Applications and limitations of laser-assisted angioplasty

Eurj Vasc Surg 3, 61-70 (1989)

Applications and Limitations of Laser-assisted Angioplasty E d w a r d B. Diethrich, Ela T i m b a d i a and Ilhan Bahadir From the Department of Cardiovascular Surgery, Arizona Heart Institute, and the Cardiovascular Center of Excellence at Humana Hospital--Phoenix, Phoenix, Arizona Laser-assisted angioplasty is rapidly evolving into a promising adjunct to or replacement Jor standard vascular procedures. A protocol was devised to evaluate the technique in a non-selected, consecutive patient population to define the applications and limitations of the technique. In a 12-month period, 358 lower-limb atherosclerotic lesions were treated with laser/balloon angioplasty [percutaneously (52%) or open (48%)] in 206 consecutive patients. Overall, the laser/balloon technique recanalised 234 lesions (65% laser success), judged clinically effective by a > 0.15 improvement in the ankle/brachial index and elimination of symptoms. Operative complications included: perforation ( 15, 4.2%): thrombosis ( 16, 4.5%); spasm ( 5, 1.4%); and false aneurysm at the puncture site (7, 2.0%). Of the 124 failures (35%) categorised for analysis, the most common cause was inability to cross the lesion in 20 cases. This experience has identified three significant clinical limitations to successful laser recanalisation: calcification, inadequate distal circulation, and inability to control restenosis/reocclusion (collapsible lesions and accelerated plaque deposition). Further research is needed to determine if thermal injury seriously compromises the safety and long-term outcome of laserassisted angioplasty. Key Words: Laser angioplasty; Perforation; Thermal injury; Thrombosis; Success rate; Patency rate; Peripheral occlusive disease.

Introduction In February 198 7, the FDA approved the argon laser for peripheral vascular revascularisation. At that time, the literature was devoid of information regarding patient selection, complications and the limitations of lasers in vascular reconstruction. Only small, experimental studies had reached publication, 1 11 and there was no significant follow-up data. To address these deficiencies as rapidly as possible, the vascular service of the Arizona Heart Institute established a protocol to explore laser-assisted angioplasty in patients suffering from peripheral vascular occlusive disease.

Presented at the 2nd Annual Meeting of the European Society for Vascular Surgery, Rotterdam, The Netherlands, September 15-16, 1988. Address correspondence and reprint requests to: Edward B. Diethrich, MD, Arizona Heart Institute, P.O. Box 10 000, Phoenix, AZ 85064, U.S.A. 0950 821x/89/010061 + 10 $03.00/0 © 1989 Grune & Stratton Ltd

Our major goal was to establish a large group of laser-treated patients in w h o m periodic, objective reevaluation would provide longitudinal data to support or refute the efficacy of laser therapy in atherosclerotic occlusive disease. Also, it provided the perfect opportunity to define the ideal patient population and identify a n y limitations of the procedure. To these ends, the protocol offered laser angioplasty to every patient as an initial intervention, reserving classical revascularisation procedures for failed laser cases or in combination with laser therapy w h e n necessary. Even lesions amenable to standard balloon angioplasty (e.g., sub-total occlusions) were lased primarily, in as m u c h as preliminary data indicated that the laser might provide a more favorable long-term o u t c o m e t h a n balloon angioplasty alone. 12 14 Balloon dilatation was used routinely following laser treatment in this protocol to optimise recanalisation. The substantiation for our "unlimited" application of the laser was based u p o n three assumptions. First, vascular surgeons have unrestricted capabilities to gain

62

E.B. Diethrich e t a / .

entry to any artery, even in the presence of extensive occlusive disease. This circumvented the access limitation of the non-surgical specialists. Secondly, laser energy should penetrate even a totally occluded arterial segment in most cases, establishing a central channel through which the dilating balloon catheter could be introduced to fully expand the artery. Lastly, a failed laser angioplasty procedure could be converted to a classical revascularisation operation, culminating in a successful outcome for the patient. By testing laser angioplasty under the broadest possible array of vascular pathologies in an unrestricted population, the limitations of the technique would be more rapidly identifiable. Furthermore, refinement of lasing techniques and optimisation of instrumentation would be facilitated by a clinical environment presenting unlimited variations of atherosclerotic disease. The data in this series, therefore, were derived from a consecutive, completely unselected group of patients with varying symptomatic disease patterns, risk factors, and vascular surgical histories. The only commonality in this cohort was the evidence of peripheral vascular occlusive disease supported subjectively by symptoms and objectively by ultrasound evaluation and arteriography.

