Predicting lschemic Complications Failed Coronary An@oplasty
After Bailout Stenting
Following
Damien Metz, MD, Philip Urban, MD, Vincent Hoang, MD, Edoardo Camenzind, MD, Pascal Chatelain, MD, and Bernhard Me/er, Mb schemic complications of percutaneous transluminal I4%coronary angioplasty (PTCA) occur in approximately of patients1 Acute vessel occlusion is estimated to occur in 2% to 11% of all PTCA procedures, and is a major cause of in-hospital related death, myocardial infarction, and emergency coronary artery bypass graft surgery (CABG).1,2 Flow interruption is usually caused by an occlusive dissection together with varying degrees of spasm,local thrombosis, and elastic recoil.3 If immediate repeat prolonged PTCA is unsuccessful, several complementary techniques may be used to attempt to restore anterogradeflow4 such asperfusion balloon catheters,5 intracoronary stenting,6 or CABG.7 Coronary stenting as a bailout procedure was lirst reported by Sigwart et al in 1987,6and has gained growing acceptance as the best alternative to CABG for a majority of cases.8-14A variety of stent designs have been developed to scaffold the arterial wall, normalize vessel lumen, and restore coronary flow after coronary disruption or occlusion.8-14However, the occurrence of ischemic events after stent implantation remains a problem,“-*3 particularly after bailout stent insertion,14,15 and may be a major cause of in-hospital morbidity and mortality.8-15 This study was therefore performed to identify in our singlecenter experience the risk factors that predispose to ischemic complications after bailout stent implantation for unsuccessful PTCA. Between April 1988 and June 1993, 3,041 patients underwent PTCA. During this period, we attempted emergencycoronary stent implantation for coronary dissection in 105 patients (3%). Four patients (4%) were not considered for the present study because of failed stent implantation (1 stent misplacement and 3 failures to reach the lesion). Therefore,the studypopulation comprised 101 patients (88 men [87%] and 13 women [13%], mean age 61 f 9 years). Initial indication for PTCA was unstable angina in 62 patients (61%), stable angina in 13 patients (13%), ongoing myocardial infarction in 2 patients (2%), and angina after acute myocardial infarction in 24 patients (24%). Mean lef ventricular ejection fraction determined from the pre-PTCA angiogram was 65 f 10%. Multivessel coronary artery diseasewaspresent in 43 patients (43%) (29 with 2-vesse1and 14 with 3-vessel disease}. All cineangiograms were reviewed by 2 experienced interventional cardiologists unaware of the clinical outcome. Lesions before and after PTCA were measured with calipers and classijied.t6-t8 Length of dissection, using the length of the inflated balloon for calibration, was also considered in the analysis. From the Cardiology Center, University Hospital, 1211 Geneva 14, Switzerland. Manuscript received October 25, 1993; revised manuscript received January 24, 1994, and accepted January 26.
