Angioscopic findings during coronary angioplasty of coronary occlusions

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135

INTERVENTIONAL CARDIOLOGY

Angioscopic Findings During Coronary Angioplasty of Coronary Occlusions FERNANDO

ALFONSO,

ROSANA

HERNANDEZ,

CAMINO

BAlqUELOS,

MD, FESC, JAVIER

GOICOLEA,

MD, FESC, MANUEL MD, FESC, PEDRO

MD, FESC,

GONCALVES,

ZARCO,

MD, JAVIER

MD, FACC, CARLOS

SEGOVIA,

MACAYA,

MD,

MD, FESC

Madrid, Spain

Objectives. This study sought to elucidate angioscopic findings in totally occluded vessels before and after intervention. Background. Coronary angioscopy allows direct visualization of the lumen surface of the coronary arteries; however, the utility of coronary angioscopy during coronary angioplasty of vessels with a total occlusion is unknown. Methods. Twenty-one consecutive patients (mean [+-SD] 58 +9 years, range 39 to 77; 3 women, 18 men) undergoing dilation of an occluded vessel were studied with coronary angioscopy. Occlusions were classified as functional in 8 patients (Thombolysis in Myocardial Infarction [TIMI] flow grade 1) and anatomic in 13 (TIMI flow grade 0). Once the guide wire had crossed the occlusion, coronary angioscopy was attempted before and after angioplasty. Results. In all patients, coronary angioscopy before dilation visualized protruding material occluding the coronary lumen where the guide wire was wedged. The occlusion consisted of red thrombus in 19 patients (90%) (2 with isolated occlusive thrombus, 17 with thrombus associated with atherosclerotic plaque) and protruding yellow plaque in 2 patients (10%). However, on angiog-

raphy only 7 occlusions (33%) had data consistent with thrombus (p < 0.01 vs. coronary angioscopy). Successful dilation was obtained in 20 patients. After dilation, coronary angioscopy was repeated in 18 patients, revealing residual thrombus with plaque in 16 (89%) and a residual yellow plaque in 2. In addition, coronary angioscopy revealed coronary dissections in 13 patients (72%); however, angiography revealed dissections only in 10 patients (55%) and residual thrombus in 2 (10%) (p < 0.001). In one patient, coronary angioscopy visualized silent distal embolization of a red thrombns not previously recognized on angiography. Conclusions. Before intervention, coronary angioscopy provides unique insights into the pathologic substrate of occluded coronary vessels. An occlusive plaque with thrombus is the most common underlying substrate in these lesions. After successful dilation, angiographicaUy silent mural thrombus is seen in most patients. This information could be used to assist in the selection of candidates and type of coronary interventions and could also prove to be of prognostic value in patients with occluded vessels.

Percutaneous coronary angioscopy is a new technique that provides unique information on the intracoronary lumen surface that is complementary to that obtained with angiography (1-3). Several studies (1-6) have demonstrated the high sensitivity of coronary angioscopy to readily visualize atherosclerotic plaque, intracoronary thrombi and intimal flaps. Although coronary angiography is the reference standard in the evaluation of patients with coronary arte~' disease, some of its limitations are now well recognized (7,8). During coronary interventions, the ability of angiography to determine the underlying substrate in occluded vessels or in lesions with a complex angiographic appearance, as well as to assess the results after dilation, is limited, and angioscopy may prove useful in this regard (9,10). Percutaneous transluminal coro-

nary angioplasty of occluded vessels still represents a therapeutic challenge (11-14). Results of angioplasty in this setting are much worse than those obtained in other types of lesions, and several studies have focused on the identification of clinical and angiographic predictors of dilation success (1114). In addition, a high restenosis rate has been reported after angioplasty of occluded vessels (15,16). The reasons for the higher restenosis rate in these lesions are at present unknown, but a suboptimal initial result or the presence of angiographically unrecognized dissections or thrombi, may be implicated. To our knowledge, no previous studies have defined the angioscopic findings of lesions with total occlusions. Accordingly, we designed this prospective investigation to elucidate angioscopic findings in totally occluded vessels, both before and after intervention.