Materials and Methods

Equipment All procedures were performed in a cardiovascular operating room equipped with a new nonmetallic, carbon fiber surgical table (model 205, International Surgical Systems) developed especially for vascular laser procedures. The table, supported by a pedestal at one end, provided complete clearance beneath and allowed 15 ° side-to-side roll with 20 ° Trendelenburg and reverse Trendelenburg tilt. Intraoperative arteriography and fluoroscopy were available via a surgical C-arm roentgenographic unit (Diagnost OP-C, International Surgical Systems) integrated with a 3/4 inch videotape recorder and monitor for constrast injection visualisation. An Eigen disk was also used to provide still images of selected arteriographic segments on a second monitor, which greatly enhanced lasing capabilities in complex situations. A metric ruler (USA XRAY) was placed on the table beneath the patient's pelvis, calibrated from the level of the umbilicus, to provide reference measurements. At the time this study began, the only FDA-approved laser delivery system for peripheral vascular use was the Trimedyne argon device (Optilase 900, 0 - 1 2 watts outEur I Vase Surg Vol 3, February 1989

put). Subsequently, the same manufacturer received approval for an Nd: YAG system (Optilase 10OO, 0 - 6 0 W output), which was substituted for the argon model due to its ability to energise probes up to 5.0 m m in diameter. In both systems, the laser energy was used to heat varying sizes of metal-tipped probes attached to 6 0 0 g optical fibers (Trimedyne, Inc.). Typically, this "hot tip" design allowed no laser energy to escape; however, one model, the Spectroprobe (Trimedyne, Inc.), had a sapphire tip with a 2 p central window which emitted 1 0 - 2 0 % direct laser light. The most commonly used hot tip probe was the 2.5 m m size (Laserprobe-SLR). Smaller probes from 1.O to 2 . O m m were reserved for the infra-popliteal arteries, while the 3.5 and 5 . 0 m m models, powered by the YAG laser, were useful in the iliac system. The Spectraprobe, with its raw laser energy preceding the metal tip, was used primarily in calcified arteries resistant to the closed beam probes. Another version of the 2.O and 2.5 m m closed beam probes sometimes used had a channel placed eccentrically on the side of the probe's tip (Laserprobe-PLR Flex) for passage over a 0.035 inch guidewire. This probe was employed whenever a wire had been used to cross the lesion initially, allowing lasing to be accomplished over the wire. In all procedures, whether arterial access was percutaneous or through an incision (open), an introducer with sheath (Cordis) was used, usually an 8 or 9 French. However, when larger arteries were encountered, a 12 French introducer was necessary to accommodate the 3.5 m m probe. Any larger probes required the open technique without an introducer sheath. Guidance was provided by a new hydrophilic, 1 4 5 c m , 0.035 inch guidewire (Glidewire, Medi-tech, Inc.) is This wire became u n c o m m o n l y slippery when wet, which made it extremely effective in negotiating even the most severely stenosed lesions. For post-lasing dilatations, a variety of balloon catheters were employed, depending on the nature of the lesions. In the superficial femoral and popliteal arteries, the most frequently used balloons were 4, 5, or 6 m m by 10 cm (Medi-tech, Inc.); the iliac arteries required the 8 or 10 m m by 8 cm models. Time of dilatation ranged from 30 to 60 s at atmospheric pressures ranging from 6-17, depending on the balloon characteristics.

Patient population In a one-year period from February 1987, we evaluated 206 consecutive patients (149 males; 57 females) aged 35 to 91 years (mean age: 68) with symptoms of peripheral atherosclerotic occlusive disease. All patients

Laser Angioplasty

demonstrated severe claudication and/or rest pain; 25 patients (12%) had ankle ulcers and 18 (9%) threatened limb loss. Twenty-four percent (49) of the patients had diabetes mellitus, 87% (179) smoked or had a history of recent smoking, 63% (130) were hypercholesterolemic, 55% (113) were hypertensive, and 52% (107) had concomitant disease in the coronary arteries. An arterial Doppler examination (preferably with exercise if symptoms and physical examination permitted) was made to establish a baseline ankle/brachial systolic pressure index (ABI) for use in evaluating long-term patency. Documentation of the lower extremity arterial system was accomplished using translumbar, retrograde or antegrade arteriography, depending on the location of the lesions: translumbar a0rtography and antegrade studies were used if both iliac arteries were totally occluded or both common femoral arteries (CFA's) were severely diseased. Lesions were categorised according to location, severity, and absence of arterial run-off. The position of the plaque in the limb's vascular tree was assigned to one of four arterial segments: the iliac (from its origin to the inguinal ligament), the superficial femoral (SFA), the popliteal, and the tibial peroneal branches. These four categories were then further divided to reflect the severity of disease (occlusion or stenosis < 70%), the availability of run-off, and in the SFA, the occurrence of multiple stenoses within this long segment. (Occlusions in 15 vascular grafts were selected for treatment as well but not categorised.) In limbs with more than one involved segment (e.g., an iliac occlusion and an SFA stenosis), each lesion was classified separately for long-term evaluation of the influence of lesion location on a successful outcome. Also categorised and recorded during this protocol were pertinent intraoperative observations and/or events which caused procedural failure or might eventually impact long-term success. The coding system devised recorded seven main categories: (Table 1) mechanical difficulties unrelated to the interaction of the laser and artery (e.g., problems with the wire, introducer/sheath, probe, fiber, delivery system, or access route); failure to cross the lesion; inability to enter the proper distal channel; absence of distal arterial run-off; presence of underestimated proximal lesion; collapsible lesions; and slow flow. Also to be considered as sources of failure in laser-assisted angioplasty were potential complications of the procedure, notably perforation and thrombosis. Patients electing laser angioplasty were informed that a standard bypass graft procedure might have to be performed if the laser failed to establish an adequate artarial channel. Two days before angioplasty, patients were placed on antiplatelet therapy (325 mg/day aspirin and 75 mg tid dipyridamole).

