doi: 10.1161/hc4401.098294
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(Circulation. 2001;104:2289.)
© 2001 American Heart Association, Inc.
Clinical Investigations and Reports |
Clinical and Angiographic Factors Associated With Asymptomatic Restenosis After Percutaneous Coronary Intervention
From Cardialysis, Westblaak 92, 3012 KM Rotterdam, Netherlands.
Correspondence to Peter Ruygrok, Cardiology Department, Green Lane Hospital, Private Bag 92-189, Green Lane West, Auckland, New Zealand. E-mail pruygrok{at}ahsl.co.nz
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Abstract |
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Background— Angiographic restenosis after percutaneous coronary interventional procedures is more common than recurrent angina. Clinical and angiographic factors associated with asymptomatic versus symptomatic restenosis after percutaneous coronary intervention were compared.
Methods and Results— All patients with angiographic restenosis from the BENESTENT I, BENESTENT II pilot, BENESTENT II, MUSIC, WEST 1, DUET, FINESS 2, FLARE, SOPHOS, and ROSE studies were analyzed. Multivariate analysis evaluated 46 clinical and angiographic variables, comparing those with and without angina. The 10 studies recruited 2690 patients who underwent percutaneous revascularization and 6-month follow-up angiography (86% of those eligible). Restenosis (
50% diameter stenosis) occurred in 607 patients and was clinically silent in 335 (55%). Male sex (P=0.008), absence of antianginal therapy with nitrates (P=0.0002) and calcium channel blockers (P=0.02) at 6 months, greater reference diameter after the procedure (P=0.04), greater reference diameter at follow-up (P=0.004), and lesser lesion severity (percent stenosis) at 6 months (P=0.0004) were univariate predictors of asymptomatic restenosis. By multivariate analysis, only male sex (P=0.04), greater reference diameter at follow-up (P=0.002), and lesser lesion severity at 6 months (P=0.0001) were associated with restenosis without angina.
Conclusions— Approximately half of patients with angiographic restenosis have no symptoms. The only multivariate predictors of silent restenosis at 6 months were male sex, greater reference diameter at follow-up, and lesser lesion severity on follow-up angiography.
Key Words: angioplasty • restenosis • stents
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Introduction |
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Restenosis remains the major shortcoming after percutaneous intervention, with reported rates, in recent times, varying between 10% and 40%. A combination of patient factors, such as diabetes, lesion variables including length and vessel size, and type of revascularization device, all influence the likelihood of restenosis.1–4 With the evolution of core laboratories, such as Cardialysis in Rotterdam, large databases of clinical and angiographic data provide a unique opportunity to identify factors that may influence the restenotic process.
One consistent observation of studies evaluating patient outcome after percutaneous coronary interventional procedures is the disparity between the incidence of restenosis in those patients undergoing systematic angiographic follow-up 6 months after the interventional procedure and the rate of repeat target lesion revascularization in those with clinical follow-up and symptom-driven repeat angiography.5,6 The clinically driven repeat revascularization rate is often 
50% the angiographic restenosis rate, and routine angiography 6 months after the intervention clearly influences the likelihood of reintervention.7
There is little information on the differences in patient or lesion characteristics between patients who develop restenosis with recurrent symptoms and those in whom restenosis is clinically silent. This study evaluates patients from 10 interventional coronary angioplasty or stent trials, each enrolling between 102 and 1054 patients, with planned 6-month follow-up angiography. Multivariate analysis was used to assess clinical or angiographic factors that might be associated with asymptomatic as opposed to symptomatic restenosis.
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Methods |
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Patient Population
Patients enrolled in 10 percutaneous coronary interventional studies5,6,8–15 undertaken over a period of 9 years who underwent planned 6-month angiographic follow-up were considered for analysis. Of these studies, 2 were randomized trials of stent deployment versus balloon angioplasty (BENESTENT I, BENESTENT II), 6 were registries of newer stent designs (BENESTENT II pilot, DUET, FINESS 2, ROSE, SOPHOS, WEST I), 1 assessed the efficacy of intravascular ultrasound–guided stent implantation (MUSIC), and another studied the effect of a cholesterol-lowering agent on restenosis rates in patients undergoing balloon angioplasty (FLARE) (for abbreviations and acronyms see Table 1). The 10 studies are summarized in Table 2. Baseline characteristics of patients enrolled in these studies are shown in Table 3. All clinical information was monitored and forwarded to the core laboratory (Cardialysis, Rotterdam) and entered into the study databases. Studies were approved by institutional ethics committees, and written informed consent was obtained from all patients.