From the Cardiopulmona~'Department, Hospital Univcrsitario"San Carlos," Madrid, Spain. Manuscript receivedAugust 12, 1994; revised manuscript received Dcccmber 30, 1994,accepted March 28, 1995. Address for correspondence: Dr. Fernando Alfonso, Departamento de Cardiopulmonar, Hospital Universitario "San Carlos," Ciudad Universitaria, Plaza de Cristo Rey, Madrid 28040, Spain. @1995 by the American Cullcgc of ('artlitfl¢~g3

(J Am Coll Cardiol 1995;26:135-41)

Methods Patients. From May 1993 to March 1994, a total of 92 consecutive patients with an occluded vessel underwent coronary angioplasty at our institution. Of these, 29 patients were 0735-1097/95/$9.50 0735-1097(95)00186-8

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ALFONSO ET AL. CORONARY ANGIOSCOPY IN OCCLUDED VESSELS

Table 1. Baseline Clinical and AngiographicCharacteristics Age (yr)

58 _+9

Female gender Reason for PTCA Unstable angina Post-MI angina Silent ischemia* Previous MI Thrombolytic therapy Previous CABG Multivessel disease LVEF (%) Collateral circulation Occluded vessel LAD RCA LCx

3 (11~;) 10 (48%) 9 (42q,~) 2 (10%) 12 (57%) 8 (38%) 2 (10%) 10 (48%) 64 + 14 14 (66%) 8 7 6

*After myocardial infarction (MI). Data presented are mean value + SD or number (%) of patients. CABG = coronary artery bypass graft surgery; LAD left anterior descending coronary artery; LCx = left circumflex coronary artery: LVEF = left ventricular ejection fraction; PTCA - percutaneous transluminal coronary angioplasty; RCA = right coronary artery.

excluded from the study because the guide wire was unable to cross the occlusion: 12 for direct angioplasty in the treatment of acute myocardial infarction; 12 for vessel size <2.5 ram; and 16 for a tortuous or very short (<1 cm) proximal coronary segment. In the remaining 23 patients a coronary angioscopy examination of the occluded vessel was attempted during elective angioplasty. Two patients were excluded because of very poor angioscopic images. The remaining 21 consecutive patients with satisfactory angioscopic images constitute the study group. Two of these patients have been included in a previous report (17). Baseline clinical and angiographic characteristics of the 21 patients are detailed in Table 1. The elapsed time from the start of ischemic symptoms and from the final symptomatic status to coronary angioplasty was 11.8 _+ 9 months and 35 _+ 12 days, respectively (mean _+ SD). On the basis of clinical information (change in the pattern of angina, date of myocardial infarction), only five occlusions (23%) were considered to be chronic (>3 months). All patients gave informed consent to the study, which was performed according to a protocol approved by the Institutional Review Board allowing the use of angioscopy during angioplasty. Coronary angioplasty procedures and angiographic definitions. Twenty patients underwent conventional balloon coronary angioplasty, and one was treated with extraction atherectomy. Coronary angioplasty procedures were performed according to standard techniques, as previously described (18,19). Efforts were made to cross the occlusion as carefully as possible. A progressive approach with the serial use of floppy, intermediate and stiff guide wires was advocated. If conventional guide wires were not successful in crossing the occlusion, a Magnum wire (Schneider, Zurich, Switzerland) was used and was subsequently exchanged for a 0.014-in. (0.036 cm) wire. Coronary angioplasty success was defined as a residual stenosis <50% in the absence of complications (18,19). Serial electro-

