amount of atherosclerotic material, we may have reduced thrombus incorporated in the vascular scar and limited intimal proliferation. Finally, the population size was rather small compared with size in other controlled studies6,21 and the selected angiograms may have created systematic bias in our results.
strated that patients with myocardial infarction had less pronounced improvement in percent fractional shortening (/5 { 12% for segment 7, p õ0.05), reflecting a persistent significant depression in LV contractility. Similarly, segmental motion improvement in inferior and basal regions at control was smaller in LV segments with previous myocardial infarction. Again, improvement in regional contractility was observed in the absence of restenosis only, and was far more pronounced in anterior than inferior zones. For the entire group with left anterior descending artery lesions, we found a weak, although significant, negative correlation between percent diameter stenosis at control, and the variation in the percentage of segment shortening in the anterior wall (r Å 00.28, p õ0.03; r Å 00.26, p õ0.01; r Å 00.26, p õ0.02 for zones 7, 8, and 9, respectively).
Improvement in left ventricular regional wall motion:
When myocardial perfusion is chronically altered, revascularization of dysfunctional areas has demonstrated its usefulness in preserving LV contractile function.10 – 12 Improvements in regional wall motion and global ejection fraction of the left ventricle after coronary bypass surgery are well recognized.22,23 These clinical observations can be explained by the concept of ‘‘hibernating myocardium,’’ which could be due in part to chronic myocardial ischemia but also to repeated episodes of acute ischemia that culminate in stunning of cardiac muscle.24,25 After coronary angioplasty, and particularly in the setting of unstable angina, improvements in LV wall contractility have been conclusively documented.11,14,25 – 27 Accordingly, we found in this prospective study a significant variation in LV wall motion that was detected from analysis of end-diastolic and end-systolic ventricular contours. A more thorough study using a frame-by-frame approach on the overall cardiac cycle may have strengthened our conclusions. In previous studies, we followed midterm evolution in patients treated with balloon angioplasty for left anterior descending artery lesions and we found ben-
DISCUSSION After results of the large controlled trials,4,5 the interest in DCA has been questioned.3 Nevertheless, the advantage of optimal atherectomy was clearly indicated in retrospective studies that used the matching approach.16 All strategies that have aimed at an optimal increase in the vascular lumen have limited the incidence of restenosis even though late decrease in vessel lumen appears to be more pronounced using DCA.3,9,17 Our data on restenosis seems to be somewhat surprising since the population included a large proportion of patients with unstable angina. However, our optimizing technique added complementary balloon angioplasty to a great number of cuts (on the average 20 to 30 per lesion) whose efficacy was demonstrated by the substantial amount of atheroma fragments generally collected. By using large devices and postdilation for most arteries, even for those as small as 3.0 mm in diameter, we obtained, on average after the procedure, a minimum lumen diameter ú3.0 mm. These results are almost identical to those found in the Optimal Ath550
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eficial effects on asynergy of the anterior wall and on asynchrony of the anterior segments during the contraction phase. Other parameters reflecting regional dysfunction, such as shortening of contraction duration, were also significantly improved in the absence of angiographic restenosis.12 In the present study, wall motion in the myocardial zone revascularized with atherectomy improved in a significant manner, whereas parameters of LV loading did not significantly change from baseline values. In fact, we observed a tendency toward an increase in LV systolic and mean aortic pressures. The improvement was more marked for anterior segments, and less pronounced for inferior and basal segments of the left ventricle. As reported in studies dealing with coronary balloon angioplasty, angiographically visible restenosis limits recovery of regional contractility.28 The binary distinction of restenosis may appear arbitrary since recent studies in humans have found that attenuation of the coronary blood flow reserve exists for stenosis as low as 40%.7,8 Indeed, we found a significant correlation between the degree of stenosis and 6-month variations in percent fractional shortening for all 95 patients. By contrast, even though there is a correlation between percent diameter stenosis and the consecutive decrease in coronary perfusion reserve, the predictive value of the angiographic severity of a given lesion remains uncertain.8 Accordingly, we cannot draw individual conclusions on the outcome of myocardial perfusion from our study. LV dysfunction may recover spontaneously after repeated episodes of ischemia or after the acute phase of myocardial infarction. Some investigators found no significant variations when ventricular volumes and segmental motion were measured after the 10th day of infarction, but others have clearly shown that recovery of LV function was possible after a delay of 5 weeks.29 Although we obtained no data concerning myocardial viability and cardiac metabolism, improvement in segmental wall motion favors the persistence of a heterogeneous population of myocytes having different degrees of functional alterations.23 Unfortunately, clinical follow-up only was available for patients who developed myocardial infarction after DCA; thus, our data cannot be extended to procedures associated with creatine kinase elevation more than twofold normal.30 Study limitations: Patients were prospectively selected on the basis of angiographic criteria, and the group with previous myocardial infarction may have had a reduction in the magnitude of variation in LV contractility since improvement in regional wall motion was significant but obviously smaller in this subset. However, the distribution of patients with myocardial infarction was not different according to the coronary territory treated or the incidence of restenosis. Pathophysiologic consequences of coronary blood flow changes on LV function are strongly influenced by the dominance of the right coronary system, and complementary analysis performed using another radiologic projection may have reinforced
data demonstrating the benefit of revascularization apparent in this study that focused on the left coronary system. Acknowledgment: We gratefully acknowledge the technical assistance of Dominique Fernandez and Francoise Noailles for preparing the manuscript, and Gerard Gouverneur for his help with the statistical analysis.