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All patients who underwent 6-month angiographic follow-up and had complete clinical and angiographic data were analyzed. In the Benestent II and SOPHOS studies, only those assigned to angiographic follow-up were enrolled. Of interest were those who had no symptoms of angina at 6-month clinical follow-up and angiographic restenosis, defined as a 50% diameter stenosis at the treated site. Forty-six clinical and angiographic factors were entered into a univariate and multivariate analysis to establish whether any were predictive of asymptomatic or silent restenosis (Table 4).
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Angiographic Analysis
All procedural and follow-up angiograms were sent to the core laboratory (Cardialysis) and analyzed by the Cardiovascular Angiography Analysis System, which was validated previously.16,17 For each patient, several matched angiographic views were obtained after intracoronary administration of nitrates. Patients with an unsuccessful procedure or without angiographic follow-up were excluded from the analysis. For patients who had undergone multilesion coronary angioplasty, the most severe restenotic lesion at follow-up was entered into the analysis. The minimal luminal diameter (MLD) and reference diameter obtained by an interpolated method were determined on an end-diastolic frame.
Statistical Analysis
Statistical analysis was performed with the SAS version 6.12 software package (SAS Institute). Continuous variables were compared by Student’s t test and the categorical variables by the Fisher’s exact test. We performed a logistic regression on the dependent variable Y, where Y=1 for patients with asymptomatic restenosis and Y=0 for patients with symptomatic restenosis. As explanatory variables. We considered 46 clinical and angiographic variables. We executed a univariate logistic regression defined by the formula log[P(Y=1)/P(Y=0)]=A+BxX, where X is the explanatory variable, A the intercept, and B the regression parameter. Multivariate logistic regression defined by the formula log[P(Y=1)/P(Y=0)]=A+B(1)xX(1)+B(2)xX(2)+...+B(n)xX(n), with X(1),...,X(n) as the explanatory variables, A the intercept, and B(1),...,B(n) the regression parameters, was then performed. With the stepwise procedure, a group of explanatory variables was selected that as a group were multivariately significant. Logistic regression analysis was also performed for the patients treated with an intracoronary stent. A value of P
0.05 was considered significant.
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Results |
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In the 10 studies, 4013 lesions were treated in 3774 patients. In 2 studies (BENESTENT II and SOPHOS), patients were allocated to 6-month clinical and angiographic follow-up or clinical follow-up alone; thus,
50% of the patients from these studies were not included in our analysis. Nineteen percent of patients declined follow-up angiography, leaving 2690 patients with complete clinical and 6-month angiographic data. Of these patients, restenosis, defined as a 50% diameter stenosis, occurred in 607, giving a restenosis rate of 23%; in 335 patients (55%), this was not associated with symptoms of angina. Most patients had moderate restenosis; only 5% had 70% diameter stenosis.
The significant univariate predictors of silent as opposed to symptomatic restenosis (diameter stenosis 50%) were male sex, absence of nitrate and calcium channel blocker use at 6-month follow-up, reference diameter after the procedure, reference diameter at 6-month follow-up, and lesion severity at 6 months (MLD and percent diameter stenosis) (Table 4). The cumulative frequency curves for MLD and diameter stenosis comparing those with symptomatic and asymptomatic restenosis are depicted in the Figure. By multivariate analysis, only male sex (P=0.04, OR 1.65, 95% CI 1.02 to 2.70), greater reference diameter at follow-up (P=0.002, OR 1.73, 95% CI 1.22 to 2.48), and lesser lesion severity (percent stenosis) at 6-month follow-up angiography (P=0.0001, OR 0.93, 95% CI 0.91 to 0.96) were associated with silent restenosis.
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Mean vessel caliber was smaller in women than men (reference diameter 2.74 versus 2.88 mm, P=0.01), and women also tended to have a smaller mean MLD than men at follow-up angiography (MLD 0.97 versus 1.02 mm, P=0.27). There was no difference between women and men in mean percent diameter stenosis (64.5% versus 64.2%, P=0.87).
An analysis was also performed on patients who were treated with an intracoronary stent. Of the 1469 patients who received stents from a variety of manufacturers, 242 developed restenosis (16%), of whom 58% were asymptomatic (as opposed to 53% in the balloon group, P=0.317). The univariate predictors of asymptomatic restenosis were unstable angina at screening (P=0.019), absence of calcium channel blocker (P=0.023) and nitrate (P=0.0002) use at 6-month follow-up, and presence of heparin use at the time of screening (=0.0179). By multivariate analysis, unstable angina at the time of screening (P=0.03) and absence of nitrate use at 6 months (P=0.0001) were associated with silent restenosis.
