Transcatheter therapy of thrombotic-occlusive lesions in saphenous vein grafts

transcatheter Occlusive Felipe

therapy of ThromboticLesions in Saphenous Vein Grafts

A. Ceceiia,

MD, and

David

H. Hoelzinger,MD

Saphenous vein graft (SVG) disease, a form of accelerated atherosclerosis, remains a therapeutic conundrum. The use of stents after excluding the presence of thrombus has proved highly successful at short- and long-term follow-up. We report on 60 severely symptomatic patients with multiple subtotal and total thrombotic SVG occlusions who were treated with a combination of intragraft urokinase-verapamil infusion and insertion of multiple biliary stents. Stent deployment had a 100% success rate. No case of clinical subacute thrombosis

was registered, and major in-hospital complications were uncommon (< 1%). The clinical outcome was encouraging, with a 12-month event-free survival rate of 87% in the 57 evaluable patients. This method of therapy appears to be highly successful in the treatment of thrombus-containing occlusive SVG disease, in preventing the “no-reflow” phenomenon, and in lessening1 the incidence of periprocedural non-Q-wave myocardial infarction. (Am J Cardiol 1996;78:3 l-36)

eoperation has historically been the therapy for aphenous vein graft (SVG) disease, but the Rs considerable risk, complications, technical diffi-

(80%) had severe (class III or IV) angina. The patient inclusion criteria included the presence of angina pectoris, no contraindication to anticoagulation therapy (acetylsalicylic acid, dextran, dipyridamole, ticlopidine, heparin, and warfarin) , and the presence of thrombus at angiography with a total occlusion (Thrombolysis in Myocardial Infarction [ TIMI] 0 to I) or functional/subtotal thrombotic multiple lesions (TIM1 II) (Table 11). The anatomic entry criteria included aorto-ostial stenoses (Figure 1) , diffuse long ( > 15 mm) lesions, ulceration (Figure 2)) tandem lesions, and total occlusions. Informed consent was obtained from all pati’ents according to the guidelines of the institutional review board of the St. Luke’s Medical Center. Urokinase infusion: The SVGs to the left coronary artery system were systematically approached u,sing a 10Fr hockey-stick guiding catheter and the grafts to the right coronary artery with a 1OFr multipurpose guide. Intravenous meperidine 25 mg, an intragraft bolus of 500,000 IU of urokinase, and 200 pg of verapamil given over 5 minutes preceded guidewire advancement. A 0.014-inch high-torque guiding wire (S’E’ort; Advanced Cardiovascular Systems, Santa Clara, California) was advanced to cross the lesion(s), and over this guiding wire, an intracoronary infusion cathleter (Tracker- 18 side-holes; Target Therapeutics, Fremont, California) was positioned within the graft covering the length of the lesion(s). A continuous infusion of urokinase was started at a rate of 150,000 IU/hour through the infusion catheter (distal) port and 20..000 II-I/hour through the guiding catheter (proximal) port, and maintained for 8 to 12 hours. Angiogralphy was performed before removing the infusion system through the guiding catheter port. Twenty patients received 8 hours of infusion of urokinase for a total of 1,360,OOO IU; 40 patients received 12 hours of urokinase for a total dose of 2,040,OOO IU. A heparin bolus and drip was used during ulrokinase infusion to keep the partial thromboplatstin

culties, and high cost have prompted some investigators to develop alternative treatments, such as percutaneous transluminal coronary angioplasty, ‘9’ directional 3,4 or extraction’ atherectomy, and excimer laser angioplasty.6 Unfortunately, all of these treatment strategies are limited by a considerable periprocedural complication rate and a high incidence of restenosis.7-” With the advent of stents, 13,14balloon-expandable and self-expanding, the treatment of focal and, frequently, more unfavorable SVG lesions has produced significantly better short- and long-term clinical results, I5 although early occlusion has been a problem in some series.” The remaining challenge is the treatment of the SVG totally occluded by a large thrombus obliterating ~1 stenotic lesion throughout the extent of the graft. Preliminary work on the treatment of these lesions by combined stenting and thrombolysis has yielded good results.16 We present our experience in 60 patients with chronic total occlusions of SVGs that were recanalized by long-term infusion of urokinase and treated with biliary tubular slotted stents.

