Tear or Dissection After Coronary Angioplasty

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1 1035 Tear or Dissection After Coronary Angioplasty Morphologic Correlates of an Ischemic Complication Alexander J.R. Black, MB, BS, David L. Namay, MD, Alan L. Niederman, MD, Nicholas J. Lembo, MD, Gary S. Roubin, MB, PhD, John S. Douglas Jr., MD, and Spencer B. King III, MD Intimal tear or dissection is an important descriptor of ischemic complications after coronary angioplasty, but only the minority of patients will develop an acute ischemic event. To identify additional factors that may predict the development of an ischemic event when arterial disruption occurs during otherwise uncomplicated angioplasty, the records of 1,346 patients prospectively identified as having tear or dissection without immediate vessel closure were examined. Ischemic complications, defined as ischemic chest pain, myocardial infarction, the need for coronary bypass surgery, or death, occurred in 120 patients (9%). Significant multivariate correlates of an ischemic complication were the presence of unstable angina or a totally occluded vessel before angioplasty and diameter stenosis of greater than 30% after angioplasty. Detailed geometric and videodensitometric analysis of the postdilatation angiograms of a subset of 96 consecutive patients was carried out. Ischemic complications occurred in 11 patients (11%). Multivariate analysis revealed that the independent correlates of complications, in decreasing order of importance, were the length of the tear or dissection (p=0.001), diameter stenosis after angioplasty (p=0.001), cross-sectional area after dilatation measured by videodensitometric methods (p= 0.013), and the presence of extraluminal contrast (p=0.044). When tear or dissection occurs during otherwise uncomplicated coronary angioplasty, patients at risk of developing delayed ischemic complications can be identified and may benefit from measures designed to minimize this risk. By controlling for the geometric or mechanical factors that result in tear or dissection, it has been possible to identify factors not previously thought associated with ischemic complications. Further studies are warranted to assess therapeutic approaches in patients undergoing coronary angioplasty for total coronary occlusion or unstable angina pectoris. (Circulation 1989;79: ) I schemic complications of percutaneous transluminal coronary angioplasty (PTCA) occur in approximately 4% of patients and constitute the major cause of morbidity and mortality associated with this procedure.1'2 When vessel closure occurs during PTCA, appropriate management can be instituted. However, approximately half of the ischemic complications that occur as a result of PTCA do so after the patient has left the catheterization laboratory.3 The correlates of ischemic syndromes complicating PTCA have been examined in some detail.1-7 From the Andreas Gruentzig Cardiovascular Center, Cardiology Division, Departments of Medicine and Radiology, Emory University Hospital, Atlanta, Georgia. Presented in part at the 60th Annual Scientific Sessions, American Heart Association, Anaheim, California, November Address for reprints: Dr. Spencer B. King III, Andreas Gruentzig Cardiovascular Center, Emory University Hospital, 1364 Clifton Road NE, F606, Atlanta, GA The presence of intimal tear or arterial dissection after PTCA consistently figures as a significant predictor of ischemic complications. With the advent of techniques and devices8'9 that may minimize the likelihood of ischemic complications after angioplasty, it would be useful to identify, with the information available at the completion of the procedure, which patients with tear or dissection are at risk of developing complications after leaving the catheterization laboratory. Effective lumen diameter or area or both are probably of major importance in determining the hemodynamic consequences of arterial disruption. Both are difficult to estimate or measure in the dilated lesion, but recently developed geometric and videodensitometric techniques may be helpful. Accordingly, this study was carried out to identify the correlates of delayed ischemic complications in patients with intimal tear or dissection after PTCA and, specifically, to examine quantitative angiographic indexes that may be useful.