1. Hinohara T, Robertson GC, Selmon MR, Vetter JW, Rowe MH, Braden LJ,
McAuley BJ, Sheehan DJ, Simpson JB. Restenosis after directional coronary atherectomy. J Am Coll Cardiol 1992;20:623–633. 2. Fishman RF, Kuntz RE, Corrozza JP, Miller M, Senerchia CC, Schnitt SJ, Diver DJ, Safian RD, Baim DS. Long-term results of directional atherectomy: predictors of restenosis. J Am Coll Cardiol 1992;20:1101–1110. 3. Umans VAWM, Robert A, Foley D, Wijns W, Haine E, de Feyter PJ, Serruys PW. Clinical, histologic and quantitative angiographic predictors of restenosis after directional atherectomy: a multivariate analysis of the renarrowing process and late outcome. J Am Coll Cardiol 1994;23:49–58. 4. Topol EJ, Leya F, Pinkerton CA, Whitlow PL, Hofling B, Simonton C, Masden RR, Serruys PW, Leon M, Williams DO, King SB III, Mark DB, Isner JM, Holmes DR, Ellis SG, Lee KL, Keeler GP, Hinohara T, Califf RM. A comparison of directional coronary atherectomy with coronary angioplasty in patients with coronary artery disease. N Engl J Med 1993;329:221–227. 5. Adelman AG, Cohen EA, Kimball BP, Bonan R, Ricci DR, Webb JG, Laramee L, Barbeau G, Traboulsi M, Corbett BN, Schwartz L, Logan AG. A comparison of directional coronary atherectomy with balloon angioplasty for lesions of the left anterior descending coronary artery. N Engl J Med 1993;329:228– 234. 6. Simonton CA, Leon MB, Kuntz, Popma JJ, Hinohara T, Bersin RM, Yock PG, Wilson BH. Acute and late clinical and angiographic results of directional atherectomy in the Optimal Atherectomy Study (OARS) (abstr). Circulation 1996;92(suppl I):I–545. 7. Wilson RF, Johnson MR, Marcus ML, Aylward PEG, Skorton DJ, Collins, White CW. The effect of coronary angioplasty on coronary flow reserve. Circulation 1988;77:873–885. 8. Uren NG, Melin JA, De Bruyne B, Wijns W, Baudhuin T, Camici PG. Relation between myocardial blood flow and the severity of coronary artery stenosis. N Engl J Med 1994;330:1782–1788. 9. Kuntz RE, Safian RD, Carrozza JP, Fisjman RF, Monsour M, Baim DS. The importance of acute luminal diameter in determining restenosis after coronary atherectomy or stenting. Circulation 1992;86:1827–1835. 10. Braunwald E, Kloner RA. The stunned myocardium: prolonged, postischemic ventricular dysfunction. Circulation 1982;66:1146–1149. 11. de Feyter PJ, Suryapranata H, Serruys PW, Beat K, van der Brabd M, Hugenholtz PG. Effects of successful percutaneous transluminal coronary angioplasty on global and regional left ventricular function in unstable angina pectoris. Am J Cardiol 1987;60:993–997. 12. Colle JP, Legoff G, Carfora A, Delarche N, Kilpatrick DD, Besse P. Longterm beneficial effects of PTCA on early segmental relaxation in disease of the left anterior descending artery. Angiology 1988;39:466–478. 13. Reiber JHC, van der Zweet PMJ, von Land CD, Koning G, Loois G, Zorn I, van der Brand M, Gerbrands JJ. On-line quantification of coronary angiograms with the DCI system. Medicamundi 1989;34:89–98. 14. Colle JP, Legoff G, Ohayon J, Bonnet J, Bricaud H, Besse P. Quantitative frame by frame analysis of regional contraction and lengthening on left ventricular cineangiograms: application to the study of normal left ventricles and left ventricles with mitral valve prolapse. Clin Cardiol 1986;9:43–51. 15. Ingels NB, Daughters GT, Stinson EB, Alderman EL. Evaluation of methods for quantitating left ventricular segmental wall motion in man using myocardial markers as a standard. Circulation 1980;61:966–972. 16. Umans VAWM, Keane D, Foley D, Boersma E, Melkert R, Serruys PW. Optimal use of directional coronary atherectomy is required to ensure long-term angiographic benefit: a study with matched procedural outcome after atherectomy and angioplasty. J Am Coll Cardiol 1994;24:1652–1659. 17. Kuntz RE, Hinohara T, Robertson GC, Safian RD, Simpson JB, Baim DS. Influence of vessel selection on the observed restenosis rate after endoluminal stenting or directional atherectomy. Am J Cardiol 1992;70:1101–1108. 18. Foley DP, Melkert R, Serruys PW. Influence of coronary vessel size on renarrowing process and late angiographic outcome after successful balloon angioplasty. Circulation 1994;90:1239–1251. 19. Arbustini E, De Servi S, Bramucci E, Porcu E, Costante AM, Grasso M, Diegoli M, Fasani R, Morbini P, Angoli L, Boscarini M, Repetto S, Danzi G, Niccoli L, Campolo L, Lucreziotti S, Specchia G. Comparison of coronary lesions obtained by directional coronary atherectomy in unstable angina, stable angina, and restenosis after either atherectomy or angioplasty. Am J Cardiol 1995;75:675–682.
