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Circulation. 1996;93:2106-2113

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(Circulation. 1996;93:2106-2113.)
© 1996 American Heart Association, Inc.

Articles

Angioscopic Predictors of Early Adverse Outcome After Coronary Angioplasty in Patients With Unstable Angina and Non–Q-Wave Myocardial Infarction

Sergio Waxman, MD; Michael A. Sassower, MD; Murray A. Mittleman, MD, DrPH; Stuart Zarich, MD; Akira Miyamoto, MD; Karen S. Manzo, RN; James E. Muller, MD; George S. Abela, MD; Richard W. Nesto, MD

From the Institute for Prevention of Cardiovascular Disease, Boston, Mass, and Cardiovascular Division, Deaconess Hospital, Harvard Medical School, Boston, Mass.

Correspondence to Richard W. Nesto, MD, Cardiovascular Division, Deaconess Hospital, One Deaconess Rd, Boston, MA 02215.


*    Abstract
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 *Abstract
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Background Clinical and angiographic criteria have a limited ability to predict adverse outcome in patients with unstable angina who are undergoing percutaneous transluminal coronary angioplasty (PTCA). We investigated whether the use of angioscopy can improve prediction of early adverse outcome after PTCA.

Methods and Results Angioscopic characterization of the culprit lesion was performed before PTCA in 32 patients with unstable angina and 10 with non–Q-wave infarction. Seven patients (17%) had an adverse outcome (myocardial infarction, repeat PTCA, or need for coronary artery bypass graft surgery) within 24 hours after PTCA. Six of 18 patients with a yellow culprit lesion had an adverse outcome compared with 1 of 24 in whom the culprit lesion was white (P=.03). Six of 20 patients with plaque disruption suffered an adverse outcome compared with 1 of 22 with nondisrupted plaques (P=.04). Six of 17 patients with intraluminal thrombus had an adverse outcome, whereas only 1 of 25 patients without thrombus suffered an adverse outcome (P=.01). Yellow color, disruption, and thrombus at the culprit lesion site were associated with an eightfold increase in risk of adverse outcome after PTCA. The prediction of PTCA outcome based on characteristics of the plaque that were identifiable by angioscopy was superior to that estimated by the use of angiographic variables.

Conclusions In patients with unstable angina and non–Q-wave infarction, angioscopic features of disruption, yellow color, or thrombus at the culprit lesion site can identify patients at high risk of early adverse outcome after PTCA. Angioscopy was superior to angiography for prediction of PTCA outcome.


Key Words: angioplasty • prognosis • coronary disease • angioscopy • thrombus


*    Introduction
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Percutaneous transluminal coronary angioplasty for the treatment of unstable angina carries a high risk of early and late adverse outcomes, such as abrupt closure, myocardial infarction, need for emergency bypass surgery, repeat PTCA, and restenosis.1 2 3 Although various clinical and angiographic criteria have been identified that are associated with adverse outcomes, such as diabetes mellitus,4 female sex,5 advancing age,6 7 lesion complexity by angiography,4 5 8 9 and angiographic evidence of thrombus at the culprit lesion site,4 5 10 their ability to predict outcome remains relatively low. Of these criteria, the angiographic presence of an intraluminal thrombus has been associated most consistently with an increased risk of early adverse outcome.11 12 13 14

Angiography is the standard method used to image the coronary arteries during interventional procedures. Although information about the degree of stenosis can be obtained readily, the angiogram has only a limited ability to detect the presence of an intraluminal thrombus.15 Intracoronary angioscopy can provide direct images of the endoluminal surface of the culprit lesions and is a superior tool for the detection of thrombi.16 17 18 We hypothesized that with angioscopy, it may be possible to identify lesion-specific characteristics associated with an adverse outcome after PTCA and thereby improve risk stratification of patients who undergo this procedure.

We performed coronary angioscopy at the time of PTCA in patients with unstable angina and non–Q-wave infarction and analyzed outcomes to determine whether angioscopy can identify characteristics of culprit lesions predictive of early adverse outcome.