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Table 1. Intraoperativefailure codesfor laser-assisted angioplasty Category

Description

Mechanical

Due to sheath, wire, balloon, probe,* fibre, delivery system, accessroute

Failure to cross

Due primarily to calcification

No re-entry

Due to inability to re-enter the proper distal lumen

No run-off

Due to insufficientdistal arterial circulation

Proximal lesion

Due to undetected or underestimated lesion proximal to lased segment

Collapsible lesion Due to lesion'sreturn to pretreatment configuration Slow flow

Due to haemodynamicand physicalconditions hampering flowto distal vessels (e.g., small arteries, iatrogenic incisional flaps, extensive dissection planes, etc.)

*Does not include mechanicalinjury, i.e., perforationor dissection.

Operative procedures The operative approach was determined by the location of the lesions and the necessity for exposure of the common femoral artery. Since the initiation of our protocol, we favoured the percutaneous route, and it predominated in the approach to iliac, mid-SFA and popliteal lesions. In general, the open technique was required for approach to the common femoral, profunda femoris, and superficial femoral arteries in instances of: (1) complete occlusion of the common or external fliac artery (with absent femoral pulse) if percutaneous needle insertion was not possible; (2) common femoral or profunda femoris lesions in conjunction with SFA occlusion and stenoses; or (3) extensive atherosclerotic disease preventing introduction of the sheath at the site of percutaneous entry. Epidural block was our preferred form of anaesthesia for laser-assisted procedures regardless of the entry technique. This mode of anaesthesia produced a profound sympathetic response which eliminated, to a great extent, the vasospasm observed with local anaesthesia. When an epidural block was contraindicated (in patients with previous spinal operations or in whom a thrombolytic agent might be used), local or, more rarely, general anaesthesia was employed. The techniques for laser angioplasty via the percutaneous or open routes have been reported in detail, 162o but in brief, the percutaneous approach was begun with antegrade needle insertion under fluoroscopic control at the site of the femoral pulse. A 0.035 inch guidewire was passed through the needle to the SFA and Eur] VascSurg Vol 3, February 1989

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E . B . D i e t h r i c h e t al.

advanced as far as possible. With the needle removed, the appropriately sized introducer sheath was positioned in the c o m m o n and proximal superficial femoral arteries. A small bolus of contrast material (Omnipaque 350, Winthrop Laboratories) was injected through the sheath to confirm its location and identify the most proximal arterial obstruction. Following sheath placement, 2 5 0 0 units of heparin sodium were administered intravenously and the dosage repeated as necessary to keep the activated coagulation time over 200 s. Prior to use, the probe was tested in saline for the presence of laser energy (as evidenced by bubbles at the tip). Lasing was begun at 12 W with the probe constantly moving in a to-and-fro motion to prevent the probe from sticking to the vessel wall and accumulating charred debris on the tip. If an artery was totally occluded and lasing could not be done over a wire, contrast material was injected continuously during probe movement to monitor its location in relation to the artery, identify side branches, and avoid misdirection. Lasing continued until the probe either created an open channel' in a total obstruction or "debulked" a tight stenosis. If long occlusions or multiple stenotic segments were found in tandem, treatment continued in stepwise fashion until all lesions were treated. The probe was withdrawn under continuous activation so that the tip exited the sheath clean without carbon particles. Once the artery was opened, retrograde blood flow was observed through the sheath's side tubing. Because the largest sized probes available during this study could not completely recanalise an artery in most cases, balloon dilatation was necessary to fully expand the vessel. If the inflation characteristics of the balloon indicated substantial residual plaque, the compromised segment was released and redilated. Following successful dilatation, a final control arteriorgram was taken before the treated arteries were released to smooth the intima. This final lasing, termed "glazing", was performed at the 12 W treatment energy setting, presumably enhancing long-term patency by reducing surface irregularities to give a more satisfactory blood-intimal interface. Heparinisation was not reversed following the procedure, and the patient was transferred to the recovery room with the sheath in place. Removal of the sheath took place after the activated coagulation time had fallen below 150 s. Used whenever the needle could not be placed percutaneously, the open approach began with a vertical incision exposing the CFA from the inguinal ligament distally to its bifurcation into the origin of the profunda femoris artery and the proximal SFA. Heparin was given intravenously prior to clamping the c o m m o n femoral and profunda femoris arteries. In the open technique, there Eur I Vasc Surg Vol 3, February 1989