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20. Bauters C, Lablanche JM, MacFadden EP, Hamon M, Bertrand ME. Re-
and functional recovery of ischemic human myocardium after angioplasty. J Am Coll Cardiol 1991;18:966–978. 26. Rosing DR, Cannon RO III, Watson RM, Bonow RO, Mincemoyer R, Ewels C, Leon M, Lakatos E, Epstein SE, Kent KM. Three-year anatomic, functional and clinical follow-up after successful percutaneous transluminal coronary angioplasty. J Am Coll Cardiol 1987;9:1–7. 27. van den Berg EK, Popma JJ, Dehmer GJ, Snow FR, Lewis SA, Vetrotec GW, Nixon JV. Reversible segmental left ventricular dysfunction after coronary angioplasty. Circulation 1990;81:1210–1216. 28. Melgares R, Prieto JA, Azputarte J. Significant coronary restenosis limits the recovery of regional left myocardial dysfunction achieved after successful coronary angioplasty. Eur Heart J 1993;14:866–875. 29. Galli M, Marcassa C, Bolli R, Giannuzzi P, Temporelli PL, Imparato A, Orrego S, Giubbini R, Giordano A, Tavazzi L. Spontaneous delayed recovery of perfusion and contraction after the first 5 weeks after anterior myocardial infarction. Evidence for the presence of hibernating myocardium in the infarcted area. Circulation 1994;90:1386–1397. 30. Kugelmass AD, Cohen DJ, Moscucci M, Piana RN, Senerchia C, Kuntz RE, Baim DS. Elevation of the creatine kinase myocardial isoform following otherwise successful directional coronary atherectomy and stenting. Am J Cardiol 1994;74:748–754.
lation of coronary angioscopic findings at coronary angioplasty to angiographic restenosis. Circulation 1995;92:2473–2479. 21. Baim DS, Kuntz R, Sharma SK, Fortuna R, Feldman R, Senerchia C, DeFeo T, Popma JJ, Ho KKL, for the BOAT investigators. Acute results of the randomized phase of the balloon versus optimal atherectomy trial (BOAT) (abstr). Circulation 1995;92(suppl I):I–544. 22. Vanoverschelde JLJ, Wijns W, Depre´ C, Essamri B, Heyndrickx GR, Borgers M, Bol A, Melin JA. Mechanisms of chronic regional postischemic dysfunction in humans. New insights from the study of noninfarcted collateral-dependent myocardium. Circulation 1993;87:1513 – 1523. 23. Marwick TH, MacIntyre WJ, Lafont A, Nemec JJ, Salcedo EE. Metabolic responses of hibernating and infarcted myocardium to revascularization. A follow-up study of regional perfusion, function, and metabolism. Circulation 1992;85:1347–1353. 24. Shen YT, Vatner SF. Mechanism of impaired myocardial function during progressive coronary stenosis in conscious pigs. Hibernation versus stunning? Circ Res 1995;76:479–488. 25. Nienaber CA, Brunken RC, Sherman CT, Yeatman LA, Gambhir SS, Krivokapich J, Demer LL, Ratib O, Child JS, Phelps ME, Schelbert HR. Metabolic
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rate (ú50% stenosis in diameter) at control was 23%. In patients without restenosis, there were no significant changes in LV volumes or in LV pressures. In this subgroup, ejection fraction improved significantly in the left anterior descending group (mean difference 3 { 10%, p õ0.04). Moreover, there was an increase in fractional shortening of all anterior segments (mean difference 11 { 16%, p õ0.005). Improvement in fractional shortening was less marked in the right coronary artery group even without restenosis. We conclude that: (1) optimal DCA can achieve a low restenosis rate in selected large vessels, (2) long-term beneficial effects on regional LV function are possible, particularly in patients with left anterior descending disease and in the absence of coronary restenosis. Q1997 by Excerpta Medica, Inc. (Am J Cardiol 1997;79:545–552)
irectional coronary atherectomy (DCA) was first proposed in order to reduce the incidence of reD stenosis after balloon angioplasty but controlled
tions (3.3%). Three patients (2.5%) developed myocardial infarction defined as new Q waves in the electrocardiogram and/or creatine kinase myocardial isoform more than twofold normal values. All these patients completed clinical follow-up, and 95 underwent angiography at 6 months, giving a 81% angiographic control rate in successful procedures. Thirteen of the controlled patients (12%) initially had a slight elevation in creatine kinase above the upper limits of normal. The remaining patients were either symptom-free or had Canadian Cardiac Society class 1 or 2 angina with medical treatment. None required cardiac revascularization either by coronary bypass surgery or repeat coronary angioplasty. Eligible patients who all had symptomatic ischemic heart disease were selected if the reference diameter of the selected vessel was ú3.0 mm. Otherwise, indication for DCA was determined according to the anatomic condition of the targeted vessel and morphologic criteria of the lesion to be treated.1 – 5 Patients who presented with restenosis after previous angioplasty were not included in this study. Atherectomy procedure: DCA was performed with large catheters (size 7Fr in 87% of cases) according to the usual procedure to eliminate as much residual stenosis as possible.6,9 Enlargement of the vascular lumen was obtained through a stepwise approach that comprised multiple cuts at low (10 to 20 psi) and then at high pressure (40 to 60 psi). Additional angioplasty using high-pressure inflation with a noncompliant balloon was almost systematically used to complete the atherectomy. Mean ratio of balloon size over reference diameter never exceeded 1.1. A pre-