Coronary angioplasty was pegormed according to current clinical practice. All patients were receiving either long-term aspirin 100 mglday or intravenous aspirin 250 to 500 mg before the PTCA procedure. Full heparinization was established with an intravenous bolus of 10,000 to 20,000 U. Intravenous nitroglycerin (2 to 6 mglhour) was administered if unstable angina occurred. PTCA was peformed using 6Fr to 9Fr guiding catheters, and 0.014- to 0.021-inch guidewires. The balloon catheters were predominantly of monorail design. Bailout stent implantation was performed when angiographic coronary artery dissection (with either established occlusion or angiographic appearancessuggestive of a high risk of subsequentocclusion) developed after PTCA. Chest pain was present in 79% of patients and significant intracoronary ST-segmentchanges in 90%.t9 Before proceeding to stenting, repeat prolonged inflations with the sameballoon catheter,or a larger one if needed, was always attempted. A perfusion balloon catheter was not routinely used.If the dissection proved refractory to repeat inflations, and the coronary anatomy was considered suitable for stenting, without contraindication for intensive short-term anticoagulation, bailout stent implantation was attemptedafter obtaining informed consent. Intravenous urokinase (0.5 to 1 million U) was given to 54 patients (53%) before or after stent implantation when thrombus was thought to play a major role. When a decision was made to proceed with stenting, heparin was supplementedif needed,aiming for an activated clotting time level of >300 seconds.A dextran infusion was given occasionally, principally in our early experience.Articulated Palmaz-Schatzballoon expandable stents, manually crimped onto the previously used monorail balloon, were usedin 82 patients (81Yo).A selfexpandable stent (Wallstent Medinvent) was used in 16 patients (16%) and a Wiktor or Gianturco-Roubin stent was usedfor 2 (2%) and 1 (1Yo)patient, respectively. Complete cover of the dissection site with the prosthesis was usually attempted. After implantation, further balloon inflations were generally performed to optimize the angiographic appearance and smooth inflow and outflow irregularities. Different approaches to puncture site hemostasiswere used over time: either the arterial sheath was taken out when the activated clotting time reached 1.50 to 180 seconds, and hemostasis was achieved with external compression alone, or, more recently, the sheath was sometimeswithdrawn immediately after completing the procedure (n = 32), and local hemostasiswas then achieved with a combination of a collagen-sealing device (Vasoseaf”, Datascope) and an external compressionsystem(Femostop’“, Radi Medical Systems).A heparin infusion was begun to obtain a partial thromboplastin time of 55 to 70 secondsor an activated clotting time of 180 to 220 seconds,or both. Oral BRIEFREPORTS 271
TABLE I Baseline Clinical Characteristics Angioplasty
Age Men Unstable angina LVEF (%) Multivessel coronary disease
TABLE Ill Clinical and Angiographic Characteristics Stent Implantation
Before Balloon
Group I (n = 28)
Group II (n = 73)
Odds Ratio*
61 f10 22 (79%) 21 (75%) 66 f 13 13 (46%)
61 +9 66 (90%) 41 (56%) 64 f 9 30 (41%)
0.4 2.3 1.2
l Univariate. LVEF = left ventricular ejection fraction mean.
TABLE II Baseline Angiographic Characteristics loon Angioplasty
Coronary artery Left anterior descending Left circumflex Right Lesion type AHAIACC A Bl 82 C Nominal balloon diameter (mm) Reference vessel diameter (mm) Stenosis (%) Restenosis TIMI grade O-l flow Previous myocardial infarction Coronary thrombus
Before Bal-
Group I (n = 28)
Group II (n = 73)
Odds Ratio”
14 (50%) 5 (18%) 9 (32%)
43 (59%) 7 (10%) 23 (32%)
0.7 2.0 1 .o
3 (11%) 10 (36%) 6 (21%) 9 (32%) 3.1 + 0.3
7 (10%) 21 (29%) 23 (32%) 22 (30%) 3.1 * 0.3
1.1 1.7 0.6 1.2 -
3.2 + 0.3
3.1 f 0.3
-
87 + 9 3 (11%) 1 (4%) 8 (29%)
88+9 5 (7%) 4 (6%) 18 (25%)
1.6 0.64 1.3
5 (18%)
15 (21%)
0.9
Pain TIMI O-2 flow Dissection morphology lntraluminal Extraluminal Spiral Dissection class (NHLBI classification) B C D E F Length (mm) Length >20 mm Collateral vessels
Before Odds Ratio* (95% Cl;
Group I (n = 28)
Group II (n = 73)
V&e
24 (86%) 20 (71%)
55 (75%) 36 (49%)
NS <0.05
1.9 2.6 (1.4-4)
13 (46%) 7 (25%) 8 (29%)
41 (56%) 23 (32%) 9 (12%)
NS NS NS
0.7 0.7 2.8
5 (18%) 3 (10%) 5 (18%) 8 (29%) 7 (25%) 29 f 23 16 (57%)
23 (32%) 14 (19%) 9 (12%) 12 (16%) 13 (18%) 15+11 19 (26%)
NS NS NS NS NS <0.0005
2 (7%)
3 (4%)
NS
0.4 0.5 1.5 2.0 1.5 3.6 (1 h9.2) 1.8
Wnivariate. Cl = confidence interval; NHLBI = National Heart, Lung, and Blood Institute; TIMI = Thrombolysis in Myocardial Infarction trial.