was often no need to clamp the SFA since it was generally occluded at its origin. With the arteries crossclamped, an arteriotomy was made in the CFA for introduction of the laser probe. The incision was extended approximately 3 m m into the SFA. If a significant obstruction existed in either the profunda femoris or common femoral arteries, a classical endarterectomy was performed, intentionally terminating near the origin of the SFA. The probe was introduced and passed distally to create a 2 cm channel in the SFA. The catheter sheath was then inserted through the arteriotomy for use in further lasing, balloon dilatation, and contrast injection. The procedure continued as described in the percutaneous technique, with concomitant lesions lased and dilated sequentially. Once all lesions were treated, the arteriotomy in the CFA was closed with a knitted Dacron patch. If a profunda endarterectomy had been performed, the patch on the CFA was extended to the profunda femoris artery as well.

Additional procedures In order to obtain total revascularisation of all limbs treated, an assortment of vascular procedures were performed concomitantly with the laser angioplasty. Primarily, these involved the profunda femoris artery and the placement of grafts proximally in unlased arterial segments to improve distal flow.

Postoperative care Patients were observed in the Intensive Care Unit overnight for signs of bleeding or a change in pulse status. The aspirin (325 mg/day) and dipyridamole ( 7 5 m g tid po) therapy begun 2 days prior to operation was reinstituted as soon as oral intake was tolerated. Discharge from the hospital usually took place 1-2 days after operation. While procedural success of the laser technique was determined intraoperatively by arteriography, follow-up evaluation and exercise arterial Doppler examination were performed within 10 days after discharge to confirm the symptomatic and hemodynamic Success of the procedure (based on relief of symptoms and a > 0.15 improvement in the ABA). Doppler studies (and arteriography in a randomly selected subset of patients) were scheduled at six-month intervals for documentation of long-term results. Return

Laser Angioplasty

65

Table 2. Postoperative results of laser-assisted angioplasty in 206 consecutive, unselected patients (358 arterial segments lased in 285 limbs) No. of lesions

Category I

II

(Iliac) A Occlusion B Stenosis (SFA) A Occlusion proximal mid B Occl/no run-off C Stenosis/mult lesions

Laser success*

75 (21%) 48 27 213 (59%)

46 (61%) 25(52%) 21 ( 7 8 % )

Ave. A ABI 0.22±0.15 O.28:t:O.12

152 (71%)

91 45 7 70

51 (56%) 42 (93%) 0 59(85%)

IIl (Popliteal) A Occlusion B Occl/no run-off C Stenosis

28 (8%) 18 4 6

13 (46%) 10(56%) 0 3 (50%)

l).18 +O.09 O.01 ±0.02 0.174-0.14

lV (Tibial/Peroneal) A Occlusion B Occl/no run-off C Stenosis

27 (8%) 7 l 19

l 3 (48%) 2(29%) 0 11 ( 5 8 % )

0.17±0.15 -0.16±0.13

(Grafts) A Vein B Prosthetic

15 (4%) 7 8

10 (66%) 3(43%) 7 (88%)

0.18±0.15 0.154- 0.07

234(65%)

0.184-0.11

358

Totals

0.23 ± 0.14 0.29 ± 0.08 --O.O1 4-O.03 0.25-t-0.10

*Success based on return of pulses, absence of symptoms, and > 0.15 improvement in ABI over preoperative value.

of s y m p t o m s or failure to i m p r o v e after o p e r a t i o n were indications for earlier a r t e r i o g r a p h i c investigation.

