Aggressive clinical pattern of angina at restenosis following coronary angioplasty in unstable angina

Warner et al. November 1992

American Heart Journal

Triple vessel angioplasty: acute outcome and long-term results. J Am Co11 Cardiol 1988;12:42-8.

8. O’Keefe JH, Rutherford BD, McConolroy DR, Johnson WL, Georgi LV, Ligon RW, Shimshak TM, Hartzler GO. Multi- vessel coronary angioplasty from 1980 to 1989: procedural results and long-term outcome. J Am Co11 Cardiol1990;16:1097- 1102.

9. Cowley MJ, Vetrovec GW, Wolfgang TC. Efficacy of percutaneous transluminal coronary angioplasty: technique, patient selection, salutatory results, limitations, and complications. AM HEART J 1981;101:272-80.

10. DiSciascio G, Cowley MJ, Goudreau E, Vetrovec GW, Kelly K. Staged approach to multivessel coronary angioplasty; strate- gic consideration and results. J Intervent Cardiol 1988;1:175- 80.

11. Nath A, DiSciascio G, Kelly KM, Vetrovec GW, Testerman C, Goudreau E, Cowley MJ. Multivessel coronary angioplasty early after acute myocardial infarction. J Am Co11 Cardiol 1990;16:545-50.

12. Cowley MJ, Dorros G, Kelsey SF, Van Raden M, Detre K. Acute coronary events associated with percutaneous transluminal coronary angioplasty. Am J Cardiol 1984;53:12C-6C.

13. Cutler SJ, Ederer F. Maximum utilization of life table method in analyzing survival. J Chronic Dis 1958;8:699-712.

14. Vandormael MG, Deligonul U, Kern MJ, Kennedy H, Galan K, Chaitman B. Restenosis after multilesion percutaneous transluminal coronary angioplasty. Am J Cardiol1987;60:44B- 7B.

15. Finci L, Meier B, DeBruyne B, Steffenino G, Divernois J. Rutishauser W. Angiographic follow-up after multivessel percutaneous transluminal coronary angioplasty. Am J Cardiol 1987;60:467-70.

16. Mata LA, Bosch X, David PR, Rapold HJ, Corcos T, Bourassa MG. Clinical and angiographic assessment 6 months after double vessel percutaneous coronary angioplasty. J Am Co11 Cardiol 1985;6:1239-1344.

17. Vandormael MG, Diligonul U, Kern MJ, Harper M, Presant S, Gibson P, Galan K, Chaitman BR. Multilesion coronary angioplasty: clinical and angiographic follow-up. J Am Co11 Cardiol 1987;10:246-52.

18. Myler RK, Top01 EJ, Shaw RE, et al. Multiple vessel coronary angioplasty: classification, results, and patterns of restenosis in 494 consecutive patients. Cathet Cardiovasc Diagn 1987;13:1-15.

19. Deligonul U, Vandormael MG, Kern MJ, Zelman R, Galan K, Chaitman BR. Coronary angioplasty: a therapeutic option for symptomatic patients with two and three vessel coronary disease. J Am Co11 Cardiol 1988;11:1173-9.

20. Ellis SG, Cowley MJ, DiSciascio G, Deligonul U, Top01 EJ. Bulle TM, Vandormael MG, and the Multivessel Angioplasty Prognosis Study Group. Determinants of 2-year outcome after coronary angioplasty in patients with multivessel disease on the basis of comprehensive preprocedural evolution in complications for patient selection. Circulation 1991;83:1905- 14.

Aggressive clinical pattern of angina at restenosis following coronary angioplasty in unstable angina

The frequency, clinical pattern, and timing of recurrent angina following successful single-lesion percutaneous transluminal coronary angioplasty (PTCA) was assessed in a consecutive group of 104 patients with stable angina and in 85 with unstable angina. In addition, the relationship between lesion morphology and angiographic features and the pattern of recurrent angina was determined. Restenosis, defined as recurrence of symptoms with >50% stenosis at the site of PTCA, occurred in 25 (24%) of the stable group and in 23 (27%) of the unstable group (p = NS). The pattern of angina at repeat presentation was aggressive in nature in 8% of the stable group and in 48% of the unstable group @ = 0.002). The time interval between the recurrence of symptoms and repeat coronary angiogram or PTCA was longer in the nonaggressive group than in the aggressive group, 16 + 12.1 and 5 f 6.8 weeks, respectively (p < 0.003). The key factors predicting the recurrent angina pattern identified by multiple logistic regression analysis were the angina status pre-PTCA (p = 0.001) and the presence of double-vessel disease (p = 0.01). An aggressive pattern of angina at the time of restenosis is frequent in patients with unstable angina at the time of PTCA, and close post-PTCA surveillance is necessary in these patients. (AM HEART J 1992;124:1174.)