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Discussion |
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Large studies of patients undergoing percutaneous coronary intervention with planned 6-month angiographic follow-up have identified the clinical and angiographic predictors of restenosis. These studies have also demonstrated that angiographic restenosis is more frequent than clinically driven repeat target lesion revascularization. This analysis demonstrates that >50% of patients with angiographic restenosis have no symptoms of angina 6 months after the intervention. Our finding that 55% of patients with restenosis were asymptomatic is similar to the 48% reported in the study by Hernandez et al,18 which was a rigorous evaluation of 277 consecutive patients with restenosis after balloon angioplasty. Earlier studies reporting a lower proportion of asymptomatic restenosis have major design limitations, including small numbers of patients, incomplete angiographic follow-up, and variable time to follow-up angiography.19–21
In this series of patients enrolled in 10 percutaneous intervention studies, the overall restenosis was 23%; only 20% of those with restenosis had 70% diameter stenosis. Univariate predictors of asymptomatic restenosis were male sex and absence of antianginal medication use, greater reference diameter after the procedure, greater reference diameter at follow-up, and lesser lesion severity at 6-month follow-up. By multivariate analysis, only male sex, reference diameter at follow-up, and lesser lesion severity at 6 months were associated with asymptomatic restenosis. This suggests that there are more similarities between symptomatic and asymptomatic patients with restenosis than there are important differences.
Previous studies have demonstrated that the angiographic MLD rather than percent diameter stenosis predicts recurrent symptoms after coronary intervention, with a threshold of 1.35 to 1.50 mm.22,23 This is consistent with our finding that men were more likely than women to have restenosis without symptoms, because the women in this study had smaller-caliber arteries than men, no difference in percent diameter stenosis, and a trend toward a smaller MLD.
Other factors relating to attitude and perception of pain may also play a role. Several studies have documented a sex bias in referral for diagnostic procedures and treatment of patients with coronary artery disease.24–27 The initial diagnosis of angina in women is made more slowly than in men, because chest pain is often attributed to other causes.27 After intervention, however, men may experience less pain, may experience pain that they do not identify as a recurrence of angina, or may not admit to recurrent symptoms. Alternatively, women, once proven to have coronary artery disease, may present earlier with recurrent angina. A combination of these factors may contribute to the sex difference.
Absence of use of nitrates and calcium channel blockers at follow-up was a univariate predictor of asymptomatic restenosis. Although recurrent symptoms would be expected to precede the reinstitution of antianginal treatment, cause and effect are not self-evident. It is possible that those with a restenotic lesion of lesser severity had no symptoms and therefore did not receive medication, whereas those with a more severe progressive lesion may have been treated with escalating doses of antianginal agents. Although symptomatic patients may be on more medication, it is also plausible that patients on more treatment may have fewer symptoms. By multivariate analysis, lesser lesion severity was in fact a predictor of asymptomatic restenosis, suggesting that moderate restenosis (lesion severity 50% to 60%) may often be associated with no recurrent symptoms. Repeat intervention on such lesions may not be warranted, because they are associated with a good clinical outcome and may regress over the next 2 to 5 years.28–30 Routine 6-month follow-up angiography and resultant higher rates of repeat intervention may be related to a lower 10-year mortality rate.7,31
The predictors of asymptomatic restenosis in the subgroup undergoing stent deployment were absence of the use of nitrates at 6-month follow-up and unstable angina at initial presentation. It is possible that stents may have a "plaque-stabilizing" effect in the relief of symptoms in acute coronary syndromes (as opposed to stable angina).
An unexpected finding was that diabetes was not a predictor of asymptomatic restenosis. Patients with diabetes are more likely than those without to have suffered a silent myocardial infarction and are less likely to have symptoms in association with myocardial ischemia during treadmill stress testing or Holter ECG, perhaps because of a sensory neuropathy.32,33 Conversely, one reason that those with diabetes may have worse angina than those without is that diabetes is associated with reduced collateral development.34 Such collateral formation may be particularly important in the prevention of angina when there is slow and progressive lesion development, as occurs with restenosis. Hence, a lack of collateral formation may offset a tendency toward reduced symptoms from diabetic neuropathy, with diabetes having no net effect on silent versus symptomatic restenosis.