Results Based u p o n the classification system for arterial p a t h o logy in this protocol, a r t e r i o g r a p h y identified 3 58 treatable lesions in both the n a t i v e vessels a n d v a s c u l a r grafts of the 2 0 6 patients (2 85 limbs): 75 (21%) C a t e g o r y I ifiac lesions (48 occlusions a n d 2 7 stenoses); 2 1 3 (59%) Category II SFA lesions ( 1 3 6 occlusions, 70 stenoses, a n d 7 occlusions w i t h o u t run-off); 28 (8%) Category III popfiteal lesions (18 occlusions, 6 stenoses, a n d 4 occlusions with no run-off); 27 (8%) Category IV t i b i a l / p e r o n e a l lesions (7 occlusions, 19 stenoses, a n d 1 occlusion w i t h o u t run-off); a n d 15 (4%) v a s c u l a r grafts (7 vein a n d 8 prosthetic). Slightly over half the angioplasties to t r e a t these lesions were performed p e r c u t a n e o u s l y (52%). Table 2 presents the p r o c e d u r a l results a n d t h e a v e r a g e degree of h e m o d y n a m i c i m p r o v e m e n t in these four a r t e r i a l categories a n d their subdivisions. Overall, pulses w e r e restored, s y m p t o m s were abolished, a n d a n k l e / b r a c h i a l indices were i m p r o v e d in 2 3 4 (65%) procedures. The ABI rose from a n a v e r a g e p r e o p e r a t i v e

v a l u e of 0 . 6 1 + 0 . 1 8 to 0 . 7 9 + 0 . 2 4 ( P > O . 0 5 ) postoperatively. Compilation of the events associated with the 35% failures is s h o w n in Table 3. The most c o m m o n incident w a s the inability of the laser probe to open a c h a n n e l or cross a lesion [20 (6%) failures: 7 ifiac occlusions, 11 SFA lesions, a n d t w o p e r o n e a l stenoses]. As anticipated, calcification w a s the p r i m a r y reason, a c c o u n t i n g for 78% (14) of these failures. The inability of the probe to re-enter the true l u m e n distal to the lesion was n e a r l y as c o m m o n , o c c u r r i n g m o s t often in SFA occlusions (17 of the 19 r e - e n t r y failures). T e c h n i c a l p r o b l e m s w i t h the sheaths, wires, or probes were e n c o u n t e r e d o n l y in the p r o x i m a l lesions (six lilac a n d four SFA), also t h e site of a n o c c a s i o n a l difficulty w i t h the access route. A m o n g the h a e m o d y n a m i c variables influencing o u t c o m e , slow flow (16 cases) a n d poor arterial run-off (12) were p a r t i c u l a r l y o m i n o u s b e c a u s e even further surgical i n t e r v e n t i o n could often n o t provide a d e q u a t e circulation. Two i n s t a n c e s of u n d e r e s t i m a t e d p r o x i m a l lesions w e r e successfully rectified by a s u b s e q u e n t laser treatm e n t of the o b s t r u c t i n g plaque. Of the 14 lesions w h i c h w e r e classified as collapsible ( r e t u r n to their pre-lased stenotic configuration), two in the ifiac arteries were successfully treated w i t h i n t r a v a s c u l a r stenting w h e n t h a t t e c h n i q u e b e c a m e available. EurJ Vasc Surg Vol 3, February 1989

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E.B. Diethrich etal.

Table 3. Causes of immediate failure in 124 laser-assisted angioplasties

Table 4. Additional procedures performed with laser-assisted angioplasty

Arterial segment Patch angioplasty Cause

lilac

SFA

Mech

6

4

Cross

7

11

Re-entry Run-off

-2

Prox L

Popliteal Tib/Per Grafts ---

--

10

2

--

20

17

1

1

--

19

2

3

2

3

12

1

2

--

1

Collap L

6

6

2

--

--

14

Flow

8

5

2

--

1

16

7

4

4

--

15

9

2

5

--

16

61

15

14

5

124

Perf

--

Throm Totals

29

117

Totals

Mech = mechanical difficulties unrelated to laser-tissue interaction Cross - failure to cross the lesion Re-entry = failure to re-enter tile lumen distal to the lesion Run-off - absence of arterial run-off Prox L - presence of underestimated/untreated proximal lesion Collap L - collapsible lesion Flow - slow flow Perf = failure due to perforation Throm failure due to thrombosis in immediate postoperative period

Endarterectomy

84

Profundaplasty

27

Thrombectomy

16

Pseudoaneurysm resection

7

Sympathectomy

3

Grafts: Femorol-femoral Femoral-popliteal Aorto-bifemoral Aorto-femoral

8 18 3 14

Table 5. Results in 85 patients returning for re-evaluation Total number of lesions: Patent vessels* Long-term failures

129 ( 36% of all treated lesions) 105 (82%) at 180 days 24 (18%) presenting at 104 days (ave)