2 1036 Circulation Vol 79, No 5, May 1989 FIGURE 1. Angiogram and illustration of a segment ofleft anterior descending coronary artery after dilatation. Arrows indicate an intraluminal filling defect ("tear"). Methods Patients The study population consisted of patients retrospectively identified from the PTCA database who left the catheterization laboratory with angiographic evidence of tear or dissection after otherwise uncomplicated coronary angioplasty. If occlusion of the dilated artery occurred during the procedure, whether permanent or corrected after subsequent dilatation, "in-lab closure" was considered to have occurred, and the patient was excluded from this analysis, as were patients in whom ischemic complications were associated with isolated side-branch closure. Patients undergoing repeat angioplasty, angioplasty of coronary bypass grafts, or angioplasty for evolving myocardial infarction were also excluded. A total of 1,346 patients composed the study group. less than 50%. Angiographic evidence of dissection was considered present if there was marked irregularity of the vessel wall after PTCA, luminal filling defect suggestive of intimal flap, or extravasation of contrast outside the lumen after dilatation. When dissection was considered present, selected patients received prolonged inflations with slightly larger balloons in an attempt to "tack back" the dissection flap. Heparin infusion after PTCA was used in 255 patients (19%), usually when there was a large dissection or angiographic evidence of intraluminal thrombus. Procedural Details Detailed Angiographic Analysis The 96 most recent consecutive angiographic films were subjected to detailed morphologic analysis by two experienced angiographers who were unaware of the outcome of the patient. Dissection was classified as either a linear intraluminal filling defect (tear, Figure 1), an extraluminal opacity (cap, Figure 2), or a spiral dissection (Figure 3). Of note, some overlap occurred between these descriptions depending to some extent on the angiographic projection, and when the two angiographers disagreed, a third was asked to arbitrate. In addition, the length of the dissection was measured and was recorded whether or not it exceeded the length of the stenotic lesion or the length of the dilatation balloon. An estimate was made of whether or not vessel wall contrast staining occurred in the region of the dissection. As well as measuring stenosis severity after PTCA with digital calipers, we also assessed the minimum cross-sectional area of the dilated segment by videodensitometry (XR-70, Vanguard Instrument, Melville, New York), with the known diameter of the angioplasty guiding catheter as a calibration reference. Angioplasty was performed with standard techniques and equipment as previously described.1"412 The procedure was considered angiographically successful if the diameter stenosis after PTCA was Ischemic Complications The following were considered ischemic complications of PTCA: death, coronary artery bypass Clinical and Angiographic Variables Unstable angina was defined as angina of recent (<2 months) onset or recent change, including angina present at rest. The number of diseased coronary arteries was defined as the number of major epicardial coronary arteries or their major branches with 50% or more diameter stenosis. Coronary artery obstruction is expressed as percent luminal diameter reduction, which was measured by a digital caliper system and reported as the average of two orthogonal views.10 Because of the difficulty in classifying angiographic evidence of arterial damage as 'intimal tear" or "dissection,"' the term "dissection" is used throughout this paper to refer to any degree of angiographic arterial disruption.

3 Black et at Tear or Dissection After PTCA 1037 FIGURE 2. Angiogram and illustration of a segment of left anterior descending coronary artery after dilatation. Arrows indicate a crescentic extraluminal accumulation of contrast ("cap"). surgery judged necessary because of ischemia, myocardial infarction (rise of creatine kinase to >three times the upper limit of normal for our laboratory together with the presence of some myocardial creatine kinase iso-enzyme, or the development of pathologic Q waves on the electrocardiogram or both), chest pain or electrocardiographic changes resulting in recatheterization, and recurrent chest pain with ischemic electrocardiographic changes. Only those complications that occurred during hospitalization for PTCA were considered. All clinical, angiographic, procedural, and outcome variables were prospectively recorded by physicians on standard forms, audited for completeness, and stored in a computerized data base. Statistical Analysis Discrete variables were compared with the x' or Fisher's exact test where appropriate, and the significance of linear trends was assessed by x2 analysis. Continuous variables were compared between groups by the Student's t test. A probability (p) less than 0.05 was considered significant. Multivariate analysis was performed with multiple logistic regression, including those variables that were significant at thep<0.1 level in the univariate analysis. Analysis was carried out with a commercial statistical package (BMDP Statistical Software). Continuous variables are expressed as mean±sd. For discrete variables, the crossproduct (or odds) ratio was calculated whenp <0. 1 (probability of event occurring when condition exists multiplied by the probability of no event when condition does not exist divided by probability of event when condition does not exist multiplied by probability of no event when condition exists). FIGURE 3. Angiogram and illustration of a segment of left anterior descending coronary artery after dilatation. Arrows indicate a spiral tear.

