CLINICAL STUDIES
Long-term (10-year) outcome in patients with unstable angina pectoris treated by coronary balloon angioplasty
David A. Halon, MB, ChB, FACCa,
Moshe Y. Flugelman, MDa,
Amnon Merdler, MDa,
Hedy Rennert, MPH*,
Johnny Shahlaa and
Basil S. Lewis, MD, FRCP, FACCa
a Cardiovascular Research Unit, Department of Cardiology, Lady Davis Carmel Medical Center and the Bruce Rappaport School of Medicine, Technion-IIT, Haifa, Israel
* Department of Community Medicine and Epidemiology, Lady Davis Carmel Medical Center and the Bruce Rappaport School of Medicine, Technion-IIT, Haifa, Israel
Manuscript received January 23, 1998;
revised manuscript received July 2, 1998,
accepted July 24, 1998.
Address for correspondence: Dr. David A. Halon, Department of Cardiology, Lady Davis Carmel Medical Center, 7 Michal Street, Haifa 34362, Israel
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Abstract
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Objectives. We sought to examine completed 10-year survival and event-free survival in patients with stable and unstable angina pectoris treated by coronary balloon angioplasty.
Background. Patients with unstable angina are at increased risk for recurrent acute coronary events.
Methods. The study included 208 consecutive patients (133 with stable and 75 with unstable angina pectoris) undergoing angioplasty from 1984 to 1986. The balloon crossed the lesion in 185 patients (121 with stable and 64 with unstable angina pectoris). Angioplasty was performed in patients with unstable angina pectoris 12 ± 15 days (median 8) after symptom onset. Patients with unstable angina pectoris were classified retrospectively into Braunwald class I (n = 3), class II (n = 20), class III (n = 28), class B (n = 52) and class C (n = 12). Follow-up data were obtained from hospital charts, telephone interview and official death certificates where applicable. The study had >80% power to detect a clinically significant 20% difference in survival and a 20% difference in event-free survival between the stable and unstable patient groups.
Results. Despite similar baseline characteristics, early (40-day) mortality was slightly higher in patients with unstable angina (4.7% [3 of 64 patients] vs. 0.8% [1 of 121 patients], p = NS). Long-term outcome was not different, because survival curves were parallel thereafter (10-year survival was 83% for those with stable and 77% for those with unstable angina, p = NS). Survival free of myocardial infarction or coronary artery bypass graft surgery at 10 years was 53% in patients with stable and 47% in patients with unstable angina (p = NS), and survival free of infarction, bypass surgery or repeat angioplasty was 32% for both groups at 10 years. In patients with Braunwald class III unstable angina, 10-year survival was 80%, as compared with 85% in other patients with unstable angina, due to the early hazard (p = NS). Survival and event-free survival were similar in patients who had had a recent myocardial infarction (Braunwald class C) and in patients with acute electrocardiographic changes. Repeat hospital admissions were not more frequent in patients with unstable angina (3.1 ± 3.5 vs. 3.0 ± 2.6, p = NS).
Conclusions. Ten-year survival and event-free survival were similar in patients with stable and unstable angina pectoris treated by coronary balloon angioplasty, with no evidence of an increased rate of recurrent cardiovascular events in the unstable group.
The clinical syndrome of unstable angina pectoris defines a group of patients with coronary disease who are at increased risk of fatal and nonfatal myocardial infarction (MI) and sudden cardiac death. More than 20% of patients with unstable angina have a non–Q wave MI during the initial hospital period, and another 3% have a new episode of MI in the following 6 weeks (1). Unstable angina is associated with in-hospital or 6-week mortality of 1.5% to 2.5% (1,2) and 1-year mortality of up to 10% (2). Recurrent hospital admission is necessary in one-third of the patients.