Causes of failure in 19 retreated~ F o u r o t h e r lesions in t h e SFA w e r e r e l e a s e d w i t h initial success; h o w e v e r , t w o r e s t e n o s e d w i t h i n o n e m o n t h . A m o n g t h e c o m p l i c a t i o n s p r o d u c i n g failure w e r e t h r o m b o s i s ( 1 6 cases, 4 . 5 % ) a n d p e r f o r a t i o n (15 cases, 4.2%). N o n e of t h e p e r f o r a t i o n s r e q u i r e d o p e r a t i v e corr e c t i o n o t h e r t h a n e l e c t i v e bypass g r a f t i n g to r e v a s c u l a r ise distal tissue. Of t h e 16 t h r o m b o s e s , 1 0 w e r e m a n a g e d w i t h t h r o m b o l y t i c t h e r a p y ( u r o k i n a s e infusion); six r e q u i r e d t h r o m b e c t o m y . (Also s e e n w e r e five i n s t a n c e s of s p a s m (1.4%), a n d s e v e n cases of false a n e u r y s m s at t h e p u n c t u r e site (2.0%), b u t t h e s e w e r e n o t a s s o c i a t e d w i t h failure.) A t o t a l of 2 0 lesions (5%) w e r e r e l a s e d in t h e i m m e diate p o s t o p e r a t i v e period, p r i m a r i l y for t h r o m b o s i s a n d restenosis; e i g h t w e r e s u c c e s s f u l ( t w o of t h e collapsible lesions a n d six of t h e t h r o m b e c t o m i s e d arteries). I n o r d e r to p r o v i d e a n o p t i m a l o u t c o m e for e a c h p a t i e n t r e g a r d l e s s of t h e p e r f o r m a n c e of t h e laser t h e r a p y , a v a r i e t y of a d d i t i o n a l p r o c e d u r e s w e r e p e r f o r m e d (Table 4) to g u a r a n t e e or assist in o b t a i n i n g a d e q u a t e c i r c u l a tion. T h e m a j o r i t y of t h e s e w e r e p a t c h a n g i o p l a s t i e s o v e r t h e SFA incision; h o w e v e r , 8 4 e n d a r t e r e c t o m i e s , 2 7 p r o f u n d a p l a s t i e s a n d 16 t h r o m b e c t o m i e s w e r e also n e c e s sary. T h r e e s y m p a t h e t c o m i e s w e r e p e r f o r m e d , a n d a n a s s o r t m e n t of grafts w e r e p l a c e d to c o m p l e m e n t t h e laser Eur] Vasc Surg Vol 3, February 1989

Restenosis (producing thrombosis in 7)

15

Progressive plaque formation

3

Undetected proximal lesion

1

* As determined by absence of symptoms and maintenance of a > O.15 improvement in the ABI over the preoperative value. ]"As determined by arteriography.

a n g i o p l a s t y . Despite all efforts, 10 p a t i e n t s in this series eventually required amputation. As of t h e t i m e of this report, 85 ( 4 1 % ) of t h e 2 0 6 p a t i e n t s in this series h a v e b e e n r e - e v a l u a t e d for r o u t i n e f o l l o w - u p or r e t u r n of s y m p t o m s (Table 5). I n 62 of t h e p a t i e n t s , r e p r e s e n t i n g 8 2 % of t h e t r e a t e d lesions s e e n in f o l l o w - u p ( 1 0 5 of 1 2 9 ) , a r t e r i a l p a t e n c y h a s b e e n m a i n t a i n e d , as j u d g e d by a b s e n c e of s y m p t o m s a n d a c o n t i n u e d > O. 15 i m p r o v e m e n t in ABI o v e r t h e p r e o p e r a t i v e value. T w e n t y - t h r e e p a t i e n t s w i t h 2 4 lesions ( 1 8 % ) h a v e e x p e r i e n c e d r e t u r n of s y m p t o m s a n d a c o r r e s p o n d i n g d i m i n u t i o n of t h e i r ABI's ( a v e r a g e 0 . 1 5 4 - 0 . 0 8 d r o p in ABI). A v e r a g e t i m e to r e t u r n of s y m p t o m s in this g r o u p w a s 1 0 4 days. A r t e r i o g r a p h y h a s d o c u m e n t e d r e s t e n o s i s in all p a t i e n t s ; 19 lesions h a v e b e e n r e t r e a t e d . I n 15, t h e

Laser Angioplasty

lesion appeared to have restenosed at the lasing site, producing thrombosis in seven instances. In three, progressive atherosclerotic plaque had formed at the treated site, and in one, a previously undetected proximal lesion had induced restenosis.