METHODS Study patients: From May 1993 to May 1995, 60 consecutive symptomatic patients (55 men and 5 women; mean age 65 + 9 years) having 147 lesions were treated with intragraft urokinase (Abbokinase@; Abbott Laboratories, North Chicago, Illinois) infusion and the Palmaz (biliary) tubular slotted stent (Johnson & Johnson Interventional Systems, Warren, New Jersey) (Table I). Most patients From the “Charles A. Barrow” Heart Lung Center, St. Luke’s Medical Center, Phoenix, Arizona. Manuscript received October 4, 1995; revised manuscript received and accepted January 9, 1996. Address for reprints: Felipe A. Cece?ra, MD, 4444 North 32rd Street, No. 230, Phoenix, Arizona 85018.

0 1996 by Excerpto All rights reserved.

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Inc

0002.9149/96/$15.00 PII SOOO2-9149(96)00190-7

31

TABLE

I Baseline

Clinical

Characteristics

of

60

Patients

Number

Characteristics Angina class* I II III IV Recent myocardial Diabetes mellitus Systemic hypertension Hypercholesterolemia

(%)

0 12 (20) 21 (35) 27 (45) infarction+

9 (151 12 (20) 33 27

(>220

mg/W Age of graft (mean 2 SD mos) Mean (+SD %) left ventricular ejection fraction l Unstable angina pain, including pain + Recent myocordiol * Hypercholeskrolemia

of Patients

(55) (45)

100249 0.38 -t 0.12

= recent increase in frequency and intensity of the chest at rest. infarction = ~6 weeks. = serum cholesterol > 220 mg/dl or history of onti-

lipidemic therapy. The age of the sophenous vein graft was calculated from the date of bypass graft surgery. Saphenous vein graft lesions not previously treated with endovascular

procedures

were classified

QS de nova.

time between 60 and 90 seconds. Fibrinogen was maintained at > 120 mg/dl. Stent deployment: The biliary stent, approved by the U.S. Food and Drug Administration Advisory Panel in February 1991 for the treatment of biliary tract disease, has been used extensively in patients with SVG stenoses >50% diameter with an estimated reference vessel diameter >4.0 rnm.15 Hockey-stick or multipurpose guiding catheters (10Fr) were routinely used. A 0.016inch S’Port wire was advanced to the distal grafted coronary artery. The lesion(s) was predilated using an angioplasty balloon (Synergy, Mansfield, Watertown, Massachusetts) 1.0 or 1.5 mm smaller than the reference lumen diameter of the SVG catheter before inflation. Through the central lumen of this catheter, urokinase 250,000 IU was given as a bolus, and verapamil 400 I-18 was administered over 5 minutes. After predilatation, a 4.0 to 6.0 mm (20 mm length) Schwarten LP (PSG) dilatation system was used to deliver a 10 mm ( P104) manually crimped biliary stent. If the lesion was long enough to require multiple stents, these were delivered 1 by 1 from the distal to the proximal lesion area, each being overlapped with the adjacent stent for 1 to 1.5 mm. An average of 3 stents was used per patient. After final dilatation using a noncomplaint highpressure balloon, all stents were interrogated by intravascular ultrasonography. A 2.9Fr 30 MHz monorail ultrasound catheter (CVIS, Sunnyvale, California) was used exclusively. The criterion for optimal stent expansion was an intrastent vessel cross-sectional area at least as great as the cross-sectional area of the distal reference lumen.17 Anticoagulation protocol: Antithrombotic therapy was given before and after stent deployment in our first 35 patients, as has been routine with this stent.” These patients received acetylsalicylic acid 325 mg, dipyridamole 75 mg 3 times daily, and a calcium 32

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FIGURE

1. After thrombolysis, marginal branch displayed sion with ulcerated plaque treated with single Palmaz 2 overlapped biliary stents

saphenous vein graft to obtuse critical o&al lesion and proximal [Hack arrows). O&al lesion was biliary stent and proximal lesion (open arrows).