Unstable angina results from a critical reduction in coronary blood flow, usually after an acute change in the pathology of a coronary lesion. Possible mechanisms underlying plaque destabilization include endothelial damage, erosion or rupture of the fibrous cap and changes in plaque cellularity and vascularity (3). Rupture of a plaque is associated with platelet aggregation, intermittent generation and lysis of thrombus and episodes of distal microembolization, which together with changes in coronary vascular tone produce instability of coronary blood flow (4–7). In conjunction with the localized pathophysiologic event, patients with unstable angina show evidence of a systemic response, including activation of the coagulation system and an acute systemic inflammatory reaction (8–10) mediated by the immune system (11). The hypercoagulable state and systemic inflammatory markers may persist for at least 6 months, even in patients who have no further clinical episodes, and may predate the episode of unstable angina pectoris (12) or acute MI and may be a risk factor for its occurrence (13–15).
Revascularization using percutaneous transluminal coronary angioplasty provides an effective therapeutic modality in patients with unstable angina and coronary lesions amenable to balloon dilation (16–25). The acute local and more prolonged systemic processes operative in the patient with unstable angina could form the basis for an increased rate of recurrent events in patients with unstable angina pectoris. However, although patients with unstable angina were included and reported in angioplasty follow-up studies (21,26–30), the question of long-term outcome after angioplasty for unstable angina pectoris, with appropriate subset grouping and analysis, has not been addressed in detail. This study examined the completed 10-year outcome in patients with unstable angina pectoris treated by coronary balloon angioplasty, taken from a cohort of consecutive patients entered prospectively in the mid-1980s into the Lady Davis Carmel Medical Center Interventional Registry. We compared the results with those of patients undergoing angioplasty for stable angina pectoris during the same period to determine whether dilation of the culprit lesion alters the prognosis or whether patients with unstable angina have an adverse long-term prognosis due to recurrent unstable or acute events.
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Methods
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Patient group.
During the period 1984 to 1986, 227 patients underwent percutaneous transluminal coronary angioplasty for coronary artery disease in a single cardiology department. Survival data were available for 224 of the patients (98.6%) (three foreign nationals could not be traced), and late events and symptomatic status were obtained in 97% of the survivors. In 14 patients the procedure was performed in the context of acute MI without recurrent angina pectoris or evidence of recurrent ischemia, and these patients were removed from the present analysis. Two other patients in whom the classification of stable and unstable angina was not clear were excluded: one who underwent angioplasty in close proximity to bypass surgery for a technical graft problem and another who underwent angioplasty after atypical chest pain related to a noncardiac interventional stress.
Unstable angina was defined as a recent deterioration in anginal symptoms leading to hospital admission or presentation to the emergency room with pain at rest. Of the 208 patients in this study, 75 (36%) had unstable and 133 (64%) had stable angina pectoris. The lesion could not be crossed by the angioplasty wire or balloon catheter in 11 patients (15%) in the unstable and 12 patients (9%) in the stable group (p = NS), so that dilation was actually performed in 185 patients (64 with unstable and 121 with stable angina).
The mean time from symptom onset to angioplasty in patients with unstable angina was 12 ± 15 days (median 8).
Baseline patient characteristics.
The baseline characteristics of patients with stable and unstable angina pectoris are given in Table 1. There was no difference between the two groups with regard to age, gender, diabetes mellitus, hypertension and the presence of multivessel coronary artery disease. Single-, double- or triple-vessel disease was defined as the number of systems (left anterior descending, circumflex or right coronary artery) with one or more narrowings of >60% in a coronary artery or any of its major branches, or both, in the worst angiographic view. A slightly larger number of patients with unstable angina (p = NS) had undergone a previous MI. Almost 10% of patients in both groups had undergone previous coronary artery bypass graft surgery.
Subclassification of patients with unstable angina pectoris.