*    Methods
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Patient Population
Between October 1991 and March 1994, we performed coronary angioscopy before PTCA in 46 patients with unstable angina and non–Q-wave myocardial infarction at the Deaconess Hospital, a tertiary-care referral hospital. Approximately 2300 patients underwent PTCA for unstable angina and myocardial infarction during this period. Patients were considered candidates for angioscopy if the following criteria were met: (1) patients had unstable angina or non–Q-wave infarction as defined below; (2) PTCA was carried out as a second procedure after previous angiography, since a separate Institutional Review Board consent was required for angioscopy; (3) the culprit lesion was anatomically suitable for angioscopy (see below); and (4) angioscope catheters and staff skilled in angioscopy were available at the time of PTCA. Written informed consent for coronary angioscopy was obtained from all patients before angioplasty. The protocol was approved by the Institutional Review Board of Deaconess Hospital.

Unstable angina was defined on the basis of modified TIMI III criteria19 as chest discomfort of new onset that occurred at rest or with a crescendo pattern and lasted more than 5 minutes but less than 6 hours. The discomfort must have been accompanied by objective evidence of ischemic heart disease and by creatine kinase enzyme levels less than twice the upper limit of normal. Objective evidence of ischemic heart disease was defined as new ECG evidence of ischemia in at least two contiguous leads (either >0.1-mV ST-segment elevation lasting less than 30 minutes or >0.1-mV ST-segment depression 80 ms after the J-point or T-wave inversion) or a history of previous myocardial infarction. A non–Q-wave myocardial infarction was defined by the aforementioned criteria for ischemia plus the presence of an elevation in creatine kinase enzyme levels more than twice the upper limit of normal in the absence of new ECG Q waves that were diagnostic of infarction.

To be considered for angioscopy, patients had to meet the following criteria: (1) the culprit lesion had to be located in the proximal to middle portions of a coronary artery with a luminal diameter >2.0 mm and <4.0 mm; (2) the segment of the artery proximal to the stenosis had to be nontortuous; and (3) cuff balloon inflation of the angioscope had to be possible at a site not subtended by a major side branch. The above criteria assured safety and coaxial positioning of the angioscope to optimize image acquisition.

Angioscopic Equipment
The angioscope used (Imagecath, Baxter Healthcare Corp) was a two-part assembly that consists of a 1.5-mm-diameter (4.5F) delivery/balloon occlusion catheter and fiber-optic bundle combined into a single system that is compatible with a standard 8F guiding catheter. The fiber-optic bundle, housed inside the catheter, consists of a 3000-pixel fused bundle surrounded by ten 120-µm light fibers with an objective lens at the tip. A conventional 0.014-in angioplasty guidewire is used in this monorail system, with a loop incorporated on the tip of the optic bundle, which allows for direction and advancement of the system over the wire. The shaft of the optic bundle is 0.6 mm in diameter, and the construction of the system allows the bundle to be advanced up to 5 cm beyond the catheter tip. A channel for irrigation with crystalloid for the displacement of blood is provided, as well as a second channel for the low- pressure (1-atm) inflation of a Kraton rubber occlusion cuff located at the tip of the catheter, which is expanded with a saline/contrast mixture to obstruct blood flow transiently. Custom connectors connected the angioscope to a standard fiber-optic light source and to a miniature video camera. The image on the monitor during the procedure was magnified to 36 times the size of the actual image. Angioscopic images were recorded on a videotape for review and storage.

Procedures
All procedures were performed through a percutaneous femoral approach. All patients received aspirin before the procedure and intravenous heparin to maintain an activated clotting time of >300 seconds. Angioscopy was performed at the time of angioplasty as described previously.20 After angioscopy, PTCA was performed in the usual manner. Neither procedural nor postprocedural therapy was influenced by the pre-PTCA angioscopic findings. Routine post-PTCA angioscopy was not performed because repeated passage of the angioscope catheter may affect the PTCA result, as has been suggested by other investigators.21 After PTCA, an intravenous infusion of heparin was continued for a minimum of 12 hours to maintain an activated partial thromboplastin time of 45 to 65 seconds. The femoral access sheath was removed 4 to 6 hours after the heparin was discontinued.

Definitions
Data were collected prospectively and clinical, angiographic, and angioscopic variables were recorded. In patients with single-vessel disease, the culprit lesion was considered to be the most severely stenosed lesion in the affected vessel. In patients with multivessel disease, the culprit lesion was defined as the most severe stenosis in the artery that supplied the ischemic area, as identified by ECG localization. The position of the angioscope in relation to the culprit lesion was confirmed by fluoroscopy.