lewith

antagonist in the 24 hours preceding stent placement. Intravenous dextran-40 (100 ml/hour) was started 2 hours before the procedure and then maintained at 50 ml/hour until a therapeutic heparin dosage (partial thromboplastin time >50 seconds) was achieved after sheath removal. Intravenous heparin ( 10,000 to 15,000 IU) was given to maintain a transprocedure activated clotting time between 250 and 290 seconds. Sheaths were,removed using the Femostop device (USCI) immediately after the procedure when the activated clotting time was <150 seconds. Continuous intravenous heparin was restarted 6 hours after sheath removal and continued until the prothrombin time international normalization rate (INR) was between 2.5 and 3.5 using warfarin. Patients were maintained on acetylsalicylic acid, dipyridamole, warfarin, and the calcium antagonist for 3 months and then on acetylsalicylic acid continuously. In our next 25 patients, dipyridamole and dextran40 were eliminated. In patients who had lesser amounts of thrombus (type III), in whom no thrombus was visible (type I) at angiography after intragraft urokinase infusion, and in whom interrogation by intravascular ulrrasonography showed optimal stent deployment, I7 heparin was not restarted after sheath removal. These patients were treated with TABLE

II

Thrombus

Type Type Type Type

1 II Ill IV

Type

V

From Research

Burden

Classification

No visible Possible Definite Definite Definite Protocol

M95-283:

thrombus thrombus thrombus < 1 cm in length thrombus l-2 cm in length thrombus > 2 cm in length Initial

reconolizotion

of occluded

vein by-

pass grafts with introcoronary infusion of urokinase (recombinant, human). A thrombus was defined as the presence of a noncalcified filling defect circumferentiolly outlined by contrast on 1 3 sides (see Ref. 12). On the basis of previous pathologic studies, totally occluded grafts were presumed to contain thrombus.

JULY 1, 1996

FIGURE 2. Treatment of ulcerated saphenous vein graft (SVG). A, graft to right coronary artery has thromhotic total occlusion bvbite arrow] after successful angioplasty. B, recanalization of SVG after urokin&e’ bolus. Open arrow marks site of anaioolastv. C, after 12-hour urokinase drip, ulcer%d plaque (white arrow) is apparent. f5; after insertion of 3 biliary stems. Two were deployed overlapped /b/a& arrow) with single 10 mm stent (open arrow) covering ulcerated plaque. E, fully recanalized SVG.

acetylsalicylic acid 325 mg twice daily for 5 days and ticlopidine 250 mg twice daily. Thereafter, acetylsalicylic acid was given in a dose of 325 mg once daily and the ticlopidine dosage remained unchanged for 3 months; at that time, ticlopidine was discontinued and acetylsalicylic acid was continued. In patients with a heavy burden of thrombus (type IV or V) before urokinase infusion, even though angiography showed no thrombus after urokinase infusion, heparin was restarted after sheath removal and continued until the prothrombin time (INR) was between CORONAW

2.5 and 3.5 with the use of warfarin. Patients continued to receive acetylsalicylic acid and warfarin for 3 months. Angiographic analysis: The single view that identified the most severe stenosis (“worst view”) was selected for quantitative analysis by the senior author and an independent observer. Standard qualitative morphologic criteria” were used to assess lesion length, ostial location ( <3 mm from the origin of the SVG), eccentricity (if the lesion occupied the outer quarter of the vessel lumen), angulation >45”,