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cardiograms (ECGs) and creatinine kinase (CK) levels (every 8 h) were recorded for 2 days after the procedure. Patients with elevation of CK levels twice or more the upper normal limit of our laboratory were classified as having a non-Q wave myocardial infarction. Coronary flow before and after intervention was determined after the administration of 0.2 mg of intracoronary nitroglycerin, according to Yhrombolysis in Myocardial Infarction (TIMI) criteria (20). Total occlusions were classified as anatomic (TIMI flow grade 0) or functional (TIMI flow grade 1), as previously suggested (16). The modified American College of Cardiology/American Heart Association classification (21,22) was used to define the target lesions. On angiography thrombus was considered present in cases of an intraluminal filling defect or in TIMI flow grade 0 occlusions with staining of contrast material or concave borders, or both. Angiographic dissections were classified according to the National Heart, Lung, and Blood Institute definition (23). Coronary angioscopy and imaging protocol. A commercially available angioscope (Baxter Healthcare Corporation, Edwards LIS Division) was used in all patients. This catheter (1.5 mm in diameter, 125 cm in length) can be advanced through standard 8F guiding catheters. The angioscope includes two independent units that can move independently. The outer catheter contains a compliant (volumetric) rubber balloon and the irrigation port. The inner catheter (0.6 mm in diameter) houses the optic bundle, which telescopes independently of the cuff. The fiberoptic bundle consists of a 3,000pixel fused bundle surrounded by light fibers with an objective lens at the tip. After adjusting the imaging system for focus, intensity of light and white balance, the angioscope is advanced over a 0.014-in. guide wire. Before imaging, the cuff of the balloon is gently inflated (up to 5 mm in diameter) with a pressure <1 arm using a mixed solution (50% saline and 50% contrast material) that permits its visualization on fluoroscopy. Lactated Ringer's solution is infused (warm jacket on power injection) to clear blood from the area of interest. The angioscope is connected to a fiberoptic light source and to a miniature video camera. The image of the monitor is magnified, displayed on-line during the procedure and recorded on a 0.5-in. super-VHS videotape for subsequent playback and analysis. In the present study, the fiberoptic bundle was advanced under continuous fluoroscopic guidance and its distal tip marker positioned in the area of interest with respect to angiographic landmarks. Care was taken to document during fluoroscopy that the position of the optic bundle was relatively centered within the arterial lumen and - 1 cm proximal to the site of the total occlusion. The angioscope was then advanced until adequate visualization of the region corresponding to the angiographic lesion site was achieved. Attempts were made to obtain a complete circumferential visualization of the intraluminal structures causing the occlusion of the vessel. This required various angioscopic runs (mean 2.3 +_0.3). Before intervention, no attempt was made to cross the lesion with the imaging device. However, after successful dilation the angioscopic study was repeated, and a

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137

Figure 1. Top left, Angioscopic visualization of a coronary occlusionrevealing a protruding occlusive thrombus (T), in which the guide wire (GW) is wedged, associated with yellow plaque (P). Bottom left, After dilation, a residual disrupted plaque with mural thrombus (angiographically silent) is visualized. Top right, Coronary occlusion revealing a large occlusive thrombus with a yellow plaque. Bottom right, After dilation, residual thrombus associated with disrupted plaque is visualized.

detailed examination of the previously occluded area was performed. On angioscopy, thrombi were defined as red intraluminal structures that persisted despite flushing and were either flat and adherent to the vessel wall (mural thrombus) or protruded into the coronary lumen (including occlusive thrombus). Disrupted tissue, either flapping or nonmobile, but overhanging the vessel lumen, was classified as coronary dissection. Atheromatous plaques were classified as mural (nonprotruding) or protruding into the lumen (including occlusive plaques). Plaques with a relatively homogeneous yellowish color were considered to represent xanthomatous plaques. Angioscopic images were classified by two experienced observers. In case of disagreement a consensus was reached after joint review of the videotape. Quantitative coronary angiography. Quantitative angiographic measurements were performed at the lesion site and in the proximal coronary segment used as reference. A commercially available, previously validated system (ARTREK, Quantim 2000I, QCS, lmageComm Systems, Inc.) and standard

methods were used (24,25). In our previous experience (26) reproducibility of measurements has been good, but the system does not allow quantification of lesions with total occlusions. An arbitrary value of 0 mm (100% stenosis) was therefore assumed before angioplasty for occlusions with a TIMI grade 0 flow, as previously suggested (27). A stenosis severity of 99% was assigned for lesions with TIMI grade 1 flow when automatic measurements could not be performed. Statistical analysis. Continuous variables are expressed as mean value _+ 1 SD and categoric data as absolute values and percent. Contingency tables were evaluated by the chi-square test or Fisher exact test when appropriate. A p value <0.05 was considered statistically significant.