J. Brendan Foley, MD, MRCP (UK), Robert J. Chisholm, MD, Andrew A. Common, MD, CM,” Anatoly Langer, MD, and Paul W. Armstrong, MD Toronto, Ontario, Canada

From the Division of Cardiology, Department of Medicine, and “the Reprint requests: Paul W. Armstrong, MD, Division of Cardiology. St. Department of Radiology, St. Michael’s Hospital, University of Toronto. Michael’s Hospital, 30 Bond St., Toronto, Ontario, Canada M5B lW8. Received for publication April 6, 1993; accepted May 20, 1992. 4llf40539

1174

Volume 124

Number 5 Aggressive angina of post PTCA restenosis 1175

Unstable angina and myocardial infarction are clinical syndromes that result from a complex interaction between atherosclerotic plaque rupture, mural thrombus formation, platelet activation, and vaso- constriction.1-5 Percutaneous transluminal coronary angioplasty (PTCA) has been performed in unstable angina with a primary success rate of between 84% and 90 5% , which is comparable to that in stable angina. 6-g Major procedure-related complications, however, such as myocardial infarction, the need for emergency coronary artery bypass surgery, or death occur in 10 I’0 to 12 71 of procedures, a frequency ap- proaching twice that encountered in stable angina.63 7~ 10, l1 There is conflicting evidence as to whether restenosis in unstable angina is more frequent than in stable angina, and restenosis rates in unstable angina have been reported to be between 25% and 385 .l’-15 Little information exists concerning the clinical profile at the time of restenosis of patients who have undergone PTCA in stable and unstable angina.

The aim of this study was to determine whether there were differences in the frequency, timing, or clinical pattern of angina at the time of restenosis in patients in whom PTCA was performed in the setting of stable versus unstable angina. In addition, the relationship between the clinical pattern of the recurrent angina and the angiographic features and morphology of the lesion dilated was determined.

METHODS Patient population. During the B-month period be-

tween January 1988 and June 1989,447 PTCA procedures were performed at St. Michael’s Hospital. The study group consisted of patients who had undergone their first successful single-lesion PTCA of a native vessel, other than the left main stem, over this time period. Successful PTCA was defined as ~20% reduction in the percentage diameter stenosis, with a final residual stenosis <50%, without major in-hospital complications. One hundred eighty-nine consecutive patients were eligible for the study, of whom 104 had stable angina and 85 had unstable angina. The other patients were not eligible for the following reasons: 147 had multilesion, multivessel, or bypass graft PTCA performed; 56 underwent PTCA of a restenotic lesion; and one had the left main stem dilated. PTCA was unsuccess- ful in 54 patients; this was because of the inability to cross the lesion with the guide wire in 41 patients (19 of whom had total occlusions), failure to cross with the balloon in two patients, inadequate dilatation in three patients, the need for emergency bypass surgery in six, myocardial infarction in one patient, and death in one patient. The stable group was drawn from the elective PTCA list. The unstable group consisted of patients who during a hospital admission had PTCA performed because of a crescendo pattern of angina that included an episode of rest pain, or because of an episode of angina at rest greater than 20

minutes in duration in the absence of myocardial infarction, or those who had persistent postinfarct unstable angina. Thirty-seven (44 % ) of the unstable angina group had persistent postinfarct unstable angina, 18 had received systemic thrombolytic therapy, and 27 had sustained a non-Q wave infarct.

PTCA was performed by one of two primary operators and followed standard techniques. Patients received aspirin and a calcium antagonist before PTCA. Aspirin was continued throughout the period of follow-up, and calcium antagonists were continued for between 3 to 6 months. All other antianginal medication was left to the discretion of the attending cardiologist.

All of the patients were systematically followed at our institution and were reviewed in the clinic at 3 and 6 months following the PTCA, or more frequently if clini- cally indicated. Coronary angiography was performed in patients with recurrent angina. Restenosis was defined as >50 ‘; stenosis at the site of a previously successful PTCA. Repeat coronary angiography was planned with a view to proceeding to PTCA if a suitable lesion was identified. In those patients in whom restenosis occurred, the time intervals between the initial PTCA and the recurrence of symptoms, and between the recurrence of symptoms and repeat angiography/PTCA were quantitated.