4 1038 Circulation Vol 79, No 5, May 1989 TABLE 1. Ischemic Events in Patients With Tear or Dissection Event n % Chest pain or electrocardiographic changes without documented vessel closure 19 (1.4) Reclosure documented at repeat catheterization without infarction or bypass surgery 23 (1.7) Non-Q wave myocardial infarction 27 (2.0) Q wave myocardial infarction 27 (2.0) Emergency coronary bypass surgery 48 (3.6) Death 4 (0.3) Total Patients* 120 Total number of patients studied was 1,346. *Individual patients may have 1 or more events. TABLE 2. Correlates of Ischemic Complications in Patients With Tear or Dissection Ischemic Results All Patients Ischemic complications occurred in 120 (9%) of 1,346 patients included in this study (Table 1). The distribution of individual events is as follows: four patients died (0.3%), 48 (3.6%) required emergency coronary bypass surgery, and Q wave myocardial infarction developed in 27 (2%). Death, emergency coronary bypass surgery, or the development of Q wave myocardial infarction occurred in 59 (4%) of the patients. The remaining complications were non-q wave myocardial infarction in 27 patients (2%), vessel reclosure documented at repeat catheterization without myocardial infarction or bypass surgery in 23 (1.7%), and chest pain or electrocardiographic changes without documented vessel closure in 19 (1.4%). Significant univariate correlates of the development of an ischemic complication (Table 2) were unstable angina that was present in 74% of patients who developed a complication compared with 61% of those who did not (p<0.01), total coronary occlusion before angioplasty (47% vs. 38%,p<0.05), diameter stenosis after PTCA (32+18% vs. 26±12%, p<0.001), and minimum luminal cross-sectional area (2.6± 1.4 vs. 3.3± 1.4 mm2,p<0.05, available in 202 patients). These last two variables were also significant correlates of complications when dichotomized (see table). The other clinical and angiographic variables analyzed were not significantly correlated with complications, with the exception of hypertension that was present in 47% of patients with complications compared with 38% of those without (p=0.054). This variable was sufficiently significant to be included in the multivariate analysis. Multivariate correlates of complications (Table 3) were a diameter stenosis after PTCA of 30% or more (p=0.001), total coronary occlusion before PTCA (p=0.037), and the presence of unstable angina before PTCA (p=0.030). Patients Undergoing Detailed Morphologic Analysis There were 11 patients of 96 in this subgroup who experienced ischemic complications after PTCA. One patient died, one required emergency coronary bypass surgery, two required repeat angioplasty for No ischemic Correlate complication (n = 120) complication (n = 1,226) p Odds ratio Age (yr) 57±9 56±10 NS Gender (males) 81 (67) 904 (74) NS... Unstable angina 83 (74) 681 (61) < Hypertension 57 (47) 471 (38) Cigarette smokers* (n=1,315) 80 (69) 828 (69) NS Total occlusion 12 (10) 62 (5) < Lesion length (mm) 8.4± ±4.6 NS Calcified lesions 8 (7) 84 (7) NS Eccentric lesions 66 (55) 644 (53) NS Tortuous site dilated 4 (17) 22 (12) NS... Vessel size (mm, n=202) ±0.52 NS Multivessel disease 42 (35) 391 (32) NS Diameter stenosis after PTCA (%) 32±18 26±12 < Diameter stenosis >30% after PTCA 60 (50) 445 (36) < Minimum calculated cross-sectional area (mm2, n=202) 2.6± < Cross-sectional area <2.0 mm2 (n=202) 13 (11) 52 (4) < Gradient after PTCA (mm Hg, n=1,072) 15.5± ±8 NS... Total number of patients studied was 1,346; numbers in parentheses are percentages. PTCA, percutaneous transluminal coronary angioplasty. *Former or current smokers.