anticoagulation (acenocoumarol)and dipyridamole (225 mglday) therapy was begun on the evening of the stent implantation and given for 3 to 6 months. Heparin was continued until the international normalized ratio was >2.3. Complete bed rest was maintained for 48 hours. Aspirin (100 mglday) was continued indejmitely. Stent implantation was considered technically successful tf the stent could befully deployed within the target lesion. Angiographic successwas defined as a technically successfulimplantation with no residual stenosis >50% and normal flow. An ischemic event was defined as the occurrence of either Q-wave or non-Q-wave myocardial infarction, the needfor CABG, or death during the hospital postprocedure period. Non-Q-wave myocardial infarction was defined as the occurrence of chest pain associated with elevation in creatine kinase above twice the upper limit of normal. Data concerning the clinical in-hospital course was obtained from prospectively collected data of all interventional procedures. Several technical and angiographic parameters were included in the analysis and are listed in Tables I to IV Stent implantation was defined as deferred ifperformed after the patient had initially left the catheterization lab-
oratory. Occlusion of a signij?cant side branch artery was defined as an artery with an initial vesseldiameter of >I .5 mm with flow grade ~3 after stent implantation according to the Thrombolysis In Myocardial Infarction (TIM) trial. Continuous data are presented as mean f 1 SD. Comparisons of group differences were performed by using chi-square analysis (with Yates’ correction when necessary)for discrete variables and Student’s t testfor continuous variables. The odds ratio (cross-product ratio) of discrete variables obtained with univariate analysis are presented with their 95% confidence interval when thep value was consideredsignificant at ~0.05. Using the occurrence of ischemic events as the dependent variable, we performed multivariate analysis with multiple logistic regression--including the significant variables at the p
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‘Univariate. ACC = American College of Cardiology: AHA = American Heart Association: TIMI = Thrombolysis in Myocardial Infarction trial.
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TABLE
IV Technical Characteristics
of Stenting Procedure Odds Ratio* (95% Cl)
Group I (n = 28)
Group II (n = 73)
p Value
Deferred implantation
11 (39%)
8 (11%)
<0.005
Dissection not entirely covered Occluded side branch
15 (54%)
19 (26%)
co.005
12 (43%)
5 (7%)
<0.0001
Residual thrombus
4 (14%)
3 (4%)
NS
Number of stents Implantation of multiple stents Stented segment diameter (mm) Heparin dose (U)
1.5 I 0.7 11 (39%)
1.o f 0.3 6 (8%)
<0.0001 <0.0005
2.7 rt 0.9
3.1 + 0.3
40.005
5.2 (1.8-15.2) 3.3 (1.3-8.3) 10.4 (3.1-34.5) 3.8 (1.0-13.7) 6.8 (3.8-12) -
17,700 f 4,970
19,600 f 4,700
NS
-
‘Univariate. Cl = confidence interval.