Angiographic and angioscopic images were reviewed separately by two investigators blinded to the outcome of PTCA. Stenosis severity by angiography was measured by visual assessment and expressed as percent luminal narrowing of the vessel at the culprit lesion site. Lesions were classified as type A, B, or C according to the American College of Cardiology/American Heart Association (ACC/AHA) Task Force Classification of Coronary Artery Lesions.8 Type B and C lesions were further subcategorized as suggested by Ellis et al4 and Myler et al11 (type B1 and C1, one adverse characteristic; type B2 and C2, two or more adverse characteristics). Angiographic lesion morphology was also categorized as complex or noncomplex by use of criteria adapted from Ambrose et al.22 A complex lesion was defined as a type II eccentric stenosis or a lesion with multiple irregularities and a noncomplex lesion as a concentric or type I eccentric stenosis. These two categories have been proposed as a method to separate disrupted from nondisrupted plaques.23 In accordance with TIMI criteria,24 angiographic evidence of thrombus was defined as an intraluminal filling defect with rounded, globular, or polypoid shapes that protruded into the lumen or as contrast-medium staining at the site of coronary stenosis or occlusion.

All angioscopic assessments were made from antegrade visualization of the culprit lesion. Angioscopic definitions were based on an angioscopic classification system developed by the European Working Group on Coronary Angioscopy.25 A plaque was defined as a nonmobile, elevated, and/or protruding structure clearly demarcated from the adjacent vessel wall. The predominant color of the culprit lesion, either yellow or white, was recorded. Plaque disruption was considered present when the surface of the lesion had a rough, ulcerated, or irregular appearance with visible cracks, fissures, or intimal flaps. A lesion was considered nondisrupted when its surface appeared smooth and/or shiny without irregularities. Thrombus was defined as a red, white, or mixed intraluminal, superficial, or protruding mass adherent to the vessel surface but clearly a separate structure that persisted despite being flushed with a saline solution. A white thrombus had to fulfill the additional criteria of having a shaggy, irregular, "cotton wool" appearance.21 25 Representative angioscopic images of a yellow disrupted lesion and of white and mixed thrombi are shown in Fig 1Down.



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  		Figure 1. Left, Angioscopic image of a disrupted yellow plaque. Center, A predominantly white plaque with disrupted surface and white thrombus. Right, A spherical red and white thrombus protruding into the lumen (plaque not visualized).

An early adverse outcome was defined as death, myocardial infarction, or the need for repeat PTCA or emergency coronary artery bypass surgery within 24 hours after PTCA.

Statistical Analysis
Patients with and without adverse outcomes were categorized according to angiographic and angioscopic variables, and comparisons were made between patients by use of a two-tailed Fisher's exact test. Relative risks were calculated as the ratio of the risk of experiencing an early adverse outcome for patients with a given angiographic or angioscopic characteristic compared with the risk in those without the characteristic. Ninety-five percent CIs were calculated by use of standard asymptotic variance techniques.


*    Results
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Patient Data
Forty-six patients with unstable angina or non–Q-wave myocardial infarction underwent coronary angioscopy before PTCA. In 4 patients, adequate angioscopic images could not be obtained; these patients were not included in the present analysis. The clinical characteristics of the 42 study patients are shown in Table 1Down. Thirty-two patients were categorized as having unstable angina and 10 were diagnosed as having a non–Q-wave infarction. Balloon angioplasty was performed in 37 patients (88%), directional coronary atherectomy in 4 (10%), and excimer laser angioplasty in 1 (2%). The culprit vessel was the left anterior descending artery in 22 patients (52%), the left circumflex and right coronary in 8 patients each (38%), and a saphenous vein bypass graft in 4 patients (10%). A restenosis lesion was considered to be the culprit in 6 patients (14%), each of whom presented with unstable angina. The average interval between the onset of clinical syndrome and PTCA was 7 days. Twenty-four patients (57%) were being treated with intravenous heparin and 37 patients (88%) were receiving aspirin before PTCA.