The pattern of the angina at the time of the repeat presentation was divided into two categories: (1) aggressive, that is, a rapidly accelerating pattern of angina that resulted in emergency admission of the patient to the hospital for stabilization or (2) nonaggressive, that is, angina of gradual onset that resulted in elective hospital admission for evaluation.

Coronary angiography. The coronary angiograms from immediately before and following PTCA and at the time of follow-up angiography were assessed by two experienced observers blinded to the angina status of the patients. Dif- ferences were reconciled by consensus. The percentage diameter stenosis was graded visually in the view that demonstrated its maximum severity. The site of the stenosis was considered proximal if it was before the first diagnonal branch or first septal perforator in the left anterior descending coronary artery, before the first obtuse marginal branch in the circumflex artery, and before the acute marginal branch in the right coronary artery. Complex lesion morphology was defined as a stenosis with irregularity, overhang, or both.16 Coronary artery thrombus was defined as one or more of the following: (1) a filling defect sur- rounded by contrast medium at the site of a high-grade stenosis; (2) luminal staining at the site of a high-grade stenosis or total occlusion; or (3) upward convexity or irregularity without vessel tapering at the site of an abrupt occlusion.* Intimal dissection following the PTCA was classified as one of the following: (1) a linear filling defect, (2) an extraluminal opacity, or (3) a spiral dissection.*’ Multivessel disease was defined as narrowing of ~50”; in at least two major epicardial arteries, determined from the diagnostic pre-PTCA angiogram. Progression of disease in the culprit vessel and nondilated vessels was assessed in the pre-PTCA and late follow-up angiograms. Simultaneous projection of two angiograms was performed with the de-

1176 Foley et al. November 1992


Table I. Population data

Stable angina Unstable angina (n = 104) (n = 85) p Value

Male Age W Vessel dilated

LAD RCA cx

Multivessel disease 2-vessel 3-vessel

Total occlusion Stenosis pre-PTCA Stenosis post-PTCA Proximal stenosis Clinical restenosis

73 (70%) 56 i 10

70 (68%) 17 (166) 17 (16%)

40 (38’) 20 (19°C)

4 (4 % ) 83.6 f 10.6% 26.4 + 13.8%

48 (44 % ) 25 (24:~)

57 (67%‘) 57 + 12

49 (58%) 21 (25%) 15 (18%)

23 (27%) 24 (28%)

8 (9%) 86.4 + 9.3 % 28 + 12.9%

47 (55%) 23 (27%)

NS NS

NS NS NS

NS NS NS NS NS NS NS

Cr, Circumflex coronary artery; LAD, left anterior descending artery; NS, not statistically significant (p < 0.05): RCA, right coronary artery; PTCA, percutaneous transluminal coronary angioplasty.

Table II. Angiographic feature of the restenosis patients

Nonaggressive Aggressive group * group *

(n = 35) (n = 13)

Stenosis pre-PTCA 82.3 ziz 11% 84.3 i 12.2% Stenosis post-PTCA 26.9 + 11.9% 18.6 +- 10.6%’ Stenosis follow-up 83.5 k 14.3% 83.8 + 14.3? Vessel dilated

LAD 24 (69%) 11 (86%) RCA 6 (17%) 1(7%) cx 5 (14%) 1(7%)

No oi major epicardial vessels diseased

1 vessel 16 (45 % ) 3 (2396) 2 vessels 10 (29%) 7 (54%) 3 vessels 9 (26%) 3 (23%)

Proximal stenosis 16 (46%) 9 (69% )

P Value

NS 0.03 NS

NS NS NS

NS 0.10 NS

0.04

Abbreviations and level of significance as in Table I. *See text for explanation.

gree of stenosis graded on a scale of: <25%, 25%, 50X, 75%, 95573, and 100% .18 Any increase in stenosis from <50% to 50% or more, or a change of one or more grades in stenosis ~50% between pre-PTCA and follow-up was considered progression of disease. In 25 % of those with an aggressive pattern of angina at restenosis and in 26% of those with a nonaggressive pattern of angina at restenosis, the contralateral vessel was not injected at the time of repeat angiography, so that it was not possible to assess progression of disease in the noninjected vessel. For technical reasons the angiogram was not interpretable in one patient from the unstable group at the time of late follow-up angiography.