5 Black et al Tear or Dissection After PTCA 1039 TABLE 3. Multivariate Correlates of Ischemic Complications in Patients With Tear or Dissection Correlate Coefficient p (improvement) Diameter stenosis after PTCA >30% Total occlusion before PTCA Unstable angina before PTCA Constant Total number of patients studied was 1,346. PTCA, percutaneous transluminal coronary angioplasty. delayed vessel closure, and seven had recurrent chest pain with electrocardiographic changes. No patients in this group developed myocardial infarction. A number of angiographic and morphologic variables were found to correlate with ischemic events (Table 4). Preprocedural variables associated with complications were total occlusion of the dilated segment before PTCA, which was present in 27% of the patients who developed an ischemic complication compared with 4% of those who did not (p<0.05), and length of the stenosis to be dilated (15±7 vs. 9±5 mm, p<0.02). Routinely recorded variables after PTCA associated with ischemic complications were diameter stenosis of 25% or more (91% of patients with complications vs. 61% of those without, p<0.05; see Figure 4) and calculated minimum luminal cross-sectional area (2.4± 0.7 vs. 3.2±1.4 mm2, p<0.01). The specific morphologic factors that were associated with complications were the length of the dissection (16±10 vs. 7±4 mm, p<0.05), the presence of extraluminal contrast (82% vs. 52%, p=0.056), and videodensitometric cross-sectional area less than 2 mm2 (82% vs. 52%,p=0.056; Figure 5). The length of the dissection was strongly correlated with the likelihood of developing an ischemic complication (p <0.001, Figure 6). Multivariate correlates of complications, in order of importance, were the length of the dissection (p=0.001), diameter stenosis after PTCA of 25% TABLE 4. Clinical and Procedural and Morphologic Correlates of Ischemic Complications in Patients Undergoing Morphologic Analysis Ischemic No ischemic complication complication Odds (n=11) (n=85) p ratio Age (yr) Gender (males) Unstable angina (n=83) Hypertension Total occlusion Lesion length (mm) Lesion length.15 mm Calcified lesions Eccentric lesions Tortuous site dilated Vessel size (mm) Multivessel disease Diameter stenosis after PTCA (%) Diameter stenosis.25% after PTCA Minimum calculated cross-sectional area (mm2) Cross-sectional area <2.0 mm2 Gradient after PTCA (mm Hg, n=69) 61±6 6 (55) 9 (100) 8 (73) 3 (27) 15±7 5 (45) 1 (9) 10 (91) 1 (9) 2.62± (45) 33±8 10 (91) 2.4±0.7 7 (64) 16±9 L,ength of dissection (mm) L,ength of dissection >15 mm 4 (36) L-,ength of dissection >dilatated segment 3 (27) L,ength of dissection >length of lesion 8 (72) vrideodensitometric cross-sectional area <2 mm2 9 (82),xtraluminal contrast ("cap") 9 (82) IIntraluminal filling defect ("tear") 1 (9),piral dissection 1 (9) c 'ontrast staining 7 (64) A total of 96 patients were studied; numbers in parentheses are percentages. PTCA, percutaneous transluminal coronary angioplasty. Clinical and procedural correlate 60±10 NS 54 (64) NS 60 (81) NS 44 (52) NS 3 (4) <0.02 9±5 < (14) < (14) NS 62 (73) NS 12 (14) NS NS 36 (42) NS 29±14 NS 52 (61) < ±1.4 < (32) < ±7 NS Morphologic correlate 7±4 < (4) < (5) < (44) (52) (52) (35) (3.5) NS 44 (52) NS

6 1040 Circulation Vol 79, No 5, May 1989 n= 1/25 2/24 8/47 n= 7/ /35 2/24 CO z us LL c; W. z ui -0 oa z Ob W) 4% 8.3% U Oi O' % <20% k30 DIAMETER STENOSIS POST PTCA (%) FIGURE 4. Bar graph of ischemic events after angioplasty plotted against final diameter stenosis, showing evidence of a trend to increased complication rate as stenosis increases. PTCA, percutaneous transluminal coronary angioplasty. or more (p=0.001), videodensitometric crosssectional area (p=0.013), and the presence of extraluminal contrast (p=0.044) (Table 5). TABLE 5. Multivariate Correlates of Ischemic Complications in Patients Undergoing Morphologic Analysis Correlate Coefficient p (improvement) Length of dissection (mm) Diameter stenosis after PTCA.25% Videodensitometric cross-sectional area <2 mm Extraluminal contrast ("cap") Constant A total of 96 patients were studied. Discussion Variable degrees of intimal and medial and plaque disruption occur during all PTCA procedures but may vary from mild superficial splitting to gross fissuring through the entire medial and plaque mass. Angiographic detection of intimal disruption is relatively insensitive but certainly defines relatively gross changes that are likely to be of hemodynamic significance. Although intimal tear or dissection has for many years been known to predispose patients to ischemic events,2,4 PTCA operators have become aware that vessel closure and myocardial infarction are unusual in initially uncomplicated dissection, and urgent bypass surgery is not mandatory in most cases. Defining which dissections require additional therapy has thus become important. We have shown13 that a rising transstenotic pressure gradient after dilatation is strongly associated with dissection and with ischemic complications and that the absolute gradient, though less predictive of