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  		Table 1. Clinical and Angiographic Characteristics of the Study Population (n=42 Patients)

Seven patients (17%) had an adverse outcome within 24 hours after PTCA. Four patients required repeat PTCA, two had a myocardial infarction documented by myocardial enzyme elevation, and one required emergency coronary bypass surgery because of recurrent closure during PTCA. No deaths occurred. There was no difference in the clinical characteristics between patients with and without adverse outcome.

Angiographic and Angioscopic Findings
In accordance with the ACC/AHA classification scheme, 8 lesions (19%) were classified as type A, 9 (21%) as type B1, 21 (50%) as type B2, and 4 (10%) as type C1. There were no type C2 lesions in our series. Adverse outcomes were seen in two patients in each of the A, B1, and B2 lesion categories and in one patient with a type C1 lesion (P=.6). Two angiographic characteristics (lesion complexity and thrombus before angioplasty) were analyzed separately, and their relation to outcome at 24 hours is shown in Fig 2Down. Sixteen culprit lesions (38%) had a complex morphology by angiography that was suggestive of plaque disruption, whereas 26 (62%) were classified as noncomplex. Four patients with complex lesion morphology and three with noncomplex morphology had an early adverse outcome (P=.40). Of 9 patients in whom angiographic evidence of thrombus at the culprit lesion was present, two had an adverse outcome, whereas of 33 patients in whom thrombus was absent by angiographic criteria, 5 had an early adverse outcome (P=.63). The relative risks of an adverse outcome after PTCA, given the angiographic characteristics of the culprit lesion, are shown in Table 2Down. Angiographic complexity of the culprit lesion and thrombus were associated with nonsignificant 2.2-fold (95% CI, 0.6 to 8.5) and 1.5-fold (95% CI, 0.3 to 6.3) increases in risk of an early adverse outcome, respectively.



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  		Figure 2. Relation between two angiographic characteristics (lesion complexity and thrombus before angioplasty) of the culprit lesion and early adverse outcome after PTCA in 42 patients with unstable angina and non–Q-wave myocardial infarction. n indicates the total number of patients in each group.


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  		Table 2. Relative Risk of Early Adverse Outcome After PTCA According to Angiographic and Angioscopic Characteristics of the Culprit Lesion in 42 Patients With Unstable Angina or Non–Q-Wave Myocardial Infarction

The angioscopic features of culprit lesions before angioplasty and their relation to outcome at 24 hours are shown in Fig 3Down. Angioscopy revealed the culprit lesion to be yellow in 18 patients (43%); of these, 6 had an early adverse outcome at 24 hours. Only 1 of the 24 patients whose culprit lesions were white on angioscopy had an early adverse outcome (P=.03). Plaque disruption was observed in 20 patients (48%), 6 of whom suffered an adverse outcome. In contrast, only 1 of the 22 patients with a nondisrupted plaque had an adverse outcome (P=.04). Thrombus (red, white, or mixed) was present in 17 patients (40%), 6 of whom experienced an adverse outcome, whereas only 1 of the 25 patients in whom thrombus was absent suffered an adverse outcome (P=.01). As shown in Table 3Down, when analyzed by type of thrombus, the presence of white or mixed thrombus was associated with an adverse outcome (P=.016 and P=.036, respectively), whereas red thrombus alone was not (P=NS). Treatment with heparin (n=24) or aspirin (n=37) for 24 hours or longer before PTCA was not associated with the presence or absence of thrombus or with outcome.



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  		Figure 3. Relation between the angioscopic appearance of the culprit lesion and early adverse outcome after PTCA in 42 patients with unstable angina and non–Q-wave myocardial infarction. n indicates the total number of patients in each group.


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  		Table 3. Relation Between Type of Thrombus as Assessed by Angioscopy and Early Adverse Outcome After PTCA in 42 Patients With Unstable Angina and Non–Q-Wave Myocardial Infarction

The presence of either yellow color, disruption, or thrombus at the culprit lesion site was seen in 21 patients, and an early adverse outcome occurred in 7 (33%). Conversely, there were no adverse outcomes in the 21 patients without any of the above characteristics, ie, those whose culprit lesions were white, nondisrupted, and without thrombus (P=.009). The presence of a yellow plaque, evidence of disruption, and angioscopic visualization of a thrombus at the culprit lesion site were associated with an 8.0-fold (95% CI, 1.1 to 60.7), 6.6-fold (95% CI, 0.9 to 50.2), and 8.8-fold (95% CI, 1.2 to 66.9) increase in risk of an early adverse outcome after PTCA, respectively (Table 2Up).