Study Limitations
Although there was some standardization of clinical and angiographic data collection, only the data common to all 10 study databases were included in the analysis. Collateral vessel formation, which may have a significant bearing on the presence or absence of symptoms associated with restenosis, was not assessed in a standardized manner and thus could not be analyzed.
Exclusion criteria for coronary interventional studies mean that the study population is carefully selected and probably at lower risk for restenosis than an unselected population of patients. This may influence the rate of asymptomatic restenosis and its predictors.
Conclusions
Men are more likely than women to have recurrent symptoms if they develop restenosis after percutaneous coronary revascularization. The only other multivariate predictor of recurrent symptoms was greater lesion severity at 6-month follow-up angiography.
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Acknowledgments |
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We acknowledge the sponsoring companies for their support and the Cardialysis core laboratory technicians and database managers. We would also like to thank all investigators who participated in the 10 studies analyzed.
Received June 8, 2001; revision received August 23, 2001; accepted August 23, 2001.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Kastrati A, Schomig A, Elezi S, et al. Predictive factors of restenosis after coronary stent placement. J Am Coll Cardiol. 1997; 30: 1428–1436.[Abstract]
2. Lee SG, Lee CW, Hong MK, et al. Predictors of diffuse-type in-stent restenosis after coronary stent implantation. Cathet Cardiovasc Interv. 1999; 47: 1866–1873.
3.
Serruys PW, Kay IP, Disco C, et al. Periprocedural quantitative coronary angiography after Palmaz-Schatz stent implantation predicts the restenosis at six months. J Am Coll Cardiol. 1999; 34: 1067–1074.
4.
de Feyter PJ, Kay IP, Disco C, et al. Reference chart derived from post–stent-implantation intravascular ultrasound predictors of 6-month expected restenosis on quantitative coronary angiography. Circulation. 1999; 100: 1777–1783.
5. Serruys PW, van Hout B, Bonnier H, et al. Effectiveness, costs and cost-effectiveness of a strategy of elective stenting compared to a strategy of balloon angioplasty allowing bail-out stenting in patients with coronary artery disease. Lancet. 1998; 352: 673–681.[Medline] [Order article via Infotrieve]
6. Boland JL, Corbeij HAM, van der Giessen W, et al. Multicenter evaluation of the phosphorylcholine coated Biodivysio stent in short de novo coronary lesions: the SOPHOS study. Int J Cardiovasc Intervent. 2000; 3: 215–225.[Medline] [Order article via Infotrieve]
7.
Ruygrok PN, Melkert R, Morel M-A, et al. Does six month follow-up angiography influence clinical management and outcome? J Am Coll Cardiol. 1999; 34: 1507–1511.
8.
Serruys PW, de Jaegere P, Kiemeneij F, et al. A comparison of balloon-expandable stent implantation with balloon angioplasty in patients with coronary artery disease. N Engl J Med. 1994; 331: 489–495.
9.
Serruys P, Emanuelsson H, van der Giessen W, et al. Heparin-coated Palmaz-Schatz stents in human coronary arteries: early outcome of the Benestent II Pilot Study. Circulation. 1996; 93: 412–422.
10. te Riele JAM, Piek JJ, Mudra H, et al. Clinical and angiographic results with the ACS Multi-Link DUET coronary Stent system: the DUET study. Int J Cardiovasc Intervent. 2000; 3: 97–104.[Medline] [Order article via Infotrieve]
11. Rutsch W, Kiemeneij F, Colombo A, et al. Clinical and angiographic results with the NIR stent: first international NIR endovascular stent study. Int J Cardiovasc Intervent. 2000; 3: 145–151.
12.
Serruys PW, Foley DP, Jackson G, et al. A randomized placebo-controlled trial of fluvastatin for prevention of restenosis after successful coronary balloon angioplasty: final results of the Fluvastatin Angiographic Restenosis (FLARE) Trial. Eur Heart J. 1999; 20: 58–69.
13.
de Jaegere P, Mudra H, Figulla H, et al. Intravascular ultrasound-guided optimized stent deployment: immediate and 6 months clinical and angiographic results from the Multicenter Ultrasound Stenting in Coronaries Study (MUSIC Study). Eur Heart J. 1998; 19: 1214–1223.
14. Suryapranata H, Boland JL, Pieper M, et al. Clinical and angiographic results with the beStent: the Registry for Optimal beStent Evaluation (ROSE) trial. Int J Cardiovasc Intervent. 2000; 3: 21–28.[Medline] [Order article via Infotrieve]
15. Emanuelsson H, Serruys PW, van der Giessen WJ, et al. Clinical and angiographic results with the Multi-Link coronary stent system: the West European Stent Trial (WEST). J Invasive Cardiol. 1998; 10: 12B–19B.