At the time the patients in this study underwent angioplasty, there was no generally accepted definition of patient subsets regarding unstable angina pectoris. However, patients were classified retrospectively with the aid of the medical and nursing records at the time of angioplasty, according to the Braunwald classification (31). The severity of angina was classified as class III (occurring at rest and within 48 h of angioplasty) in 28 (55%) of 51 patients with available data, class II (at rest in the previous month but not in the 48 h before angioplasty) in 20 patients (39%) and class I (occurring on minimal or rapidly decreasing effort but not at rest) in 3 patients (6%). The clinical circumstances were classified as class C (Q wave MI during the 2 weeks before angioplasty) in 12 (19%) of the 64 patients (7 of whom had class III and 2 of whom had class II anginal severity; insufficient data in 3) and as class B in the remaining 52 patients (81%) (instability not due to an extracardiac condition); (21 of whom had class III, 18 of whom had class II and 3 of whom had class I anginal severity; data unavailable in 10). The majority of patients were receiving combined therapy for angina pectoris before hospital admission (44 [86%] of 51 patients with complete data with two or more antianginal drugs before hospital admission and only 3 [6%] not receiving medication). New electrocardiographic (ECG) ST segment–T wave changes were recorded during chest pain in 31 (61%) of 51 patients.
Angioplasty procedure.
Angioplasty was performed using standard techniques and pharmacotherapy at the time. Pharmacotherapy included pretreatment with antiplatelet drugs (aspirin 100 to 325 mg daily), intravenous heparin (10,000 to 25,000 U during and in most patients for 8 to 24 h after the procedure) and intravenous, intracoronary and/or sublingual nitrates in a dose determined by the attending cardiologist during and after the procedure. After angioplasty patients were treated with aspirin and long-acting nitrates for at least 3 to 6 months, unless contraindicated.
In the 185 patients in whom the lesion was crossed, angioplasty was successful (dilation of a major vessel considered responsible for symptoms with  50% residual narrowing and no major untoward event or urgent bypass surgery) in 59 (92%) of 64 patients with unstable angina and 119 (98%) of 121 patients with stable angina (p = 0.05) (Table 2). The number of systems and vessels dilated was similar between the two patient groups. In 61% of the patients in both groups, revascularization was complete (no residual lesions >60%).
Patient follow-up.
Procedural outcome was recorded at the time of angioplasty in all patients. Follow-up data were obtained from hospital charts and supplemented by a structured telephone interview with the patient or one of his or her immediate relatives conducted by a single cardiologist. This was followed by specific inquiry, as necessary, to ascertain the functional capacity at the time of follow-up, or in the case of death, to define its cause. When information was not available, the cause of death was obtained from the official death certificate. Survival and event-free survival were recorded at a mean of 9.5 ± 0.6 years. Survival was subsequently ascertained 10 to 12 years after the angioplasty procedure (mean 11.1 ± 0.7 years) for all 185 patients who actually underwent dilation.
Statistical analysis.
Survival and event-free survival were assessed by life-table analysis using the Kaplan-Meier method, and survival curves were compared using the log-rank test. Categoric variables were compared by using the chi-square test and continuous variables by using the Student t test.
A 20% difference in survival and a 20% difference in event-free survival between the stable and unstable patient groups over 10 years were considered to be clinically significant. The study had >80% power to detect such difference in 10-year survival, given an 83% survival rate in the stable group and a two-sided alpha error of 0.05. Given an event-free survival rate of 32% at 10 years in the stable group, we calculated a power of >80% to detect a 20% difference in event-free survival (32).
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Results
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Patients in whom the lesion was not crossed.
There were no procedural or early deaths in the 23 patients in whom the lesion could not be crossed. One patient in the stable group and three patients in the unstable group had a periprocedural infarction. Early bypass surgery was performed in four patients (33%) with stable and four patients (36%) with unstable angina (p = NS) in whom angioplasty was unsuccessful.
Patient survival.
Short-term mortality (40 days) tended to be higher in patients with unstable angina (4.7% [3 of 64 patients] vs. 0.8% [1 of 121 patients], p = NS) owing to a relatively higher early mortality in a small group of very ill patients with a recent MI, postinfarction angina and heart failure (Braunwald class IIIC).
The long-term survival is shown in Figure 1. After the small, early dip in survival in the unstable group, the curves remained almost parallel throughout the long-term follow-up period. Life-table survival at 5 years was 90.6% for the unstable and 98.0% for the stable group, and at 10 years it was 76.6% for the unstable and 82.6% for the stable group (p = NS).