complications, is important. A distinction between "intimal tears" and "medial dissections" has been made by < >3 VIDEODENSITOMETRIC CROSS SECTIONAL AREA POST-PTCA (mm2) FIGURE 5. Bar graph of ischemic events plotted against videodensitometric minimum luminal cross-sectional area after angioplasty. PTCA, percutaneous transluminal coronary angioplasty. the presence of extraluminal contrast persisting at the PTCA site and by extension of the "tear" beyond the confines of the initial lesion.13 In the present study, which focused on the morphologic aspects of arterial disruption, we found that the length of the dissection, the diameter stenosis after dilatation, and the videodensitometric assessment of luminal cross-sectional area were the strongest correlates of ischemic complications. Comparison With Previous Studies Ischemic complications have been reported in approximately 4% of patients undergoing coronary angioplasty and in about 2% after leaving the catheterization laboratory.3'5 In this study, complications occurred in 9% after leaving the catheterization laboratory, reflecting the marked association of intimal tear or dissection with subsequent events. This is in keeping with the finding of Ellis et al from this institution3 of an odds ratio of 5.19 for the development of ischemic complications when tear or dissection is present. Major complications (death, emergency coronary artery bypass surgery, or Q wave myocardial infarction) occurred in 59 patients or 4% of the total. The variables previously found to correlate with ischemic complications after PTCA are female gender, the presence of unstable angina, multivessel coronary artery disease, length and eccentricity of the lesion to be dilated, localization of the lesion at a branch or bend point, and the presence of a high pressure gradient after PTCA or residual stenosis. -7 In the present study, female gender, multivessel coronary artery disease, eccentricity of the stenosis, and localization at a bend point of the artery were not significant correlates of ischemic complications. The implication of this finding is that these clinically or "geometrically" related factors are more likely to correlate with the development of arterial tear or dissection than with ischemic complications per se. The finding that a high transste-

7 Black et al Tear or Dissection After PTCA 1041 n= 0/27 4/44 3/18 4/ Z 40- p= for linear trend FIGURE 6. Bar graph of ischemic events after angioplasty plotted against length of the dissection. Significant linear trend occursfor an increased complication rate as dissection length increases. X 30- z ci % MR, 1S////// < LENGTH OF TEAR/DISSECTION (mm) notic gradient after PTCA was not important in this study may reflect the correlation of high gradient with the presence of dissection.13 On the other hand, the presence of unstable angina and the dilatation of total coronary occlusions were predictive of complications. These findings are more interesting, and in the presence of arterial dissection, the thrombotic activity of the lesion14-16 or the presence of a segment devoid of endothelial cell cover after dilatation of a total occlusion may predispose to subsequent thrombosis and worsening of the hemodynamic situation. The use of anticoagulant therapy in these patients may be more beneficial than has been shown for unselected patients without a large dissection.17 However, the present study, in which heparin use was uncontrolled, was not designed to assess the effects of therapy. Use of Videodensitometry Previous studies show that the technique of videodensitometry may provide a more useful estimate of arterial diameters after angioplasty than caliper measurement or edge detection.18"19 The probable reason for this is the relatively frequent occurrence of indistinct edges after dilatation. In view of the known association after PTCA or smaller diameters with the development of ischemic complications and the difficulties in defining the true borders of the arterial lumen when there is dissection, videodensitometry was used for assessing luminal diameters after PTCA in this study. Indeed, the multivariate model was significantly more predictive of complications when videodensitometric cross-sectional area was included together with caliper measured diameter stenosis. Clinical Implications We have previously examined clinical and angiographic factors associated with the development of acute closure after PTCA,1,3,7 enabling an estimate of the likelihood of complications when selecting patients for angioplasty. As devices and techniques are developed that may prevent acute closure, identifying which patients are at risk of this complication after leaving the catheterization laboratory will be important. This study, which uses all of the clinical and angiographic data available at the completion of the PTCA procedure, suggests that the length of the dissection, together with diameter stenosis after dilatation are most strongly correlated with subsequent ischemic events. Classification as to whether the dissection