In five of the seven patients who suffered an adverse outcome, all three adverse angioscopic characteristics were present, ie, the lesion appeared yellow and disrupted and a thrombus was present. Of the remaining two patients, one had a thrombus on a disrupted white plaque and one had a yellow, nondisrupted, nonthrombosed plaque. Angiography correctly detected thrombus in two of these patients, whereas the culprit lesions appeared complex in four patients (all of these lesions were disrupted by angioscopy).

To account for the fact that patients received different forms of percutaneous revascularization, a second analysis was performed that excluded the 4 patients who underwent coronary atherectomy and the single patient who had excimer laser angioplasty. Only the 37 patients who underwent balloon angioplasty alone were included in this analysis. Six adverse outcomes were recorded in this group. Evidence of yellow color and thrombus by angioscopy were still significantly associated with an adverse outcome (P=.005 and P=.03, respectively), and plaque disruption demonstrated a trend toward adverse outcome (P=.07). Angiographic thrombus and lesion complexity were not associated with an adverse outcome (P=.62 and P=.39, respectively).


*    Discussion
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 up arrowMethods
 up arrowResults
 *Discussion
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This study suggests that angioscopic features of disruption, yellow color, or thrombus at the culprit lesion site in patients with unstable angina and non–Q-wave infarction are associated with an eightfold increase in the risk of adverse outcome after PTCA. The data indicate that angioscopy may well be superior to angiography for prediction of risk in this setting and may provide additional insight into the pathophysiology of the acute complications of PTCA.

Abrupt closure after PTCA can result from thrombus formation,12 26 intimal dissection,27 28 vasoconstriction,29 or elastic recoil.30 It is possible that certain characteristics of culprit lesions identifiable before PTCA may predispose to development of these complications. For example, the association of a yellow plaque with adverse outcome observed in the present study may reflect an increased thrombogenic potential of such plaques. It has been hypothesized that a yellow plaque is a lesion with a lipid pool separated from the lumen by a thin cap31 and may be a substrate for thrombosis once the cap is disrupted. Fernandez-Ortiz et al32 showed that the lipid core, which contains crystalline lipids, soft lipids, phospholipids, and cellular degradation products, is the most thrombogenic component of atherosclerotic plaques. Additional insight into the thrombogenicity of plaques is available from the demonstration of Wilcox et al33 that tissue factor, a membrane-bound glycoprotein that can initiate the clotting cascade, is present in the lipid core of atheromatous plaques. Mechanical disruption of a lipid-rich plaque by PTCA could lead to exposure of tissue factor and other thrombogenic constituents present in the atheromatous core, thereby causing intraluminal thrombus formation more often than would PTCA of a fibrotic plaque. Annex et al34 recently demonstrated the presence of tissue factor in atherectomy specimens of patients with unstable coronary syndromes. In their series, tissue factor was present in directional atherectomy specimens of all four patients who suffered abrupt closure after the procedure. Pawashe and colleagues35 reported that antibodies to tissue factor inhibit arterial thrombosis after balloon injury in a rabbit model, which again points toward the role of tissue factor as a link between the atherosclerotic plaque and intravascular thrombosis.

It is possible, however, that adverse outcomes associated with yellow plaques are caused through mechanisms other than thrombosis. Using intracoronary ultrasonic imaging, Rasheed and Hodgson36 reported greater elastic recoil after PTCA in "soft" (lipid-rich) lesions compared with "hard" (fibrous) lesions. De Franco and colleagues37 reported preliminary data in which preprocedural ultrasound identification of calcified tissue adjacent to soft plaque is predictive of major angiographic dissection after coronary angioplasty. Other factors, such as endogenous thrombolysis, local flow conditions, lumen size, and arterial wall response, may also play a role in the final outcome, which would explain the finding that many patients with yellow lesions did not experience complications despite their presumably greater risk of thrombosis, recoil, and dissection.