lation protocol (group I [18%] vs group II [26%], p = NS). There were 2 cases of intracranial hemorrhage associated with the use of thrombolytic therapy, 1 with moderate long-term neurologic impairment and 1 with a fully reversible deficit, and 2 cases of retroperitoneal bleeding, both requiring transfusions and 1 contributing to the death of an 83-year-old patient. Baseline characteristics are summarized in Tables I and II, and did not differ significantly in both groups. By univariate analysis, TIM grade 0 to 2fiow just before stenting and a long dissection length were identified as predictors of ischemic events. Using 20 mm {the length of a balloon) as a cutoff value, a signijicant difference between groups I and II was also observed (Table III). Several procedural variables were identified as predictors of an ischemic event: delayed bailout stent implantation, incompletely covered dissection, occluded side branch, number of implanted stents,and stentedsegment diameter (Table IV). By multivariate analysis, only 3 variables were sign@cant independent risk factors for in-hospital ischemic complications after bailout stenting: deferred stent implantation (odds ratio [OR] 14.9, confidence interval [CI] 2.8 to 80; p
clinical decision-making regarding the possible indication for urgent or semielective bypass surgery9J2y21 None of the clinical and angiographic variables before PTCA had a predictive value for ischemic events after stenting. Pre-PTCA unstable angina, recent myocar-dial infarction, and angiographic presence of intracoronary thrombus did not significantly increase the ischemic event rate, although all of these factors could potentially favor thrombus formation within the stent. The risk with pre-PTCA unstable angina remains controversial.10J4’15 Our data differ from those reported by Haude et all4 and Nath et a1,15but these investigators included both elective and bailout stent implantation in their analysis. Herrmann et allo found no increase in complications after bailout stenting. Pre-PTCA lesion morphology according to the American Heart Association/American College of Cardiology classification was without predictive value in our series, and ischemic events also occured irrespective of dissection morphology and class prior to stent implantation. Dissection length remains a persistent predictive factor with an increasedrisk for dissection of >20 mm: Complete cover of the flap becomestechnically more difficult to perform, and multiple stents are generally required. These 2 dependentvariables have also been recognized as predictors of acute thrombosis by other authors.i3J4Contrary to Herrmann et al, however, we did not lind the presenceof intrastent thrombus at the end of the procedure to predict subsequent complications,tO probably becauseit was observed infrequently. Our study suggeststhat delay in bailout stenting is correlated with an increasedrisk of ischemic events.This is in agreementwith previous reports, showing that the peak creature kinase level and infarction rate increase with the time to stent placement after abrupt vessel closure complicating PTCA. 22,23In our series, deferred stent implantation was associated with a non-Q-wave myocardial infarction in 55% of the cases.The interval between PTCA and subsequentbailout stenting representsthe time required to return a patient to the catheterization laboratory, and partially explains the higher incidence of TIMI grade 0 to 2 flow rate before stenting in BRIEFREPORTS 273