1–3
trials have failed to confirm a clear superiority of atherectomy.4,5 However, a renewal of interest for DCA has been generated by the Optimal Atherectomy Restenosis Study which has shown lower rates of restenosis (angiographic 29.6% and clinical 18%).6 Consequently, such techniques should bring about midterm improvement in coronary flow and therefore restore ventricular function within the myocardial segments chronically exposed to ischemia.7 – 12 This study prospectively evaluated the utility of optimal DCA in 95 consecutive patients who systematically underwent 6-month follow-up angiography after a successful procedure. To investigate the hypothesis that reducing the restenosis rate would improve regional left ventricular (LV) function, we compared the coronary angiogram course of the treated narrowing with that of cardiac function estimated from segmental wall motion.
METHODS Patients: Between August 1992 and June 1995, 122 DCA procedures were performed in our center. Four were unsuccessful or gave way to complicaFrom the Catheterization Laboratory and Intensive Care Unit, IFR Coeur-Vaisseaux-Thrombose, University of Bordeaux II, Bordeaux-Pessac, France. Manuscript received May 31, 1996; revised manuscript received and accepted October 7, 1996. Address for reprints: Pierre Coste, MD, Hoˆpital Cardiologique, IFR Coeur-Vaisseaux-Thrombose, Avenue Magellan, 33604 Bordeaux-Pessac, France. Q1997 by Excerpta Medica, Inc.
0002-9149/97/$17.00 PII S0002-9149(96)00813-2
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FIGURE 1. Evaluation of regional wall motion according to the radial method percent shortening are expressed as mean { 1 SD. EF Å ejection fraction; S Å segment.
were manually traced by an independent observer. Contours were digitized and calibrated according to a computer program that takes into account distortion due to the image intensifier. LV end-diastolic volume index, LV end-systolic volume index, and LV ejection fraction were calculated according to Simpson’s rule.12 Regional wall motion was analyzed using a radial method developed by Ingels et al.12,14,15 Schematically, an index of wall displacement was measured for 10 angular sectors using a center of contraction located at 69% of the axis distance that joins the upper edge of the base of the aorta to the LV apex at end-systole. Then, segmental wall motion was expressed as a percentage of the end-diastolic value of the radius of each sector (see Figure 1). Normal values of ejection fraction and fractional shortening were calculated in a control group of 25 patients without cardiac disease or significant coronary lesions.14 Normal range values (mean { SD) were 70 { 6% for LV ejection fraction. The segments of the anterior wall, segments 6 to 10, showed the following percent shortening: S6, 35 { 5%; S7, 52 { 6%; S8, 57 { 7%; S9, 59 { 7%; and S10, 52 { 5%. For inferior and basal zones, percent shortening of segments 2 to 5 were: S2, 20 { 7%; S3, 34 { 9%; S4, 38 { 8%; and S5, 31 { 5%. To insure better reproducible measurement conditions, patients were kept under the same pharmacologic regimen between the 2 examinations, and catheterization was repeated according to the same protocol. Whenever feasible, patients had a programmed control at 6 months (average 6 { 1.9). A few of them underwent coronary angiography earlier than expected because of recurrence of unstable angina, suggesting a rapid restenosis process. Statistical analysis: Quantitative data are expressed as mean { 1 SD. Comparisons between groups were tested globally using analysis of variance for repeated measurements. When significant differences were found, comparisons within groups for continuous variables were made using Student’s paired t test. Between-group comparisons were undertaken with Student’s unpaired t test for unmatched series. Categorical variables were compared using chi-
dilation of the stenosis was necessary for 1 patient only. All patients were given aspirin (250 mg/day) and intravenous heparin (10,000 IU bolus dose) before DCA. Patients selected for follow-up had to fulfill criteria for technical success defined by: (1) residual stenosis õ50% in diameter in at least 2 different radiologic projections; (2) absence of procedural complications (vessel occlusion, myocardial infarction, emergency coronary bypass surgery, repeat angioplasty) during the hospitalization stay; and (3) no elevation in creatine kinase myocardial isoform more than twofold normal values. Quantitative analysis of angiograms: Coronary angiograms were quantified using ACA software included in Philips Digital Cardiac Imaging system (Eindhoven, The Netherlands). The reproducibility of measurements for this system has already been reported.13 Two independent observers (P.C. and S.S.) performed these quantitative analyses without knowledge of LV function data. Coronary lesions were assessed on end-diastolic images by analyzing the same segment length after systematic intracoronary injection of vasodilator (Sin1; 0.5 mg). Conditions of centering, magnification, and radiologic projections were carefully repeated during follow-up study. The guiding catheter was used as a calibration device to express measurements in absolute values. Restenosis at the site of the preceding coronary atherectomy was defined by a renarrowing of the vessel lumen ú50% in diameter on the control angiogram. Hemodynamic data and quantitative evaluation of ventricular function: Baseline values of intraventricu-