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the burden of thrombus (see Table II), and ulceration (identified by definite overhanging edges). The SVGs were considered degenerated if diffuse atheromatous changes with or without ectasia affected ~25% of the shaft. Those lesions > 15 mm in length, tandem lesions, total occlusions, and ulcerated, eccentric, or ostial lesions were considered complex. Measurements of minimal lumen diameter, reference diameter, and lesion length were obtained with electronic calipers. An automated edge-detection algorithm (Philips DCI-VD, release 4.1.4) was applied using the guiding catheter as a reference.20 Anterograde flow was graded using the TIM1 criteria.*l Abrupt closure was defined as TIM1 0 or I flow at any time during the procedure; distal embolization was defined as sustained flow TIM1 I to II and/or complete occlusion of a distal branch during the procedure.15 Intra-SVG verapamil (200 to 600 p,g) was routinely administered as a bolus before and after stenting. The reference and minimal lumen diameters were determined before and after stent deployment from the single worst view.22 Immediate (short-term) gain was defined as the improvement in minimal lumen diameter (final minimal diameter minus the prestenting diameter) .23 Periprocedural or postprocedural dissection was graded from 0 to 4,‘” and postprocedural thrombus was recorded. Special attention was given to identifying instances of the no-reflow phenomenon25 (a reduction in distal flow without apparent dissection or distal embolization) . Clinical outcome: Patients were followed using the systematization proposed by Wong et al.” Deployment success (per lesion) was said to have been achieved when the stent was deployed across the stenosis. Procedural success (per patient) was characterized by a final diameter stenosis of <50% in all treated lesions and the absence of major clinical complications (death, Q-wave myocardial infarction, or the need for bypass grafting). Clinical success (per patient) was characterized by a final diameter stenosis of <50% in all treated lesions and the absence in the next 14 days of death, Q-wave myocardial infarction, or a need for emergency bypass grafting or repeat intragraft transcatheter therapeutic procedure such as transluminal angioplasty. Patients were followed up at 1, 3, 6, 9, 12, and 18 months at office visit by the investigators, the referring cardiologists, or both, or by telephone in the case of out-of-state patients. Any major late clinical events (death, Q-wave myocardial infarction, or late site revascularization procedure) were recorded. Statistical analysis: Data were analyzed with JMP software (SAS Institute, Cary, North Carolina). Data are reported as mean + SD.

TABLE

III

Angiographic

Findings

in 147

Lesions Number

Lesion length > Tandem lesions* Total occlusion Ostial location Eccentricity Ulceration Thrombus

15 m m

burden

9 (61 96 (65) 35 (24) 147(100) type 96 (65) 37 (25) 15 (10)

* lesions

in the scme vessel within

TABLE IV in 147

Quantitative Lesions

Reference Minimum

Values

(%)

51 (35) 35 (24) 18 (12)

at lesion

Thrombus III IV V

of lesions

Angiographic

Measurements I

vessel diameter lumen diameter

clre expressed

1.5 m m of each other.

[mm) (mm)

(IS mean + SD.

Angiographic findings: Thrombus was present angiographically in all the lesions before treatment (Table III), but was absent in all lesions at the completion of urokinase infusion. No patient required

further thrombolysis. Most lesions (99; 75%) were being treated de novo. All of our patients had procedural success, with all of the stents being deployed successfully. There were no episodes of abrupt closure after stent deployment and no dissection or perforation. No angiographic evidence of thrombus was seen after the stenting procedure. These lesions, pretreated with urokinase and verapamil, were free of the no-reflow phenomenon, 25 and we had a low incidence (2%) of distal embolization. Quantitative angiography: The baseline reference vessel diameter showed large SVGs. After the procedure, there was no significant change. The final minimal lumen diameter had enlarged, with a marked reduction in the extent of stenosis (Table IV). Clinical complications and follow-up: The clinical success rate (98%) was slightly lower than the procedural success rate ( 100%). There was 1 sudden death immediately preceded by seizure activity in the intensive care unit 36 hours after stent deployment. We were not able to obtain an autopsy. In our initial group of patients receiving a full anticoagulation protocol, there was 1 retroperitoneal hemorrhage and 1 need for surgical repair of the right common femoral artery plus evacuation of a large hematoma in the right inguinal area. Only 2 patients had a greater than fivefold increase in the creatine kinase-MB fraction to warrant a diagnosis of non-Q-wave infarction. Two others had a greater than threefold increase, and 3 had an increase of greater than twofold but less than threefold.

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Two patients in addition to the 1 who died were lost to office or telephone follow-up. At 3 and 6 months, all 57 remaining patients were alive and event free. At 1 year, the event-free rate had declined to 87%, because 2 patients required target vessel revascularization (Table V) .