Statistical analysis. Parametric data were compared using unpaired two-tailed t tests. Discrete group parameters were compared using the chi square test or Fisher’s

exact test where appropriate. In those in whom restenosis occurred, the angina status pre-PTCA and the angiographic features before and following PTCA were entered into a stepwise logistic regression model with the pattern of angina at repeat presentation as the dependent variable. All data are presented as mean f SD. A value of p I 0.05 was considered statistically significant. Statistical analysis was performed using the Statistical Analysis System (SAS Institute, Cary, N.C.).

RESULTS

The stable and unstable angina groups were similar with respect to age, sex, vessel dilated, and the percentage of stenosis before and following PTCA (Table I). There was no significant difference in the clinical restenosis rate between the stable and unstable groups-25 of 104 (24%) and 23 of 85 (27 %), respectively.

In the unstable group, 11 of 23 (48%) presented with an aggressive pattern of angina at the time of restenosis. In four of these patients the first manifes- tation of restenosis was prolonged ischemic chest pain that resulted in admission to the coronary care unit. In the other seven patients there was an accelerated pattern of angina, which in four culminated in a prolonged period of angina at rest that again resulted in admission to the coronary care unit. This is in marked contrast to the stable angina group, where only 2 of 25 (8%) had an aggressive pattern of angina at the time of restenosis (p = 0.002); one of these patients presented with prolonged rest pain and the other with an accelerated pattern of angina. None of the patients with an aggressive pattern of angina at repeat presentation suffered a myocardial infarct.

There was no difference in the time interval

Volume 124


Fig. 1. A, Lesion morphology in stable and unstable patients pre PTCA. B, Lesion morphology in stable and unstable patients immediately post PTCA.

between the initial PTCA and recurrent symptoms in aggressive group and 16.0 & 12.1 weeks in the non- those with aggressive and nonaggressive patterns of aggressive group (p < 0.003). Similarly, the interval angina, 8.5 + 6.3 and 7.6 f 6.5 weeks, respectively. between the index PTCA and repeat coronary an- The aggressive nature of the angina at restenosis, giography/PTCA was shorter in the aggressive group however, resulted in a significantly shorter interval than in the nonaggressive group, 13.7 -t 6.6 weeks between the recurrence of angina and repeat coro- and 23 i 12.5 weeks, respectively (p = 0.014). nary angiography/PTCA-5.0 + 6.8 weeks in the There was a trend toward a greater frequency of



8%

Fig. 2. A, Lesion morphology pre PTCA in patients returning with aggressive and nonaggressive patterns of angina at restenosis. 8, Lesion morphology pre PTCA in patients with aggressive and nonaggressive patterns of angina at the time of follow-up angiography.

double-vessel disease in those with an aggressive The residual stenosis immediately post PTCA, how- pattern of angina at restenosis: 7 of 13 (54%) com- ever, was significantly less in those with an aggressive pared with 10 of 35 (29%) (p = 0.1) of those with a pattern of angina at repeat presentation, 18.6 f nonaggressive pattern (Table II). The mean diame- 10.6”; compared with 26.9 k 11.9% in the nonag- ter stenosis of the lesion dilated before PTCA was gressive group (p = 0.03). The mean stenosis at the similar in both groups, 82.3 t 11% in the nonaggres- time of follow-up angiography was similar in both sive group and 84.3 k 12.270 in the aggressive group. groups: 83.5 + 14.3Y in the aggressive group and

Volume 124


83.8 + 14.3% in the nonaggressive group. There was a greater frequency of proximal lesion location in the aggressive group than in the nonaggressive group-9 of 13 (69 SC ) aggressive patients versus 16 of 35 (46 96 ) in the nonaggressive group (p = 0.04). There was no significant difference between the two groups in the frequency of progression of disease between pre- PTCA and follow-up angiograms, which occurred in 1OS; of the dilated vessels in both the aggressive and nonaggressive groups and in 13% of the nondilated vessels assessed in the aggressive group and in 2 % in the nonaggressive group (p = 0.15).

Lesion morphology. Analysis of the lesion morphology before PTCA demonstrated a significant difference in the frequency of intracoronary thrombus before PTCA in the unstable group, 17 of 82 (21%), compared with 10 of 104 (8%) in the stable group (p = 0.033) (Fig. 1, A). The post-PTCA and follow-up angiograms did not reveal any significant differences between the two groups with respect to lesion morphology.