Results Angioscopic findings before intervention. All patients underwent a successful coronary angioscopic examination of the occluded vessel before intervention. In every patient coronary angioscopy was able to provide satisfactory visualization of the

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Table 2. Quantitative Coronary Analysis (mean _+ SD)

P a t i e n t s (21)

Reference Segment (mm)

MLD (mm)

Before PTCA*

2.8 + 0.4

0.1 + 0.2

98 _+ 4

After PTCA

2.8 + 0.4

2.4 + 0.6

33 -+ 25

12 10 8

Stenosis (%)

*See text for definitions of lesions not suitable for quantitative analysis. MLD = minimal lumen diameter; PTCA = percutaneous transluminal coronary angioplasW.

6 4 2 0 O-THR

O-THR÷O-PLQ

M-THR*O-PLQ

O-PLQ

19 T H R

Figure 2. Angioscopic findings in totally occluded vessels. M-THR (O-THR) = mural (occlusive)thrombus; O-PLQ = occlusiveplaque.

material causing the occlusion and in which the guide wire was wedged (Fig. 1). A complete circumferential visualization of the occlusion site (three or more quadrants) was obtained in 16 patients (76%), whereas in 5 (24%) only partial (two quadrants) visualization was achieved. In two patients only a protruding yellow plaque (without thrombus) was recognized at the lesion site. However, in the remaining 19 patients (90%), a red thrombus was seen at the site of the occlusion (Fig. 2). In 2 of these 19 patients an occlusive red thrombus was the only material visualized at the site of the occlusion, whereas in the other 17 the thrombus was associated with atherosclerotic plaque. In 6 of these 17 patients the thrombus was occlusive (accounting for most of the lumen narrowing) and straddled the atherosclerotic plaque. In the remaining 11 patients the occlusion consisted mainly of atheromatous protruding tissue, in which the thrombus was mural and localized. On angiography only 7 of these patients (33%) were considered to have data consistent with thrombus (p < 0.01 vs. angioscopy). The atheromatous material found at the lesion site was classified as protruding or occlusive in all patients. Eighteen of the plaques were yellow (nine with associated white plaques), and one was white. Coronary angioscopic examination before intervention was uneventful in all but one patient who experienced ventricular fibrillation during imaging. The arrhythmia was successfully managed with direct current cardioversion. Procedural results. At baseline angiography, 15 occlusions had TIMI grade 0 flow. After intracoronary nitroglycerin, however, two of these lesions had TIMI grade 1 flow. Thus, eventually eight occlusions were classified as having TIMI grade 1 flow and 13 with TIMI grade 0 flow. Angiographically, six lesions were classified as type B1, 11 as type B2 and 4 as type C. In two patients a Magnum wire was required to cross the lesion. Dilation of these occluded vessels required a relatively prolonged inflation time (415 _+ 100 s). Successful dilation was achieved in 20 (95%) of 21 patients, all with normal (TIMI grade 3 flow) distal runoff. The patient with a failed dilation had a TIMI grade 0 flow occlusion caused by occlusive thrombus with yellow plaque. After the initial dila-