Angioscopic evidence of thrombus was also associated with an adverse outcome after PTCA. Prior studies have reported that the presence of thrombus at the site of dilatation, as determined by angiography, is predictive of an adverse outcome and have led to the use of antiplatelet agents,38 prolonged anticoagulation before PTCA,39 40 thrombolytic41 and antithrombin agents,42 local delivery of thrombolytics by specially coated balloons,43 and use of ultrasonic44 or atherectomy devices.45 Angioscopy, however, is superior to angiography for detection of intraluminal thrombus and may allow for a better selection of patients who may benefit from these interventions. White et al46 reported preliminary data that indicated that the presence of thrombus by angioscopy performed before or after PTCA in patients with stable or unstable angina was associated with an adverse outcome. The present study differs from that report in that our study included only patients with unstable angina and non–Q-wave infarction and angioscopy was performed before PTCA in all cases.

The mechanism through which the presence of intraluminal thrombus before PTCA predisposes to an adverse outcome is still speculative. It is likely that lesions in which a thrombus is present before angioplasty are lipid-rich, disrupted lesions in which the thrombogenic constituents of the plaque have been exposed to flowing blood. The mere presence of a thrombus can stimulate additional thrombus by local release of platelet secretory products and stimulation of thrombin generation.47 48 Meyer et al49 recently demonstrated in an ex vivo perfusion system that the growth of thrombus on thrombus may be predominantly thrombin-mediated. Our data suggest that the type of thrombus may be important in determining the outcome of PTCA, as the presence of either white or mixed (red and white) thrombi before PTCA was associated with an adverse outcome. Adhesion and activation of platelets can occur at sites of endothelial denudation, plaque disruption, or high shear (tight stenosis). Local thrombin generation and subsequent platelet activation then play a major role in thrombus growth. The presence of platelet-rich thrombi at the culprit lesion site could be indicative of an active thrombotic process with a high local thrombotic propensity. Thrombus detection by angioscopy may identify a subgroup of patients in whom a more aggressive antithrombotic approach should be taken. Whether this approach will result in clinical benefit will require a larger sample size in which the type and amount of thrombus present can be correlated with PTCA outcome.

The incidence of adverse outcome within 24 hours after PTCA in our study group was 17%, which reflects the high-risk nature of the patients in the present study and the inclusion of repeat PTCA in the definition of adverse outcome. Other studies of PTCA in patients with unstable angina have reported complication rates from 5% to as high as 20%,2 3 50 51 with various criteria and time points used to define adverse outcomes. It is likely that this wide range is also due to the heterogeneous nature of patients studied, as there is variability in the criteria used for unstable angina. To this regard, controversy exists whether the incidence of complications may be related to the subtype of unstable angina. In the 1985-1986 NHLBI PTCA Registry,52 a postprocedural complication rate (defined as coronary occlusion, myocardial infarction and death, and need for emergency bypass surgery) of 15% was reported, and the immediate outcome did not appear to be related to the subcategory of unstable angina, ie, rest versus no rest, postinfarction, accelerating, or new-onset angina. Other reports1 53 indicate that the presence of rest or postinfarction angina carries a higher risk of complications after percutaneous revascularization and that in their absence, immediate outcomes are as favorable as those obtained in patients with stable angina. Tan et al50 reported a complication rate after PTCA (defined as death, Q-wave myocardial infarction, or emergency bypass surgery) of 5.2% in patients with class IV angina, which was significantly higher than that observed in all other patients (2.4%; P=.009). The pathophysiology of unstable angina therefore may determine the outcome of percutaneous interventions. This concept is supported by the present study, as we have demonstrated that PTCA outcome is related to the different characteristics of culprit lesions in patients with unstable angina and non–Q-wave myocardial infarction.