DISCUSSION Transcatheter vein graft

therapy disease:

of thrombotic-occlusive

saphe-

The angiographic presence of thrombus during stenting is evidence of a high risk for subsequent stent thrombosis.26,27 However, some apparent thrombi in SVGs have been demonstrated angioscopically to be large masses of plaque or a ruptured saphenous vein valve, and in other patients, thrombus has been found by angioscopy that was not seen at angiography.28 Therefore, we considered it mandatory to treat all of our patients with long-term intra-SVG infusions of urokinase. We achieved 100% success in clearing these conduits of thrombus and also in opening a number of the total occlusions. The potential role of intracoronary verapamil in preventing the no-reflow phenomenon7 and the poor outcome of patients with no-reflow after percutaneous coronary intervention (increased incidence of acute myocardial infarction and in-hospital death)’ have been shown. In our series, no cases of no-reflow were seen after prophylactic verapamil was introduced into the protocol. There was no evidence of Q-wave myocardial infarction, although 1 patient with severe left ventricular dysfunction died suddenly several hours after the procedure. Of interest is the low incidence (12%) of nonQ-wave infarction. An incidence of such infarction as high as 44% has been reported in patients with SVGs treated with biliary stents.’ We hypothesize that thrombolysis coupled with intra-SVG verapamil prevented thrombosis and vasospasm, which are the principal mechanisms of subendocardial infarction. The use of the radiopaque biliary tubular slotted stent in the treatment of SVG disease has proved highly successful.” When expanded, this stent exhibits greater resistance to radial compressive force than the Palmaz-Schatz intracoronary stent. Of paramount importance in the treatment of large (>5 mm) SVGs, the biliary stent permits an expansion range of 4 to 9 mm. By intravascular ultrasonography, 40% of SVG lesions have been classified as fibrotic with associated calcium content; it may be more difficult to achieve optimal final lumen dimensions in such grafts, and restenosis rates may be higher. Our use of biliary stents resulted in an excellent final minimal lumen diameter with a small residual stenosis (7 t 16%). A larger trial with long-term angiographic follow-up will decide the issue of restenosis. Two characteristics of the biliary stent make its use difficult. First, the larger and thicker material results in a stiff, sometimes inflexible, stent. Therefore, we use the 10 mm length exclusively and place multiple overlapping stents to cover longer lesions. Second, we agree with Wong et al l5 that the deploy-

nous

CORONARY

TABLE V

Clinical

Complications

and

Outcomes

in 60

Number

Complications In-hospital Major complications Death Q-wave myocardial infarction Emergency bypass grafting Other complications Non-Q-wave myocardial infarction Subacute thrombosis Vascular complications Arteriovenous fistula Pseudoaneurysm Retroperitoneal bleeding Vascular repair needed Any transfusion Follow-up time (mean ? SD mos) Death Q-wave myocordial infarction Repeat bypass grafting Repeat SVG angioplasty Event-free survival (mos) 3 6 12

Patients

of Patients

(%) -

1 (1.7) 1 (1.7) 0 0 7 (121 0 0 0 l(1.7) 1 11.7) 7 (121 18k6 0 0 l(l.7) 1 (1.7) 57 57 52

195) (95) (87) -

ment of a stent manually crimped onto a peripheral angioplasty balloon catheter without the protection of a sheath carries a significant risk of stent embolization and requires a highly skilled operator. The higher risk of bleeding and vascular complications after stent placement is proverbial. In our series, only 1 patient developed retroperitoneal bleeding, and. another had a large inguinal hematoma. Those 2 complications were early in our experience. With discontinuation of the use of dextran and dipyridamole, application of the Femostop device and lower activated clotting times (<300 seconds) and partial thromboplastin times (60 to 80 seconds), and limitation of the heparin dosage after sheath removal, the incidence of vascular complications decreased dramatically. We have observed that many patients presenting with non-Q-wave infarction and subtotal SVG occlusion on angiography develop a totally thrombosed graft in a matter of hours. Thus, there is a narrow window of opportunity in which many SVGs can be salvaged and their benefit extended, thus lessening the need for reoperation. Use of intravascular ment: Angiography

ultrasonography

for stent

deploy-

may overestimate the adequacy of stent placement in SVGs.” In the present study, using the high-pressure balloon for final dilata.tion along with intravascular ultrasonography guidance, there were no clinical events suggestive of subacute thrombosis in patients treated with the full anticoagulation protocol or in those given only antiplatelet therapy. long-term outcome: Long-term angiographic and clinical follow-un of natients with SVGs treated Iwith both Palmaz-Schatz and biliary stents has demonstrated a 6-month to l-year event-free survival rate of 80% to 82%.9,27 In 1 of the studies,27 in patients treated previously with angioplasty, the event-free