lar systolic and end-diastolic pressures, and aortic pressures were recorded with an external fluid-filled manometer by averaging values from 10 cardiac cycles with a computerized system that processed the pressure curve signal.12 LV angiograms were filmed at 50 images/s, 15 minutes before atherectomy. The LV cavity was opacified in the right oblique anterior projection (307) with 0.5 ml/kg of contrast medium using an automatic injector. Ventricular contours without ventricular premature beats only were taken into account to evaluate segmental wall motion. LV contours on end-diastolic and end-systolic frames 546
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tribution of patients treated in the days after myocardial infarction was not different with respect to the target vessel. All patients conserved contractility within the infarcted area and all had normal coronary flow (Thrombolysis In Myocardial Infarction trial grade 3) in the infarct-related vessel. The DCA procedure was performed after a period of clinical stabilization, ú5 days after an ischemic episode at rest and ¢8 days after myocardial infarction. Angiographic restenosis at six months: Figure 2 illustrates the immediate postprocedure and 6-month outcome of our population in terms of the degree of stenosis measured by quantitative angiography. Twenty-two patients (23%) had angiographic restenosis. During follow-up, none of them experienced a new myocardial infarction. Ten of these 22 patients were rehospitalized for recurrence of angina pectoris and underwent a new intervention for myocardial revascularization, either repeat balloon angioplasty (n Å 7) or coronary bypass surgery (n Å 3). Therefore, only 11% of the entire population underwent a target vessel revascularization in the territory concerned with atherectomy. No other clinical cardiac event was noted during the follow-up period. If one applies the commonly accepted criterion of ú50% stenosis in diameter at control, the restenosis rate in the right coronary artery group appeared higher than that of the left anterior descending group, but the small number of patients with restenosis limits the statistical power of this comparison. This
square analysis, or Fisher’s exact test when appropriate. Statistical analyses were performed with SAS software (SAS Institute, version 6.04, Cary, North Carolina). A p level of probability õ0.05 was retained as significant.
RESULTS Population characteristics: The population was divided into 2 subgroups according to the myocardial area to be revascularized, and therefore according to the targeted coronary vessel (i.e., right coronary or left anterior descending artery). Baseline clinical characteristics and angiographic data of the overall population and subgroup analysis are detailed in Table I. These characteristics were similar to those found in studies dealing with DCA1 – 6 and, in addition, they were similar in the 2 coronary territory subgroups. Most patients presented with unstable angina, and 46 (48%) had experienced a recent myocardial infarction in the vascular territory of the target vessel. This recruitment feature may be explained by an anatomic selection based on the morphologic characteristics of the lesions, foremost of which was intraluminal thrombus. Among the 46 patients with prior myocardial infarction, 41 had myocardial infarction õ2 months before the procedure. Among these patients, 56% were initially treated with a thrombolytic agent and coronary recanalization was angiographically documented õ6 hours after the onset of chest pain (average 3.1 { 2.3 hours). The disTABLE I Clinical and Angiographic Data of Study Population Variables Clinical data Age (yr) Male gender Hypercholesterolemia Systemic hypertension History of smoking Diabetes mellitus Family history of CAD Prior myocardial infarction Delay from myocardial infarction to DCA (d) Unstable angina 1-vessel disease Multivessel disease 7Fr atherectomy device Quantitative angiography Minimum lumen diameter (mm) Before procedure After procedure Control Reference diameter (mm) Before procedure After procedure Control % Diameter stenosis Before procedure After procedure Control Restenosis ú50%
Right Coronary Artery Group (n Å 32)
Left Anterior Descending Artery Group (n Å 63)
Total Population (n Å 95)
54 { 12 26 (81%) 25 (78%) 11 (34%) 23 (72%) 4 (12%) 14 (44%) 16 (50%) 36 { 56 22 (69%) 16 (50%) 16 (50%) 28 (87%)
56 { 12 53 (84%) 45 (71%) 31 (49%) 45 (71%) 13 (21%) 31 (49%) 30 (48%) 29 { 32 50 (79%) 39 (62%) 24 (38%) 52 (83%)
55 { 12 79 (83%) 70 (74%) 42 (44%) 68 (72%) 17 (18%) 45 (47%) 46 (48%) 31 { 41 71 (75%) 55 (58%) 40 (42%) 80 (84%)
1.29 { 0.50 3.14 { 0.50* 2.21 { 0.86‡
1.14 { 0.40 2.97 { 0.42* 2.15 { 0.72‡
1.19 { 0.44 3.03 { 0.45* 2.17 { 0.61‡
3.67 { 0.69 3.69 { 0.70 3.52 { 0.66†
3.53 { 0.63 3.49 { 0.53 3.44 { 0.58
3.58 { 0.65 3.56 { 0.60 3.47 { 0.61†
64.2 { 11.3 14.0 { 12.4* 37.1 { 20‡ 9 (28%)
67.3 { 8.45 14.8 { 9.5* 37.4 { 18.6‡ 13 (21%)
66.2 { 9.6 14.5 { 10.5* 37.3 { 18.9‡ 22 (23%)
*p õ0.001 before versus after procedure; †p õ0.02; ‡p õ0.001 control versus after procedure. Numeric values are expressed as mean { SD, categorical values are numbers and percentage of the total number in each group. CAD Å coronary artery disease; DCA Å directional coronary atherectomy.