the group with a subsequent increase in creatinine kinase. These data suggest that when the patient is an appropriate candidate and the coronary anatomy is suitable, bailout stenting should be attempted immediately after failed PTCA or threatened closure.8,22,23 An individual decision must of course be made for each patient, taking into particular account ischemic complications that would be associatedwith the unsatisfactory PTCA result if left untreated.19,24 In conclusion, even when our early experience is included, overall results of bailout stenting make it an attractive alternative to emergent CABG after failed balloon angioplasty. Early bailout stenting is less likely to be associated with in-hospital ischemic events than deferred procedures. A poor angiographic result, particularly in long lesions with multiple stent implantation, should prompt consideration of semielective surgery. 1. Detre KM, Holmes DR Jr, Holubkov R, Cowley MJ, Bourassa M, Faxon DP, Dorms GR, Bentivoglio LG, Kent KM, Myler RK, and co-investigators of the National Heart, Lung, and Blood Institute’s Percutaneous Transluminal Coronary Angioplasty Registry. Incidence and consequences of periprocedwal occlusion: the 1985-1986 National Heart, Lung, and Blood Institute Percutaneous Transluminal Coronary Angioplasty Registry. Circulation 1990;82:739-750. 2. Simpfendorfer C, Belardi J, Bellamy G, G&m K, Franc0 I, Hollman J. Frequency, management, and follow-up of patients with acute coronary occlusions after percutaneous transluminal coronary angioplasty. Am .I Cardiol 1987;59:267-269. 3. Ellis SG, Roubin GS, King SB III, Douglas JS Jr, Weintraub WS, Thomas RG, Cm WR. Angiographic and clinical predictors of acute closure after native vessel coronary angioplasty. Circulation 1988;77:372-379. 4. Scott NA, Weintraub WS, Carlii SF, Tao X, Douglas JS Jr, Lembo NJ, King SB III. Recent changes in the management and outcome of acute closure after percutaneous tmnsluminal coronary angioplasty. Am J Cardiol 1993;7 1: 1159-l 163. 5. Leitschuh ML, Mills RG, Jacobs AK, Ruocco NA, LaRosa D, Faxon DP. Outcome after major dissection during coronary angioplasty using the perfusion balloon catheter. Am .I Cardiol 1991;67:10561060. 6. Sigwat U, Puel J, Mirkovitch V, Joffre F, Kappenberger L. Intravascular stats to prevent occlusion and restenosis after transluminal angioplasty. N Engl J Med 1987;316:701-706. 7. Talky JD, Weintmub WS, Roubii GS, Douglas JS, Anderson HV, Jones EL, Morris DC, Liberman HA, Craver JM, Guyton RA, King SB III. Failed elective percutaneous transluminal coronary angioplasty requiring coronary artery bypass surgery. In hospital and late clinical outcome at 5 years. Circulation 1990;82: 1203-1213. 6. Roubin GS, Cannon AD, Agmwal SK, Macander PJ, Dean LS, Baxley WA, Breland J. Intracoronary stating for acute and threatened closure complicating percutaneous tmnslnminal coronary angioplasty. Circulation 1992;85:916-927.
9. De Feyter PJ, DeScheerder ID, van den Brand M, Laannan G, Suryapranata H, Sermys PW. Emergency stenting for refractory acute coronary artery occlusion during coronary angioplasty. Am J Cardiol 1990;66: 1147-l 150. 10. Hemnann HC, Buchbinder M, Clemen MW, Fischman D, Goldberg S, Leon MB, Schatz RA, T&stein P, Walker GM, Hirshfeld JW Jr. Emergent use of balloon-expandable coronary artery stating for failed percutaneous txmsluminal corenary angioplasty. Circulation 1992;86:812-819. 11. Haude M, Erbel R, Straub U, Dieti U, Schatz R, Meyer J. Results of intracoronary stats for management of coronary dissection after balloon angioplasty. Am J Cardiol 1991;67:691696. 12. Kiemeneij F, Laarman GJ, van den Wieken R, Sunuarganda J. Emergency corenary stenting with the Palmaz-Schatz stent for failed transluminal coronary angioplasty: results of a learning phase. Am Heart J 1993;126:23-31. 13. George BS, Voorhees WD III, Roubin GS, Fearnot NE, Pinkerton CA, Raizner AE, King SB III, Holmes DR, Top01 EJ, Kereiakes DJ, Hart&r GO. Multicenter investigation of coronary stating to treat acute or threatened closure after percutaneous transluminal coronary angioplasty: clinical and angiographic outcome. J Am Coil Cardiol 1993;22:135-143. 14. Haude M, Erbel R, Issa H, Stmub U, Rupprecht HJ, Treese N, Meyer J. Subacute thrombotic complications after intracoronay implantation of Palmaz-Schatz stats. Am Heart J 1993;126:15-22. 