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35

rate at 1 year was only 55%. In our patients with severe disease, the event-free survival rate at 1 year was 87%. Study limitations: The greatest limitation of our study is the absence of angiographic follow-up. This was a retrospective nonrandomized study, with all the inherent limitations, including the absence of a control group. We cannot identify the optimal modality of therapy in thrombotic-occlusive SVG disease, and at present, there is no way to confirm whether intra-SVG thrombolysis followed by stent insertion is preferable to other modalities of treatment such as extractional atherectomy, laser-assisted angioplasty, and newer thrombectomy devices. Future randomized trials will decide these issues. 1. de Feyter PJ, “an Suylen R-J, de Jaegere PPT, Top01 EJ, Serruys PW. Balloon angioplasty for the treatment of lesions in saphenous vein bypass grafts. J.&n Cdl Cardiol 1993;21: 1539- 1549. 2. Meester BJ. Samson M, Suryapranata H, Bowel G, van den Brand M, de Feyter PJ, Sermys PW. Long-term follow-up after attempted angioplasty of saphenous vein grafts: the Thoravcenter experience 198 I- 1988. Ew Heart J 1991;12:648-653. 3. Garratt KN, Holmes DR Jr, Bell MR, Berger PB, Kaufmann UP, Bresnahan JF, Vlietstra RE. Results of directional atherectomy of primary atheromatous and restenosis lesions in coronary arteries and saphenous vein grafts. JArn Coil Cardiol 1992;70:449-454. 4. Selmon bIR, Hinohara T, Robertson GC, Rowe MH, Vetter JW, Barzlokis TC, Braden LJ. Simpson JB. Directional coronary atherectomy for saphenous vein graft stenoses (abstr). JAwi Co/l Cardiol 1991:17:23A. 5. Safian RD. Chines CL, May MA, Lichtenberg A, Juan N. Schreiber TL, Pavlides G. Meany TB. Saws V, O’Neill WW. Clinical and angiographic results of transluminal extraction coronary atherectomy in saphenous vein bypass grafts. Circularion 1994;89:302-312. 6. Untereker WJ, Litvack F, Margolis JR, Roubin GS, Hartzler GO, White RH, Bresnahan IF, Rothbaum DA, Hart EK, Ogilby JD, ELCA Investigators. Extimer laser coronary angioplasty of saphenous vein grafts (abstr). Circulation 1991;84 (suppl II):II-249. 7. Pomerantz RM, Kuntz RE, Diver DJ, Safian RD, Bairn DS. Intracoronary verapamil for the treatment of distal microvascular coronary artery spasm following transluminal angioplasty. Cafher Cmdimasc Dingrz 1991; 24:283-285. 8. Abbo KM, Dooris M, Glazier S, O’Neill WW, Byrd D, Grines CL, Safmn R. Features and outcome of no-reflow after percutaneous coronary intervention. Am .I Cardiol 1995:75:778-782. 9. Kelley LR, Denardo S, Morris N, T&stein PS, Schatz RA. Early experience with peripheral Palmaz stents in SVBG [abstract] Circularion 1993;88(suppl I):I-308. 10. Painter J4, Mintz GS, Wong SC: Popma JJ, Pichard AD, Kent KM, Satler LF. Hong MK, Leon MB. Intravascular ultrasound assessment of biliay stent implantation in saphenous vein grafts. ilm J Cnrdiol 1995;75:731-734.