16. Haase J, Escaned J, van Swijndregt EM, et al. Experimental validation of geometric and densitometric coronary measurements on the new generation Cardiovascular Angiography Analysis System (CAAS II). Cathet Cardiovasc Diagn. 1993; 30: 104–114.[Medline] [Order article via Infotrieve]
17. Serruys PW, Foley DP, de Feyter PJ. Quantitative Coronary Angiography in Clinical Practice. Dordrecht, Netherlands: Kluwer Academic; 1994.
18. Hernandez RA, Macaya C, Iniguez A, et al. Midterm outcome of patients with asymptomatic restenosis after coronary balloon angioplasty. J Am Coll Cardiol. 1992; 19: 1402–1409.[Abstract]
19. Levine S, Ewels CJ, Rosing DR, et al. Coronary angioplasty: clinical and angiographic follow-up. Am J Cardiol. 1985; 55: 673–676.[Medline] [Order article via Infotrieve]
20. Holmes DR, Vlietstra RE, Smith HC, et al. Restenosis after percutaneous transluminal coronary angioplasty (PTCA): a report from the PTCA registry of the National Heart, Lung, and Blood Institute. Am J Cardiol. 1984; 53: 77C–81C.[Medline] [Order article via Infotrieve]
21. Popma JJ, van den Berg EK, Dehmer GJ. Long-term outcome of patients with asymptomatic restenosis after percutaneous transluminal coronary angioplasty. Am J Cardiol. 1988; 62: 1298–1299.[Medline] [Order article via Infotrieve]
22. Rensing BJ, Hermans WRM, Deckers JW, et al. Which angiographic variable best describes functional status 6 months after successful single-vessel coronary balloon angioplasty? J Am Coll Cardiol. 1993; 21: 317–324.[Abstract]
23. Legrand V, Raskinet B, Laarman GJ, et al. Diagnostic value of exercise electrocardiography and angina after coronary artery stenting. Am Heart J. 1997; 133: 240–248.[Medline] [Order article via Infotrieve]
24. Ayanian JZ, Epstein AM. Differences in the use of procedures between women and men hospitalized for coronary artery disease. N Engl J Med. 1991; 325: 221–225.[Abstract]
25. Steingart RM, Packer M, Hamm P, et al. Sex differences in the management of coronary artery disease. N Engl J Med. 1991; 325: 226–230.[Abstract]
26. Tobin JN, Wassertheil-Smoller S, Wexler JP, et al. Sex bias in considering coronary bypass surgery. Ann Intern Med. 1987; 107: 19–25.
27. Weintraub WS, Wenger NK, Kosinski AS, et al. Percutaneous transluminal coronary angioplasty in women compared with men. J Am Coll Cardiol. 1994; 24: 81–90.[Abstract]
28.
Hochman JS, Tamis JE, Thompson TD, et al. Sex, clinical presentation, and outcome in patients with acute coronary syndromes. N Engl J Med. 1999; 341: 226–232.
29.
Ormiston JA, Stewart FM, Roche AHG, et al. Late regression of the dilated site after coronary angioplasty: a 5-year quantitative angiographic study. Circulation. 1997; 96: 468–474.
30.
Asakura M, Ueda Y, Nanto S, et al. Remodeling of in-stent neointima, which became thinner and transparent over 3 years: serial angiographic and angioscopic follow-up. Circulation. 1998; 97: 2003–2006.
31. Rupprecht HJ, Espinola-Klein C, Erbel R, et al. Impact of routine angiographic follow-up after angioplasty. Am Heart J. 1998; 136: 613–619.[Medline] [Order article via Infotrieve]
32. Zarich S, Waxman S, Freeman RT, et al. Effect of autonomic nervous system dysfunction on the circadian pattern of myocardial ischemia in diabetes mellitus. J Am Coll Cardiol. 1994; 24: 956–962.[Abstract]
33. Marchant B, Umachandran V, Stevenson R, et al. Silent myocardial ischaemia: role of subclinical neuropathy in patients with and without diabetes. J Am Coll Cardiol. 1993; 22: 1433–1437.[Abstract]
34. Abaci A, Oguzhan A, Kahraman S, et al. Effect of diabetes mellitus on formation of coronary collateral vessels. Circulation. 1999; 9: 2239–2242.
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