extended beyond the lesion dilated was less predictive than the absolute length of the dissection. Because dissection length as a continuous measure was linearly correlated with complications, the use of this measurement may be of more value when planning management than the use of the somewhat arbitrary division into "intimal tear" or "dissection" as has been suggested.'3 Videodensitometry seems to provide independent information about the structure of the damaged arterial segmnent, and on-line measurement of stenosis after PTCA with this technique18 may be useful in patients with dissection. Patients with unstable angina or those undergoing PTCA for completely occluded arteries are at increased risk if their arteries develop dissection. Management strategies for these groups of patients warrant further study. References 1. Ellis SG, Roubin GS, King SB III, Douglas JS Jr, Shaw RE, Stertzer SH, Myler RK: In-hospital cardiac mortality after acute closure after coronary angioplasty: Analysis of risk factors from 8,207 procedures. J Am Coll Cardiol 1988; 11: Dorros G, Cowley MJ, Simpson J, Bentivoglio LG, Block PC, Bourassa M, Detre K, Gosselin AJ, Gruentzig AR, Kelsey SF, Kent KM, Mock MB, Mullin SM, Myler RK, Passamani ER, Stertzer SH, Williams DO: Percutaneous transluminal coronary angioplasty: Report of complications from the National Heart, Lung, and Blood Institute PTCA Registry. Circulation 1983;67: Ellis SG, Roubin GS, King SB III, Douglas JS Jr, Weintraub WS, Thomas RG, Cox WR: Angiographic and clinical predictors of acute closure after native vessel coronary angioplasty. Circulation 1988;77: Bredlau CE, Roubin GS, Leimgruber PP, Douglas JS Jr, King SB III, Greuntzig AR: In-hospital morbidity and mortality in patients undergoing elective coronary angioplasty. Circulation 1985;72: Simpfendorfer C, Belardi J, Bellamy G, Galan K, Franco I, Hollman J: Frequency, management and follow-up of patients with acute coronary occlusions after percutaneous transluminal coronary angioplasty. Am J Cardiol 1987;59:267

8 1042 Circulation Vol 79, No 5, May Ischinger T, Gruentzig AR, Meier B, Galan K: Coronary dissection and total coronary occlusion associated with percutaneous transluminal coronary angioplasty: Significance of initial angiographic morphology of coronary stenoses. Circulation 1986;74: Meier B, Gruentzig AR, Hollman J, Ischinger T, Bradford JM: Does length or eccentricity of coronary stenoses influence the outcome of transluminal dilatation. Circulation 1983;67: Sigwart U, Puel J, Mirkovitch V, Joffre F, Kappenberger L: Intravascular stents to prevent occlusion and restenosis after transluminal angioplasty. N Engl J Med 1987;316: Roubin GS, Robinson KA, King SB III, Gianturco C, Black AJ, Brown JE, Siegel RJ, Douglas JS Jr: Early and late results of intracoronary arterial stenting after coronary angioplasty in dogs. Circulation 1987;76: Scoblionko DP, Brown BG, Mitten S, Caldwell JH, Kennedy JW, Bolson EL, Dodge HT: A new digital electronic caliper for measurement of coronary arterial stenosis: Comparison with visual estimates and computer-assisted measurements. Am J Cardiol 1984;53: Roubin GS, Gruentzig AR, Casarella WJ: Percutaneous coronary angioplasty: Technique, indications and results. Cardiovasc Intervent Radiol 1986;9: Black AJR, Anderson HV, Roubin GS, Powelson SW, Douglas JS Jr, King SB III: Repeat coronary angioplasty: Correlates of a second restenosis. J Am Coll Cardiol 1988;11: Redd DCB, Roubin GS, Leimgruber PP, Abi-Mansour P, Douglas JS Jr, King SB III: The transstenotic pressure gradient trend as a predictor of acute complications after percutaneous transluminal coronary angioplasty. Circulation 1987;76: Ambrose JA, Winters SL, Stern A, Eng A, Teichholz LE, Gorlin R, Fuster V: Angiographic morphology and the pathogenesis of unstable angina pectoris. JAm Coll Cardiol 1985;5: Bresnahan DR, Davis JL, Holmes DR, Smith HC: Angiographic occurrence and clinical correlates of intraluminal coronary artery thrombus: Role of unstable angina. J Am Coll Cardiol 1985;6: Gotoh K, Minamino T, Katoh 0, Hamano Y, Fukui S, Hori M, Kusuoka H, Mishima M, Inoue M, Kamada T: The role of intracoronary thrombus in unstable angina: Angiographic assessment and thrombolytic therapy during ongoing anginal attacks. Circulation 1988;77: Ellis SG, Roubin GS, Wilentz J, Lin S, Douglas JS Jr, King SB III: Results of a randomized trial of heparin and aspirin vs. aspirin alone for prevention of acute closure and restenosis after angioplasty (abstract). Circulation 1987;76(suppl IV):IV Tobis J, Nalcioglu 0, Johnston WD, Qu L, Reese T, Sato D, Roeck W, Montelli S, Henry WL: Videodensitometric determination of minimum coronary artery luminal diameter before and after angioplasty. Am J Cardiol 1987;59: Nichols AB, Berke AD, Han J, Reison DS, Watson RM, Garcia B, Powers ER: Comparison of cinevideodensitometric and caliper measurements of coronary stenosis after angioplasty (abstract). JAm Coll Cardiol 1987;9:196A KEY WORDS * PTCA * acute closure

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