15. Nath FC, Muller DWM, Ellis SG, Rosenschein U, Chap&is A, Quain L, Zimmerman C, Top01 EJ. Thrombosis of a flexible coil coronary stent: frequency, predictors and clinical outcome. J Am CON Cardiol 1993;21:622-627. 16. Ryan TJ, Faxon DP, Gunnar RM, Kennedy JW, King SB III, Loop FD, Peterson KL, Reeves TJ, Wiiliams DO, Winters WL. Guidelines for percutaneous trans. luminal angioplasty: a.report of the ACC/AHA Task Force on assessment of diagnostic and therapeutic cardiovascular procedures (subcommittee on PICA). J Am Cd Cardial 1988;12:529-545. 17. Chesebro JH, Knatterud G, Roberts R, Borer J, Cohen LS, D&n J, Dodge HT, Francis CK, Hillis D, Ludbrook P, Markis JE, Mueller H, Passamani ER, Powers ER, Rae AK, Robertson T, Ross A, Ryan TJ, Sobel PE, Willerson J, Williams DO, Zaret BL, Braunwald E. Thrombolysis In Myocardial Infarction (TIMI) trial, phase I: a comparison between intravenous tissue plasminogen activator and inbavenous streptokinase. Clinical findings through hospital discharge. Circulation 198276: 142-154. 16. Coronary artery angiogmphic changes after percutaneous transluminal cornnary angioplasty: manual of operations. National Heart, Lung, and Blood Institute Registry, 1985-1986: Baseline form:9. 19. Pande AK, Meier B, Urban P, Moles V, Dorsaz PA, Favre J. Intracoronay electrocardiogram during coroniuy angioplasty. Am Heart J 1992124337-341, 20. Metz D, Urban P, Camenzind E, Chat&in P, Hoang V, Meier B. Improving the results of bail-out coronary stewing after failed balloon angioplasty. Cathet Cardiovasc Diagn 1994; in press. 21. Roubin GS, King SB III, Douglas JS Jr, Lemba NJ, Robinson KA. Intmcoronary stating during percutaneous tmnsluminal coronary angioplasty. Circulation 1990;81(suppl IV):IV92-IV-100. 22. Lincoff MA, Top01 EJ, Chap&is AT, George BS, Candela RJ, Muller DW, Zimmerman CA, Ellis SG. Intracoronary stating compared with conventional therapy for abrupt vessel closure complicating coronary angioplasty: a matched case control study. JAm Co11 Cardiol 1993;21:86&875. 23. Urban P, Sigwat U. The self-expanding mesh stat. In: Sigwart U, Frank GI, eds. Coronary Stats. Berlin: Springer Verlag, 1992:21-. 24. Huber MS, Mooney JF, Madison J, Mooney MR. Use of a morphologic classification to predict clinical outcome after dissection from coronary angioplasty. Am .I Cardiol 1991;68:467471.
Elective Placement of the Wiktor Stent After Coronary Angioplasty Christopher J. White, MD, Stephen R. Ramee, MD, and Tyrone J. Collins, MD ability to maximize the artery’s luminal diameter.2,3The Wiktor stent (Medtronic Interventional Vascular, San Diego, California) is one of several metallic stents in stents is to enhance the long-term patency rate of dilat- either clinical use or in clinical trials.4-15This stent is ed coronary arteries after angioplasty by reducing the composed of a single strand of tantalum wire, which is incidence of restenosis.It has been suggestedthat stents 0.005 inches in diameter, wound in a semihelical coil might have a favorable effect on restenosisbasedon their and tightly crimped on a conventional angioplasty balloon for delivery (Egure 1). The stent is 17mm in length and is mounted on a 2.5 cm long delivery balloon From the Section of Cardiology, Department of Internal Medicine, (PrimeTM,Medtronic Interventional Vascular) without a Ochsner Clinic and Alton Ochsner Medical Foundation, 1514 Jefferson covering sheath. This pilot study examines the feasibilHighway, New Orleans, Louisiana. Dr. White’s address is: Health Care ity of elective stent placement in native coronary arterInternational, Beardmore Street, Clydebank, Scotland G814DY. Manuies in patients believed to be at increasedrisk for recurscript received November 22, 1993; revised manuscript received and rent stenosis after angioplasty. accepted January 20, 1994. linical indications for vascular stents have been sought since the initial description of a stent implanC tation by Dotter in 1969.l One potential application of
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