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FIGURE 2. Cumulative percentage of patients as a function of percent diameter stenosis as estimated with quantitative coronary angiography. Pre DCA Å before directional coronary atherectomy; Post DCA after directional coronary atherectomy; Control Å control angiogram.
TABLE II Hemodynamic Data and Segmental Wall Motion in Patients Without Restenosis Before Atherectomy Right Coronary Artery (n Å 23) Ejection fraction (%) Fractional shortening (%) Segment 2 Segment 3 Segment 4 Segment 5 Segment 6 Segment 7 Segment 8 Segment 9 Segment 10 Heart rate (beats/min) LV pressure (mm Hg) End-diastolic Systolic Mean aortic pressure (mm Hg) LV volume index (ml/m2) End-diastolic End-systolic
Follow-Up Angiography
Left Anterior Descending Artery (n Å 50)
Total Population (n Å 73)
Right Coronary Artery (n Å 23)
Left Anterior Descending Artery (n Å 50)
Total Population (n Å 73)
67 { 11
59 { 15§
61 { 14
73 { 8‡
62 { 17*
65 { 15‡
23 41 45 39 37 49 53 56 47 70
29 41 38 26 19 28 32 35 35 70
27 41 41 30 25 35 39 42 39 70
26 48 51 43 42 58 62 61 51 71
25 43 42 30 27 39 44 46 39 68
25 44 45 34 32 45 50 50 43 69
{ 12 { 19 { 18 { 16 { 22 { 26 { 22 { 21 { 20 {9
{ 18 { 16 { 19 { 19\ { 19Ø { 27\ { 27Ø { 26\ { 21§ { 12
{ 16 { 17 { 19 { 19 { 22 { 28 { 28 { 26 { 21 { 11
13 { 7 126 { 21 93 { 14
17 { 8 129 { 24 94 { 16
16 { 8 128 { 23 94 { 16
89 { 24 30 { 12
103 { 38 45 { 31
99 { 35 40 { 27
{9 { 16* { 14 { 13 { 19 { 18* { 17† { 19 { 15 { 10
{ 11 { 17 { 19 { 18† { 22‡ { 27‡ { 28‡ { 28‡ { 23 { 13
{ 11 { 17 { 18* { 17‡ { 22‡ { 26‡ { 26‡ { 27‡ { 22 { 12
13 { 6 139 { 25* 95 { 14
16 { 8 141 { 29† 99 { 18
15 { 7 141 { 28‡ 98 { 17
86 { 34 27 { 20
106 { 41 45 { 39
99 { 40 39 { 34
*p õ0.05; †p õ0.01; ‡p õ0.001 before atherectomy versus at control in the same group; §p õ0.05; \p õ0.01; Øp õ0.001 right coronary artery group versus left anterior descending artery group. Values are expressed as mean { SD. LV Å left ventricular.