A recent study demonstrated the ability of angioscopy to be used as a tool to predict clinical outcome. Itoh and colleagues54 reported that in patients with stable angina, PTCA of yellow plaques as identified by angioscopy demonstrated a lower incidence of restenosis than PTCA of white plaques. It was postulated that balloon injury of hard plaques (fibrous and calcified) can cause more extensive and deeper vessel-wall damage, which would lead to an intense reparative response of intimal hyperplasia and smooth muscle cell proliferation that results in higher restenosis rates. In that study, there was no significant difference in immediate PTCA success rates between white and yellow lesions as assessed by angioscopy. In contrast to the present study, the patient population in the study by Itoh et al consisted of patients with stable coronary artery disease and had a considerably lower incidence of thrombus as assessed by angioscopy before PTCA (20% versus 40% in the present study). It is likely that the outcome of spontaneous or mechanical injury of an atherosclerotic plaque is determined by a combination of plaque-specific factors, such as lipid, ulceration, or thrombus at the culprit lesion, and non–plaque-related factors consequent to the clinical syndrome, such as a systemic prothrombotic state or increased vasoreactivity that occurs in patients with unstable angina and myocardial infarction.

The high rate of success and low incidence of complications of PTCA in patients with stable angina2 55 presumably is due to the presence of a fibrous plaque that appears smooth and white on angioscopy.56 Similarly, the favorable results in patients with unstable angina in the present study were concentrated in patients with white, nondisrupted culprit lesions. It may be that such lesions produce unstable angina through rapid smooth muscle cell proliferation, as suggested by Flugelman et al.57 This may be the case for restenosis lesions as well. White et al58 reported that these lesions are usually white and smooth by angioscopy. All six restenosis lesions in our study were white and nondisrupted and were associated with a favorable outcome after PTCA. Thus, the heterogeneity in the angioscopic appearance of culprit lesions in patients with unstable angina may reflect the complexity of this syndrome and explain its various manifestations as well as its varying prognosis and response to medical treatment and revascularization.

Limitations
Our population was a select group of patients with unstable angina and non–Q-wave myocardial infarction. Our entrance criteria limited the number of patients that could be studied. The small number of patients may not be representative of all patients with acute coronary syndromes who undergo PTCA. However, it is noteworthy that PTCA outcome can be predicted from characteristics of the plaque that are identifiable by angioscopy.

The ability of angioscopy to define plaque pathology may be limited in some cases. In our study, characterization of the culprit lesion was accomplished primarily by antegrade imaging before PTCA to avoid potential trauma to the lesion related to passage of the angioscopic device. It is possible that in some cases, the presence of poststenotic thrombi may have been underestimated. Sites of disruption may also be hidden by thrombi or, alternatively, mild forms of disruption beyond the resolution of the angioscope may be missed. Likewise, some plaques are mixed in color, ie, yellow and white, which perhaps reflects the mixed nature of their composition, and the presence of a thrombus may obscure the color definition of the plaque. In addition, the diagnosis of white thrombi by angioscopy remains somewhat controversial, as they may be difficult to differentiate from intimal disruption or flaps, which would result in overestimation of the presence of white thrombi. This may have accounted in part for the observed difference in outcomes based on the different type of thrombi. Thus, pathological studies are needed to validate angioscopic observations in vivo. Although lesion classification according to the AHA/ACC criteria did not correlate with adverse outcomes in the present study, two specific lesion morphological characteristics (angiographic complexity and thrombus) showed an evident trend, and it is possible that analysis of a larger number of patients may have shown a statistically significant association. However, angioscopy clearly was superior to angiography for prediction of outcome in this group of patients.

The results of the present study are not sufficient to recommend that angioscopy be routinely used in patients with unstable angina and non–Q-wave myocardial infarction who are undergoing PTCA. Randomized studies could be designed to improve both short-term and long-term PTCA outcomes by identification of high-risk patients, and therapies could be tailored on the basis of angioscopic examination of the culprit lesion. Demonstration of a benefit in such studies would then support routine clinical use.

Conclusions
Angioscopic features of yellow color, disruption, and thrombus at the culprit lesion site are associated with an eightfold increase in the risk of early adverse outcome in patients with unstable angina and non–Q-wave myocardial infarction who undergo PTCA. Angioscopy is more sensitive than conventional angiography to detect intraluminal thrombus, can be useful in risk stratification of patients who undergo PTCA, and may allow for better selection of patients who may benefit from alternative revascularization devices or from more intense antithrombotic intervention at the time of PTCA.


*    Acknowledgments
 
We would like to thank John Snyder and the staff of the Cardiac Catheterization Laboratory at the Deaconess Hospital for their technical support.

Received July 19, 1995; revision received October 25, 1995; accepted November 5, 1995.


*    References
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 *References
 

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