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11. Fenton SH. Fischman DL, Savage MP, Schatz RA, Leon MB, Bairn DS, King SB, Heuser RR, Curry RC, Rake RC, Goldberg S. Long-term angiographic and clinical outcome after implantation of balloon-expandable stents in aortocoronary saphenous vein grafts. ilw~ J Cardiol 199474: 1187- 1191. 12. Sherman CT. Litvack F, Grundfest W, Lee M, Hickey A, Chaux A, Kass R, Blanche C, Swan HJC, Forrester I. Coronary angioscopy in patients with unstable angina pectoris. N Engl J Med 1986:3 15:913-919. 13. Leon MB, Wong SC, Pichard AD. Balloon-expandable stent implantation in saphenous vein grafts. In: Herrmann H, Hiishfeld J, eds. Clinical Use of the Palmaz-Schatz Intracoronary Stem. Mount Kisco, NY: Futura, 1993: 111- 121. 14. Strauss BH, Sermys PW, Bertrand ME, Purl J. Meier B, Goy J-J, Kappenberger L, Rickards AF, Sigwart U. Quantitative angiographic follow-up of the coronary Wallstent in native vessels and bypass grafts (European ewperienceMarch 1986 to March 1990). Am J Cardiol 1992;69:475-481. 15. Wong SC, Popma JJ, Pichard AD, Kent KM. Satler LF, Mintz GS, Chuang YC, Hong MK, Ditrano CJ, Leon MB. Comparison of clinical and angiographic outcomes after saphenous vein graft angioplasty using coronary versus “biliary” tubular slotted stents. Cirrularion 1995:91:339-350. 16. Eagan JT Jr, Stmmpf RK, Heuser RR. New treatment approach for chronic total occlusions of saphenous veiii grafts: thrombolysis and intravascular stents. Cathet Cardiovasc Diagn 1993;29:62-69. 17. Colombo A, Hall P, Nakamura S, Almagor Y, Maielo L. Martini G, Gaglione A, Goldberg SL, Tobis JM. Intracoronary stenting without anticoagulation accompanied with intravascular ultrasound guidance. Circularion 1995;91:1676-1688. 18. Barnathan ES. Antithrombotic therapy before and after stent deployment. In: Herrmann HC: Hirshfeld JW, eds. Clinical Use of the Palmaz-Schatz Intracoronary Stat. Mount I&co, NY: Futura, 1993:43-57. 19. Popma JJ, Bashore T. Qualitative and quantitative angiography. In: Top01 EJ, ed. Textbook of Interventional Cardiology. Philadelphia: WB Saunders. 1993:10521068. 20. Kuntz RE, Safian RD, Carrozza JP. Fishman RF, Manjour M, Baim DS. The importance of acute luminal diameter in determining restenosis after coronary atherectomy or stating. Circularion 1992;86:18271835. 21. The TIMI Study Group. The Thrombolysis in Myocardial Infarction (TIMI) trial: phase I results. N Engl Jhled 1985;312:932-936. 22. Lesperance J. Hudon G, White CW, Laurier J, Waters D. Comparison by quantitative angiographic assessment of coronary stenoses of one view showing the severest narrowing to two orthogonal views. .&I J Cardiol 1989:64:462165. 23. Kumz RE, Gibson CM, Nobuyoshi M, Bairn DS. Generalized model of restenosis after conventional balloon angioplasty, stenting and directional atherectomy. J.4111 Co11 Cardiol 1993:21:15-25. 24. Reis GJ, Pomerrmtr RM, Jenkins RD, Kuntz RE, Bairn DS, Diver DJ, Schnitt SJ, Safian RD. Laser balloon angioplasty: clinical. angiographic and histologic results. JAnz Co0 Cwdiol 1991;18:193-202. 25. Piana RN, Paik GY, Moscucci M, Cohen DJ, Gibson CM, Kugelmass 4D. Carrozza JP Jr, Kuntz RE, Bairn DS. Incidence and treatment of “no-reflow“ after percutaneous coronary intervention. Circulation 1994;89:2514&2518. 26. Agrawal SK, Ho DSW, Liu MW, Iyer S. Heam JA, Cannon AD, Macander PJ, Dean LS, Bawlry WA, Roubin GS. Predictors of thrombotic complications after placement of the flexible coil stent. Am J Cnrdiol 1994:73: 1216- 1219. 27. Nath FC. Muller DWM. Ellis SG, Rosenschein U, Chap&is A, Quain L, Zimmerman C, Top01 EJ. Thrombosis of a flexible coil coronary srent:frequency, predictors and clinical outcome. JAni CON Cardio[ 1993;21:622-627. 28. Teirstein PS, Schatz RA, Wong SC, Rocha-Singh KJ. Coronary stating with angioscopic guidance. AN? J Cardiol 1995;75:344-347.

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