study confirms the importance of late loss when compared with the acute gain that was expressed by a significant enlargement of the coronary lumen after optimal atherectomy (on average 1.84 mm). More precisely, the loss index expressed as the late loss divided by the initial gain was 0.49 { 0.42. Evaluation of left ventricular function: The parameters of LV function were analyzed according to presence or absence of angiographic restenosis as previously defined. Main results are summarized in Tables II and III with respect to the vessel dilated and the restenosis process. Heart rate and mean aor548
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tic pressure did not change significantly between the 2 examinations. We observed only a mild to moderate elevation in LV systolic pressure in patients without restenosis at control (/12 { 23 mm Hg, p õ0.001). Globally, there was no significant variation in LV volumes, but ejection fraction increased in the group without restenosis (/4 { 9%, p õ0.005). In contrast, there was no significant variation in ejection fraction (03 { 9%, p Å NS) in patients with angiographic restenosis. Conversely, regional wall motion analysis demonstrated a highly significant improvement in segmental shortening, most of which was
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TABLE III Hemodynamic Data and Segmental Wall Motion in Patients With Restenosis Before Atherectomy
Ejection fraction (%) Fractional shortening (%) Segment 2 Segment 3 Segment 4 Segment 5 Segment 6 Segment 7 Segment 8 Segment 9 Segment 10 Heart rate (beats/min) LV pressure (mm Hg) End-diastolic Systolic Mean aortic pressure (mm Hg) LV volume index (ml/m2) End-diastolic End-systolic
Follow-Up Angiography
Right Coronary Artery (n Å 9)
Left Anterior Descending Artery (n Å 13)
Total Population (n Å 22)
Right Coronary Artery (n Å 9)
Left Anterior Descending Artery (n Å 13)
68 { 8
66 { 9
67 { 8
68 { 7
62 { 8
65 { 8
21 42 41 31 38 53 57 58 50 61
34 43 47 33 24 32 38 43 43 63
29 43 45 33 30 40 46 49 46 62
23 43 44 36 33 50 58 59 39 63
37 47 41 26 17 27 33 33 33 67
31 45 43 30 23 36 43 44 36 65
{9 { 21 { 20 { 16 { 18 { 20 { 17 { 16 { 17 {7
{ 22 { 20 { 21 { 24 { 26 { 32 { 29 { 28 { 20 { 10
{ 18 { 20 { 21 { 21 { 24 { 30 { 27 { 24 { 19 {9
{4 { 15 { 15 { 17 { 17 { 14 { 14 { 15 {8 {9
{ 22 { 22 { 22 { 21 { 17 { 21 { 21 { 18 { 10 {8
15 { 6 122 { 13 91 { 8
15 { 8 124 { 25 97 { 20
15 { 7 123 { 21 95 { 16
14 { 4 131 { 17 98 { 11
13 { 8 134 { 25 100 { 21
87 { 21 28 { 11
91 { 16 32 { 10
90 { 18 30 { 10
88 { 18 28 { 11
84 { 21 31 { 7
Total Population (n Å 22)
{ 18 { 19 { 20 { 20 { 18 { 22 { 22 { 21 { 9* {9
13 { 6 133 { 22* 99 { 18 85 { 19 30 { 9
*p õ0.05 before atherectomy versus at control in the same group. Values are expressed as mean { SD. LV Å left ventricular.
FIGURE 3. Segmental wall motion of the left ventricle in patients with left anterior descending lesion and without restenosis at control angiogram. Left ventricular segments (Seg) are plotted on the X-axis and fractional shortening on the Y-axis. Normal range values are indicated as mean { 2 SD. Note the absence of significant variation in percent shortening of basal segments. Abbreviations as in Figure 2.
accounted for by anterior zones (/10% and /11% for segments 7 and 8, respectively, p õ0.001). At baseline examination, regional shortening was significantly abnormal, corresponding to a net hypokinesia due to myocardial stunning in patients with unstable angina, or to depressed contractility linked to underlying necrosis (Figures 3 and 4). This feature was far more pronounced in anterior than in inferior segments. In the restenosis group, 9 patients (41%) had prior myocardial infarction, and 5 patients had inferior and 4 anterior infarction. The vascular distribution was not statistically different when compared with that of the 37 patients (51%) with prior
infarction in the group without restenosis: 11 patients had inferior and 26 anterior infarctions. Improvement in segmental wall motion was not influenced by previous infarction in the vascular territory concerned with atherectomy. Indeed, multivariate analysis of variance for repeated measurements did not show significant interaction between previous myocardial infarction and percent fractional shortening (for segment 7, F Å 2.02, p Å 0.15). In the absence of restenosis, the time course of the regional wall motion in patients with myocardial infarction did not exhibit differences when compared with that of the other patients. However, subgroup analysis demon-
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FIGURE 4. Segmental wall motion of the left ventricle in patients with left anterior descending lesion and restenosis at control angiogram. The left ventricular wall was considered to be hypokinetic if percent shortening of ¢2 contiguous segments (Seg) were õ2 SD values from the mean value. Abbreviations as in Figure 2.
erectomy Restenosis Study (3.15 mm).6 We must emphasize that most of the vessels treated in our experience were larger than those in previous reported studies. This may have favored a lower restenosis rate.17,18 Another explanation might involve the thrombotic material that is very frequently deposited on freshly ruptured plaques.19 Indeed, the residual thrombus that is left after angioplasty is considered as a strong predictive parameter of restenosis.20 By removing a large amount of atherosclerotic material, we may have reduced thrombus incorporated in the vascular scar and limited intimal proliferation. Finally, the population size was rather small compared with size in other controlled studies6,21 and the selected angiograms may have created systematic bias in our results.
strated that patients with myocardial infarction had less pronounced improvement in percent fractional shortening (/5 { 12% for segment 7, p õ0.05), reflecting a persistent significant depression in LV contractility. Similarly, segmental motion improvement in inferior and basal regions at control was smaller in LV segments with previous myocardial infarction. Again, improvement in regional contractility was observed in the absence of restenosis only, and was far more pronounced in anterior than inferior zones. For the entire group with left anterior descending artery lesions, we found a weak, although significant, negative correlation between percent diameter stenosis at control, and the variation in the percentage of segment shortening in the anterior wall (r Å 00.28, p õ0.03; r Å 00.26, p õ0.01; r Å 00.26, p õ0.02 for zones 7, 8, and 9, respectively).