When the groups were examined according to the nature of the angina at repeat presentation, pre PTCA there was a somewhat greater frequency of thrombus in patients who had an aggressive pattern of angina at repeat presentation-4 of 13 (31%) compared with 4 of 35 (1106) in the nonaggressive group (p = 0.2) (Fig. 2, A). Analysis of the late follow-up angiograms did not reveal any significant differences in the lesion morphology between the aggressive and nonaggressive groups (Fig. 2, B).

The angina status pre PTCA, along with the following angiographic parameters, were entered into a stepwise multiple logistic regression analysis model: the vessel dilated, the stenosis pre and post PTCA, the proximity of the stenosis dilated, the number of epicardial vessels diseased, and the morphology before and after PTCA. Stepwise multiple logistic regression analysis identified the angina status pre PTCA as the most potent predictor of the pattern of angina at. the time of clinical restenosis (F = 11.53, p = 0.001). Other variables identified were the presence of double-vessel disease (F = 6.81,~ = O.Ol), the stenosis post PTCA (F = 4.8, p = 0.03), and proximal lesion location (F = 3.99, p = 0.05).

DISCUSSION

The principal novel feature of this study is that restenosis following PTCA in unstable angina is associated with a greater frequency of an aggressive pat,tern of angina than in stable angina. It is inter- esting to consider the environmental factors associated with PTCA in unstable angina that might con- tribute to a different pattern of angina at repeat pre-

sentation. The mode of action of PTCA and the pathologic process of unstable angina have certain similarities. PTCA results in splitting of the atherosclerotic plaque, which is associated with platelet adhesion and release of platelet-derived vasoactive and mitogenic factors, which may be keys in the pathogenesis of restenosis.1g-22 Unstable angina is a dynamic process that results from plaque disruption, with platelet adhesion and the release of platelet-derived chemotactic and vasoactive substances.la 3* 4 The adhesion of platelets promotes the formation of thrombus as a result of an imbalance between the complex prothrombotic and endogenous fibrinolytic systems. 23, 24 The performance of PTCA in unstable angina may perpetuate or even accent the pathologic process of unstable angina, thereby promoting a different clinical presentation at the time of restenosis from that observed in stable angina.

The time interval between the index PTCA and the recurrence of symptoms was similar in those with nonaggressive and aggressive patterns of angina at the time of repeat presentation. The aggressive nature of the recurrent angina, however, was re- flected in acute hospitalization and a shorter time interval between the recurrence of angina and repeat cardiac catheterization/PTCA. These time intervals are relevant in the Canadian Health System, as the urgency with which cardiac catheterization and PTCA are performed is dictated by the clinical status of the patient.

There is a lack of comparable data in the literature. In an uncontrolled study of 35 patients with refractory unstable angina, Sharma et aLz5 reported that only 6 TU of the patients returned with refractory unstable angina at the time of restenosis. The reasons for the differences in the results of their study and ours are unclear, but may be related to different def- initions and to sample size limitations in their study.zs

Certain features of our study deserve further discussion. The present study was aimed at evaluating the pattern of angina at the time of repeat presentation. As the frequency of restenosis was not the primary end point, angiographic follow-up was only performed in those with recurrent symptoms, mak- ing it likely that the true frequency of restenosis was underestimated in both groups.13) 26 Although the percent diameter stenosis and lesion morphology were assessed visually and retrospectively, they were performed by experienced observers who were blinded to the angina status of the patients and differences were reconciled by consensus. It is therefore unlikely that any systematic bias in the interpreta- tion of the angiograms occurred. Of interest is the fact that the residual stenosis immediately post PTCA


American Hearl Journal

was less in those with an aggressive pattern of angina at repeat presentation, thus excluding underdilata- tion as the potential cause for the aggressive nature of angina at repeat presentation. The pattern of angina recurrence could have been influenced by patient or physician factors arising from the pattern of angina at the time of the index PTCA. This is unlikely, however, as the patients with aggressive angina at repeat presentation were assessed by doc- tors who were not involved in the index PTCA, and who assessed the patients on the basis of their repeat clinical presentation.

The findings of this study have a direct impact on patient management. Patients who have had PTCA performed in the setting of unstable angina should have close surveillance following hospital discharge, and should be advised to seek prompt medical atten- tion should they have a recurrence of symptoms. We conclude that an aggressive pattern of angina at the time of repeat presentation is frequent following PTCA in unstable angina, and dictates a closer post- PTCA surveillance of these patients.

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Aggressive clinical pattern of angina at restenosis following coronary angioplasty in unstable angina