tion, severe distal stenoses were appreciated downstream, and eventually the artery remained occluded despite prolonged balloon inflations. Although good collateral circulation was present, this patient sustained a non-Q wave myocardial infarction. Results of quantitative angiography are summarized in Table 2. Using the aforementioned criteria, angiographic dissections were visualized in 10 patients after intervention (2 type A dissections, 4 type B, 2 type C, 2 type E). The two patients with type E dissection eventually required coronary stenting, and despite an excellent angiographic result, one developed a non-Q wave myocardial infarction. Angioscopic findings after dilation. Repeat angioscopic study was not attempted in the two patients with a difficult dilation (and who subsequently had a non-Q wave myocardial infarction) and in the patient who required cardioversion. In the remaining 18 patients angioscopy was repeated after intervention. In all patients angioscopy demonstrated a wideopen coronary lumen at the dilated site. However, significant residual mural thrombus or irregular atheromatous tissue, or both, were appreciated on the vessel wall in most patients (Fig. 1 and 3). Residual thrombus was classified as protruding in only three of these patients, but to a lesser extent than that found before dilation. In the remaining patients residual thrombi were classified as mural. In one additional patient, distal silent embolization of thrombotic material not recog-

Figure 3. Angioscopicfindings after successfuldilation of vessels with a total occlusion. Residual thrombus was appreciated in most patients after dilation. M-THR (P-THR) = mural (protruding) thrombus. M-PLQ (P-PLQ) = mural (protruding) plaque. Patients (18) 12 10 8 6 4 2 0 M-THR+P-PLQ

P-THR*M-PLQ 16 T H R

i

M-THR+M-PLQ

M-PLQ

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139

Table 3. Angioscopic Findings in Relation to Symptoms and Anatomic Data Angina Occlusivethrombus Occlusiveplaque + mural thrombus Occlusiveplaque + occlusivethrombus Occlusive plaque Total

Duration of Occlusion

Type of Occlusion

Post-MI

Unstable

>3 mo

<3 mo

TIMI 0

TIMI 1

1 (1(1%) 6 (54%) 4 (36%) 0 (0%) I1

1 (10%) 5 (50c~-) 2 (209~) 2 (209~-) 10

0 (0%) 2 (40%) 2 (40%) 1 (20%) 5

2 (12%) 9 (57%) 4 (25%) 1 (6%) 16

1 (8%) 6 (46%) 5 (38%) 1 (8%) 13

l (12%) 5 (64%) 1 (12%) 1 (12%) 8

Data presented are number (%) of patients. Post-Ml = anginaor silent ischemiaafter myocardialinfarction; TIMI - Thrombolysisin MyocardialInfarctionflow grade.

nized on angiography was visualized on angioscopy. Tables 3 and 4 summarize angioscopic findings in relation to symptoms and angiographic data. No differences on angioscopic findings were found when patients were grouped according to these variables, Coronary angioscopy was more sensitive than angiography (16 patients [89%] vs. 2 [10%], p < 0,001) for detection of residual thrombus after dilation. In addition, angioscopy was slightly superior to angiography in the detection of coronary dissections after intervention. Thirteen patients (72%) presented with dissections on angioscopy versus 10 (55%)on angiography (p = NS). Five patients with discrete angiographic dissections showed multiple independent dissections on angioscopy (two in three patients, three in one and four in one). Although angiography did not detect dissections proved by angioscopy in four patients, angioscopy failed to visualize an angiographic type B dissection in one patient. In this patient significant collateral circulation prevented optimal definition of the dilated coronary segment, which was classified as a protruding yellow plaque by angioscopy. Coronary angloscopy after intervention was uneventful in all but two patients, where the angiographic image obtained immediately after dilation worsened after angioscopy (17). An excellent angiographic result, however, was obtained in these two patients after repeat balloon dilation.

Discussion Despite technical improvements in catheter design and the recent introduction of new devices as a therapeutic alternative for specific lesions, dilation of coronary occlusions remains a challenge. Both the immediate and late results of coronary interventions in occluded vessels are poorer than those ob-