Improvement in left ventricular regional wall motion:
When myocardial perfusion is chronically altered, revascularization of dysfunctional areas has demonstrated its usefulness in preserving LV contractile function.10 – 12 Improvements in regional wall motion and global ejection fraction of the left ventricle after coronary bypass surgery are well recognized.22,23 These clinical observations can be explained by the concept of ‘‘hibernating myocardium,’’ which could be due in part to chronic myocardial ischemia but also to repeated episodes of acute ischemia that culminate in stunning of cardiac muscle.24,25 After coronary angioplasty, and particularly in the setting of unstable angina, improvements in LV wall contractility have been conclusively documented.11,14,25 – 27 Accordingly, we found in this prospective study a significant variation in LV wall motion that was detected from analysis of end-diastolic and end-systolic ventricular contours. A more thorough study using a frame-by-frame approach on the overall cardiac cycle may have strengthened our conclusions. In previous studies, we followed midterm evolution in patients treated with balloon angioplasty for left anterior descending artery lesions and we found ben-
DISCUSSION After results of the large controlled trials,4,5 the interest in DCA has been questioned.3 Nevertheless, the advantage of optimal atherectomy was clearly indicated in retrospective studies that used the matching approach.16 All strategies that have aimed at an optimal increase in the vascular lumen have limited the incidence of restenosis even though late decrease in vessel lumen appears to be more pronounced using DCA.3,9,17 Our data on restenosis seems to be somewhat surprising since the population included a large proportion of patients with unstable angina. However, our optimizing technique added complementary balloon angioplasty to a great number of cuts (on the average 20 to 30 per lesion) whose efficacy was demonstrated by the substantial amount of atheroma fragments generally collected. By using large devices and postdilation for most arteries, even for those as small as 3.0 mm in diameter, we obtained, on average after the procedure, a minimum lumen diameter ú3.0 mm. These results are almost identical to those found in the Optimal Ath550
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eficial effects on asynergy of the anterior wall and on asynchrony of the anterior segments during the contraction phase. Other parameters reflecting regional dysfunction, such as shortening of contraction duration, were also significantly improved in the absence of angiographic restenosis.12 In the present study, wall motion in the myocardial zone revascularized with atherectomy improved in a significant manner, whereas parameters of LV loading did not significantly change from baseline values. In fact, we observed a tendency toward an increase in LV systolic and mean aortic pressures. The improvement was more marked for anterior segments, and less pronounced for inferior and basal segments of the left ventricle. As reported in studies dealing with coronary balloon angioplasty, angiographically visible restenosis limits recovery of regional contractility.28 The binary distinction of restenosis may appear arbitrary since recent studies in humans have found that attenuation of the coronary blood flow reserve exists for stenosis as low as 40%.7,8 Indeed, we found a significant correlation between the degree of stenosis and 6-month variations in percent fractional shortening for all 95 patients. By contrast, even though there is a correlation between percent diameter stenosis and the consecutive decrease in coronary perfusion reserve, the predictive value of the angiographic severity of a given lesion remains uncertain.8 Accordingly, we cannot draw individual conclusions on the outcome of myocardial perfusion from our study. LV dysfunction may recover spontaneously after repeated episodes of ischemia or after the acute phase of myocardial infarction. Some investigators found no significant variations when ventricular volumes and segmental motion were measured after the 10th day of infarction, but others have clearly shown that recovery of LV function was possible after a delay of 5 weeks.29 Although we obtained no data concerning myocardial viability and cardiac metabolism, improvement in segmental wall motion favors the persistence of a heterogeneous population of myocytes having different degrees of functional alterations.23 Unfortunately, clinical follow-up only was available for patients who developed myocardial infarction after DCA; thus, our data cannot be extended to procedures associated with creatine kinase elevation more than twofold normal.30 Study limitations: Patients were prospectively selected on the basis of angiographic criteria, and the group with previous myocardial infarction may have had a reduction in the magnitude of variation in LV contractility since improvement in regional wall motion was significant but obviously smaller in this subset. However, the distribution of patients with myocardial infarction was not different according to the coronary territory treated or the incidence of restenosis. Pathophysiologic consequences of coronary blood flow changes on LV function are strongly influenced by the dominance of the right coronary system, and complementary analysis performed using another radiologic projection may have reinforced
data demonstrating the benefit of revascularization apparent in this study that focused on the left coronary system. Acknowledgment: We gratefully acknowledge the technical assistance of Dominique Fernandez and Francoise Noailles for preparing the manuscript, and Gerard Gouverneur for his help with the statistical analysis.
1. Hinohara T, Robertson GC, Selmon MR, Vetter JW, Rowe MH, Braden LJ,
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