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Figure 1 Kaplan-Meier curves of survival and event-free survival (alive without MI, bypass surgery or repeat angioplasty) for patient cohorts with stable and unstable angina pectoris. After a small, early fall in survival of patients with unstable angina, the curves remained parallel throughout the follow-up period. Event-free survival curves were similar in both patient cohorts.
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Event-free survival.
Life-table event-free survival without an MI or bypass surgery was 76.6% at 5 years and 47% at 10 years in the unstable group and 86.8% at 5 years and 52.6% at 10 years in the stable group (p = NS). The curves were linear, showing an unchanged and almost identical event rate throughout the follow-up period. When repeat angioplasty was added to the recurrent events (Fig. 1), the combined recurrent event rates remained very similar between both groups, but there was an increased early event rate in the first year due to repeat angioplasty procedures, the curves becoming less steep subsequently. Combined event-free survival rates at 5 years and 10 years were 56.3% and 32.0% for unstable and 62.8% and 32.0% for stable angina, respectively (p = NS). When the incidence of recurrent MI, bypass surgery or repeat angioplasty procedures was examined individually, there were no significant differences between the stable and unstable angina groups.
Subset analysis in patients with unstable angina pectoris.
Long-term survival and event-free survival rates for patients with stable angina and different subsets of patients with unstable angina are given in Table 3. In patients who underwent angioplasty within 2 days of the last episode of chest pain (Braunwald class III), 5- and 10-year survival rates were 90% and 80.0% as compared with 95.7% and 84.6% in the other patients with unstable angina (p = NS) (Fig. 2) and 98% and 82.6% in the stable group (p = NS). Combined event-free survival at 5 and 9.7 years was not significantly different from that in other patients with unstable angina (60.7% and 42.9% vs. 47.8% and 43.5%) or from that in patients with stable angina. In the 12 patients who underwent angioplasty for postinfarction angina (Braunwald class C), long-term survival was slightly but not significantly lower than that in other patients with unstable angina (66.7% vs. 82.7% at 10 years) or stable angina. The combined event-free survival rate in Braunwald class C was also not significantly different from that of other patients with unstable angina. Those with unstable angina in whom ischemic ECG changes were recorded before angioplasty (n = 31, 61%) had a 5- and 10-year survival rate of 90.3% and 80.6% as compared with 95.0% and 85.0% in other patients with unstable angina (Fig. 3) (p = NS). Event-free survival at 5 and 9.7 years was also not different in patients with and without ischemic ECG changes at the time of the acute event.
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Figure 2 Kaplan-Meier curves of survival and event-free survival in patients with Braunwald class II and class III unstable angina. There was a higher early mortality and event rate in patients with class III unstable angina but no further excess mortality or recurrent events during the follow-up period.
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Figure 3 Kaplan-Meier curves of survival and event-free survival in patients with unstable angina with and without acute ischemic ECG changes. There was a slightly higher early mortality in patients with acute ischemic ECG changes but no further excess mortality during the follow-up period. Event-free survival was similar in both groups.
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The mean number of repeat cardiac hospital admissions during the follow-up period was similar in the unstable and stable groups (3.1 ± 3.5 per patient for unstable vs. 3.0 ± 2.6 for stable angina) (p = NS). Functional class at the latest follow-up in surviving patients was almost identical in patients with unstable and stable angina, with two-thirds in functional class I or II (New York Heart Association) (33 [68.8%] of 48 patients with unstable angina and 67 [67%] of 100 patients with stable angina) (p = NS).
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Discussion
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The essential findings of the study were that despite an early hazard in high risk patients, the overall long-term survival and event-free survival rates in patients with unstable angina pectoris were very good and not different from that of patients with stable angina. The outcome was similar irrespective of the timing of angioplasty in relation to the onset of the acute clinical syndrome or the last episode of rest pain. These results, together with those reported by Ruygrok et al. (30), implied that unstable angina pectoris was a short-lived process limited to one or more particular coronary lesions and that on a practical level, despite probable systemic phenomena, angioplasty seems to be followed by vascular healing and plaque restabilization.