tained in other types of lesions (11-16). Whereas the initial dilation success in these patients is hampered by a high rate of subacute coronary closure, the midterm outcome is shadowed by a restenosis rate as high as 66% (11-16). The critical step during these procedures relies on successfully crossing the occluded segment with the guide wire. This, in turn, appears to be closely related to the anatomy of the occlusion. The underlying pathologic substrate of coronary occlusions in patients undergoing coronary angioplasty is largely unknown (28,29). The ideal scenario for coronary interventions would be a central fresh thrombus surrounded by the fibrocellular tissue of the atherosclerotic lesion. This would provide a path of lower resistance that may assist the passage of the guide wire across the former true lumen. In the alternative pathologic presentation, plaque rupture, resulting in a raised and protruding plaque, plays a predominant role. Some investigators (28) have suggested that such unfavorable anatomy may preclude successful recanalization of the occluded vessel and, in fact, may increase the risk of complications. Different clinical and angiographic variables have been used in an attempt to predict the anatomic substrate and hence the likelihood of procedural success in patients with coronary occlusions (11-16). Among the clinical variables, duration of the occlusion has emerged as the strongest predictor of dilation success in most series (11-16). Anatomic variables, including total versus functional occlusions, the presence of a tapered occlusion (nipple) to guide the recanalization procedure and the absence of bridging collateral vessels are also well established predictors of success (11-16). However, the angiographic information on occluded vessels is especially limited. Indirect signs of unfavorable anatomy, such as length, eccentricity, ulceration and the presence of thrombus, cannot be reliably obtained from angiogra-

Table 4. Type of Plaque in Relation to Symptoms and Anatomic Data Angina Yellow and white Yellow* White Total

Duration of Occlusion

Type of Occlusion

Post-Ml

Unstable

>3 mo

<3 mo

TIMI 0

TIMI 1

5 (45%) 5 (45%) 1 (10%) 11

4 (40%) 6 (60%) 0 (0%) 10

1 (20%) 4 (80%) 0 (0%) 5

8 (50%) 7 (44%) 1 (6%) 16

5 (38%) 8 (62%) 0 (0%) 13

4 (50%) 3 (37%) 1 (13%) 8

*In the two patients with only an occlusivered tbrombus before intervention, yellowplaque was visualized after dilation, and this feature was included in the analysis. Data presented are number (%) of patients. Abbreviationsas in Table 3.

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phy in this particular setting. Accordingly, new efforts aimed at gaining further insights into the pathologic substrate of occluded vessels are warranted. Present study. The present study demonstrates that angioscopy is a safe and useful tool for the evaluation of occluded vessels. In our series, coronary angioscopic examination was easily performed, both before and after dilation, providing unique, additional information to that obtained by angiography. Before intervention, angioscopy permitted visualization of the intracoronary material responsible for the occlusion. In all patients the guide wire appeared to be wedged into occlusive atheromatous plaque or thrombus, or both. The most common pathologic substrate was an occlusive yellow plaque associated with either occlusive or mural red thrombus. In only a few instances was the occlusion caused by isolated red thrombus or atheromatous material. Occlusive thrombi were visualized as a red, rather homogeneous material protruding into the coronary lumen. Alternatively, mural thrombi were identified as localized areas or reddish material, mainly located at the edges of an occlusive atheromatous plaque. Because all of these vessels were occluded, angina or ischemic ECG changes (a frequent problem during angioscopic studies) were absent or mild. This allowed a relatively unrestricted examination of the target lesion. In fact, the occlusion site and the adjacent coronary segment frequently could be visualized for some time, even after the infusion of Ringer's solution had been stopped and the occlusion cuff deflated. In one patient, however, ventricular fibrillation occurred during the angioscopic study. This complication may have been related to mechanical factors or, more likely, to myocardial ischemia because TIMI grade 1 flow was present before the study. After dilation, angioscopy demonstrated widely dilated coronary lumen but with a significant amount of residual atheromatous material and mural thrombus at the lesion site. The presence of extensive mural thrombus after dilation was unexpected in these vessels, which had presented a good angiographic appearance. Partially occlusive material, however, was seen in only a few patients after dilation. Coronary dissections were also identified in most patients, but in contrast to the angiographic data, many appeared to be multiple dissections. In the present study we tried to avoid guiding the interventions with respect to the angioscopic findings. In four patients, however, significant residual protruding thrombus associated with a narrowed lumen was visualized with coronary angioscopy after dilation. In two of these patients, angiography also demonstrated a poor dilation result. An additional, prolonged balloon inflation was performed with angiographic success in all four patients. Previous studies. Our findings support previous reports suggesting that coronary angioscopy is superior to angiography in the detection of coronary thrombus. Previous studies (1-3) have demonstrated the usefulness of angioscopy in recognizing intracoronary thrombus in acute coronary syndromes. In addition, the use of this technique to gain insight into the patho-