Discussion

Although the use of laser energy to treat atherosclerotic lesions with minimal or no surgical intervention offers an attractive alternative to conventional revascularisation techniques, its desirability is of little consequence in determining its suitability for this application. As with any new procedure, the guidelines for judging therapeutic efficacy, safety and patient candidacy must be derived from clinical trials designed to specifically address these issues. In early 1987, after m a n y frustrating years of disappointing experimental research with raw laser energy, an argon laser with a closed beam delivery system was approved by the FDA for atheroma ablation in the peripheral arteries. By encasing the laser energy and using it to heat a metal probe, the dangers of the open laser beam would be avoided, so researchers thought at the time. It seemed a reactionary but acceptable compromise, provided, of course, that the metal-tipped probe did not harbor some yet unidentified dangers of its own. Excited by the elegant simplicity and technological sophistication the laser represented at that time, we immediately constructed a protocol to investigate the ability of the then available laser instrumentation to safely open obstructed arteries. Our goals in this research were to: (1) evaluate safety; (2) compose patient selection criteria; (3) determine applications and limitations of the technique; (4) identify complications, and (5) judge tong-term efficacy. Our protocol was predicated upon the assumption that only an unlimited variety of pathological experiences in an unselected patient population would be adequate to thoroughly test the functional capabilities of laser-assisted angioplasty. Normally, such a broad approach to a technique's evaluation would not be feasible. However, the vascular service at the Arizona Heart Institute provided a set of circumstances which not only made this unrestricted testing possible but desirable. Because the laser angioplasty procedures would be performed by vascular surgeons in an operating room, the laser could be used initially in every peripheral revascularisation without compromising the eventual outcome of the procedure. That is, the surgeons could access a n a r t e r y without being limited to one method, and they could appropriately treat the patient regardless of the laser's performance.

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Furthermore, this varied clinical environment provided a rich medium for the evolution of the technique and its instrumentation. As situations presented themselves, new methods were devised and redesigns of equipment proposed. For example, the small probe diameters available in the beginning, which made tandem balloon angioplasty mandatory, led to the development of larger delivery systems. However, the argon laser had a limited energy output (12W) insufficient to heat the larger probe. Hence, the 60-W Nd:YAG laser was substituted for the argon at our facility. (There was no inherent difference in probe performance: the most commonly used 2.5 m m probe functioned similarly when heated with either source.) As these technological refinements became manifest, so also did certain events and observations which seemed to exert an influence on the procedure and its results. Some of these events had obvious effects on the technique's performance and produced immediate failure; others were clinical impressions whose impact might eventually surface in the form of late failures. We appropriately developed seven categories for these occurrences and added their documentation to our protocol in the hopes of finding correlations to outcome. Among those events which acutely affected the procedure were mechanical failures. These were problems relative to instrumentation and unrelated to the lasertissue interaction. Malfunction of the laser delivery system, breakage of the fibre, separation of the probe tip, defects in the sheath, access problems, and dissection or perforation due to the guidewires or balloon catheters fell into this category. Early in this series, the most common event in this category was balloon dissection (three cases); experience soon eliminated this mishap. Equipm e n t malfunction accounted for another five incidences (one case of tip separation), and two early difficulties with access to SFA occlusions prompted alterations in our open approach. Another more c o m m o n cause of acute failure was inability of the probe to cross a lesion. Usually this was due to the presence of recalcitrant calcified plaque. Even the energy of the new partial open beam probe with its preceding raw laser light was sometimes ineffective, particularly in tight stenoses. The misdirection of the probe was also a potential source of failure. It was not u n c o m m o n to find lesions situated at a junction with large collateral branches. The probe, in seeking the least resistant path, would choose the unobstructed collateral rather than the desired direction across the lesion. Continuous injection of contrast material was important here to monitor the probe's direction. In fact, it was crucial throughout the lasing process to guard against perforation. The path of the probe after entering the lesion was Eur] Vasc Surg Vol 3, February 1989