Management of patients with unstable angina pectoris.
Medical treatment with aspirin has been effective in reducing the event rate in patients with unstable angina pectoris (33,34), and the addition of heparin and low-molecular-weight heparin provided further benefit (35,36). Antiplatelet glycoprotein IIb/IIIa inhibitors decreased acute events both before and after coronary intervention (37–39). The prognosis of unstable angina may differ depending on the clinical presentation (40). Detection of minor myocardial necrosis by troponin T assay identified patients who may benefit from prolonged antithrombotic therapy (36). Coronary artery bypass surgery improved 2-year survival in patients with unstable angina who had reduced left ventricular function (27) and improved survival at 8 years in patients considered to be at high risk (29).
Angioplasty for unstable angina pectoris.
Increased risks were initially reported in patients undergoing angioplasty for unstable angina pectoris, due to an increased incidence of thrombus and instability of the plaque (16). We usually attempted to stabilize patients before angiography, although it is not clear (41,42) whether early or late outcome is different in these patients as compared with those undergoing an earlier intervention. Stammen et al. (43) performed angioplasty in patients with unstable angina at a mean of 15 days (range 1 to 76) after hospital admission and reported a similar 6-month outcome to that in patients with stable angina. Coronary angioplasty has proven to be effective (16,23,25,44), even though angioplasty of the obstructive coronary lesion does not prevent the systemic reaction and its local disruptive nature could amplify it.
A higher incidence of restenosis after balloon angioplasty in patients with unstable angina has been described by some investigators (21,45) but not all (23). Local lesion characteristics may influence the early response to angioplasty and the late event rate (23,46–49). In the National Heart, Lung, and Blood Institute’s Angioplasty Registry, the cumulative event rate at 2 years was the same for patients with unstable and stable angina (44), but at 5 years a higher crude mortality rate was reported in patients with rest angina than that in unstable angina patients without rest angina and particularly in those with postinfarction angina (50). This study highlighted the potential early hazard in patients with class IIIB unstable angina in the mid-1980s, but showed quite clearly that the later course is no different from that of patients with stable angina.
Potential study limitations.
There are several limitations to this study. The study dealt with a relatively small sample size, and this is particularly disadvantageous regarding subgroup analysis. However, because baseline characteristics and the extent of disease were similar in patients with stable and unstable symptoms and primary treatment was the same, the results do carry prognostic import, particularly in view of the long follow-up period in this patient cohort. The study had >80% power to detect a 20% difference in survival and event-free survival between patients with stable and unstable angina pectoris; subgroup analysis should be interpreted with caution.
We have no knowledge of the pathophysiology at the time of the acute event in the individual patients in this study. There were probably a number of pathophysiologic mechanisms involved, differing from patient to patient and possibly with each having a different prognosis. Subset analysis using the Braunwald classification may have corrected for such differences to some extent. It is likely that in the present era of stents, low-molecular-weight heparin (51,52) and platelet glycoprotein IIb/IIIa receptor inhibitors (37–39), the outcome of treatment in all patient groups may be different from that of patients treated over 10 years ago. Use of current treatment modalities, had they been available 10 years ago, would almost certainly have minimized the early risk in patients with class IIIC postinfarction unstable angina and would have brought the long-term survival curves for stable and unstable angina even closer together.
Clinical implications.
The data provided no evidence of a long-term predisposition toward recurrent unstable or ischemic events in patients with unstable angina pectoris treated by coronary balloon angioplasty, despite what is now known about systemic inflammatory markers and their persistence. The rehospitalization rate was similar in patients with stable and unstable angina over a 10-year period. Given that special care is taken with high risk patients with refractory postinfarction angina, coronary balloon angioplasty represents an effective therapeutic strategy in patients with unstable angina pectoris and is associated with an excellent long-term prognosis.
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Footnotes
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Dr. Lewis was supported by the Fund for the Promotion of Research at the Technion, Haifa, Israel.
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