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logic composition of atheromatous plaque has been suggested (1-6). Experimental data suggest that lipid-rich xanthomatous plaques appear to be at higher risk for disruption and subsequent thrombosis (30). This may explain the high frequency of yellow plaques associated with either occlusive or mural thrombus found in our study, which included mainly recent occlusions. Alternatively, angioscopy has been used to define the nature of abrupt vessel closure complicating coronary interventions (31). Nevertheless, for protocol reasons, patients with an abrupt closure during coronary angioplasty and those with an evolving myocardial infarction were not included in our study. Other investigators (32) have demonstrated that progressive thrombus formation may be visualized with angioscopy soon after intervention at the lesion site. This phenomenon may contribute to the pathogenesis of early elastic recoil after dilation. Alternatively, patients with progressive thrombosis may be prone to acute complications. Although we did not perform continuous angioscopic monitoring of the dilated segment, it is tempting to speculate that patients with significant residual thrombus immediately after dilation may be at higher risk for thrombus progression. This, in turn, may increase the risk of subacute closure. Further studies will be required to determine whether this mechanism may explain the high risk of subacute thrombosis and late restenosis in patients undergoing dilation of occluded vessels. Finally, angioscopy may be used to identify patients with occluded vessels who may benefit from the additional use of thrombolytic therapy. De Zwaan et al. (33) demonstrated that in patients with unstable angina, thrombolysis was only of benefit in the presence of a total or subtotal coronary occlusion. Angioscopy appears to be superior to angiography for detecting thrombus in occluded vessels and could be used to guide the use of thrombolytic agents in this setting. Limitations. We studied a relatively small cohort of patients undergoing dilation of occluded vessels. They represent a selected cohort because only patients with occlusions that could be crossed with the guide wire underwent imaging. Accordingly, our findings may not be applicable to patients with other types of lesions, including chronic total occlusions. Nevertheless, our results are probably representative of most patients undergoing attempted dilation of occluded lesions in the clinical setting. We visualized only the proximal aspect of the occlusion before intervention, and in some patients only partial visualization of the vessel circumference was achieved. However, in most patients angioscopic findings after dilation were consistent with those found before intervention. Therefore, although characterization of the obstructive material may have been incomplete, it seems likely that analysis of the proximal surface of the occlusion may provide adequate insights concerning the nature of the occlusion. In our study thrombus was defined as red material (protruding or mural) on the vessel wall. Recent studies (34) have suggested that in the early stages of coronary thrombosis a white, platelet-rich thrombus may be the predominant pathologic substrate. In the present investigation, overhanging white tissue was considered

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to represent a vessel dissection. Therefore, we cannot rule out the possibility that some platelet-rich thrombus could have been misclassified as a dissection. Conclusions and clinical implications. Coronary angloscopy is a useful tool for delineating the pathologic substrate of occluded vessels in patients undergoing coronary angioplasty. A red thrombus overlying an occlusive yellow plaque is the most frequent angioscopic finding in patients with these lesions. In addition, after successful dilation, angiographically silent residual mural thrombus is found by angioscopy in the majority of patients. Prospective studies should address the clinical implications of the additional information provided by angioscopy. Potentially, information obtained during angloscopy regarding pathologic substrate may be useful in the selection of candidates and type of intervention. Coronary angioscopy could also be used to guide the recanalization device through an intraluminal rather than a subintimal pathway. In addition, visualization of residual thrombus after angioplasty may be a marker of patients at higher risk for vessel reclosure or late restenosis. Finally, angioscopic findings may help to identify patients who may benefit from coadjuvant antithrombotic or even intracoronary thrombolytic therapy either before or after the procedure.

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