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subject to difficulty with another form of deviation, dissection of a false lumen. In order to establish an acceptable arterial channel, a probe had to not only pass through an obstruction, but it needed to exit the lesion in the true lumen beyond. The inability of the probe to reenter the correct arterial channel created a neolumen which led to at least partial failure. (In a few cases, we observed this intraoperatively and expected absent pulses, only to find the pulses present; however, failure was more common.) Associated haemodynamic events also influenced outcome. As with any revascularisation procedure, success ultimately depended upon the ability of the distal circulation to benefit from the reestablished proximal flow. In diabetic patients, for example, distal disease is common, and their lack of arterial run-off makes revascularisation much less successful. Ten of the 12 patients without adequate run-off were diabetics. In our experience, preoperative arteriograms often failed to demonstrate the infra-popliteal arteries (poor timing, slow flow due to severe proximal stenosis, etc.). However, in some patients, this was misjudged as a lack of arterial run-off. When the distal pulses were restored in these patients following laser treatment, it was attributed to the laser. However, it soon became obvious that the distal arteries had been patent but unvisuafised, not recanalised by the laser. It therefore remained valid that if there was truly no run-off, the procedure would fail with the current hot tip probe. Reduced flow proximal to a successfully lased segment was just as deleterious. In actuality, the presence of a proximal lesion impeding flow should never occur: proximal lesions are always treated primarily. On two occasions, however, the severity of an identified proximal lesion was underestimated, resulting in inadequate pressure to a treated distal segment. These patients were released successfully, and this prompted us to be more aggressive in treating subcritical stenoses. Another not u n c o m m o n cause of eventual failure was related to the composition of atherosclerotic plaques. Many lesions have a significant fibrotic component. Although these lesions were easily lased and dilated by the balloon, the fibrous "elastic memory" would return the artery to its pretreatment state. This happened both acutely on the operating table or weeks later, leading to subsequent reocclusion. A final haemodynamic factor was classified as "slow flow", and it included several factors which would account for lack of flow sufficient to maintain distal arterial integrity. Among these were small arteries, extensive dissection planes, and iatrogenic intimal flaps at the incision site. Identification of the latter prompted alteration in the patch grafting technique used to close incisions. Although many of these "failure codes", as they Eur J VascSurg VoI 3, February 1989

were known, represented some of the limitations of laserassisted angioplasty, we have amassed sufficient experience to identify three primary road-blocks to a successful laser recanalisation. First is calcification. With today's commercially available technology, many calcified lesions will remain untreatable. However, new laser configurations being studied are showing great promise in dealing with this problem. Another limitation which precipitates acute failure is the lack of adequate distal circulation. There appears little hope that viability can be restored once the end arterial system is compromised. Finally, the ability to control restenosis/reocclusion is vital to arterial patency. The use of longitudinal studies such as ours to follow the course of patients over years will be instrumental in uncovering the causes of reclosure and dealing with them effectively. At the present, we see a strong trend towards restenosis and accelerated plaque deposition at sites of treated subcritical stenoses. It may well be that thermal injury plays a great part in this. In fact, tissue injury either mechanically or thermally induced has become a prominent consideration in laser angioplasty failure. A major complication of the procedure is mechanical arterial damage due to perforation (4.2% in this series). In the beginning of our study, we observed five different types of arterial injury inflicted by the probe; however, not all the injuries were clinically relevant. To more accurately correlate probe deviation with clinical outcome, we composed three categories of perforation, with injuries ranging from the simplest form of dissection to the most deleterious type of adventitial rupture. Class I: This category encompassed dissections which did not penetrate the adventitia. In the first scenario, the laser probe left the true lumen or the intended plane of dissection, deviating into an aberrant pathway. It may shear an arterial side branch, but it eventually relocated distally in the correct, open arterial channel. There was no adverse reaction to this dissection and, in most cases, the situation went unnoticed. A more consequential event was the laser probe deviating into the atherosclerotic plaque, usually when it encountered calcium deposits. Unlike the clinically satisfactory situation above, however, the probe did not re-enter the true distal lumen or create a satisfactory dissection plane that could restore arterial continuity. Under these circumstances, the procedure was usually abandoned with no untoward consequences. Class II: In this situation there was true arterial wall penetration through the adventitia with two possible outcomes. In the first, contrast material was seen outside the arterial wall, but without active bleeding. Here, in the more common situation, the probe had penetrated the

Laser Angioplasty

artery in an area of dense atherosclerotic material, so little if any blood was flowing through that segment. Occasionally, such an injury was attended by leakage of blood from the artery. Because of the severe disease, the blood flow was under very low pressure, so clot formation sealed the penetration site. No operative intervention was required. Class HI: This was the same type of damage as in Class lI, but the active bleeding continued through the perforation site and surgical intervention was necessary to control the haemorrhage. The Class I perforation with no re-entry is identical to the failure code of the same description. Because we have not encountered any Class III perforations, our 15 instances of mechanical arterial injury listed in Table 2 as perforation represent Class II injuries only. One perhaps iatrogenically induced form of thermal arterial injury may relate to the concentration of laser energy on minimally diseased arterial tissue. A prime example is the technique of glazing, relasing of the dilated segment purported to smooth the disrupted plaque. While the concept of welding tissue to remove surface irregularities which might encourage plaque formation is logical, the temperature at which this should be done is still under investigation. When we began this study, we glazed the arteries at 5 W of energy, which produced an intra-arterial temperature of 120°C. We then altered the glazing energy, increasing it to the treatment level of 12 W. This produced a temperature of about 4 0 0 - 4 5 0 ° C at the probe tip. Studies have shown that temperatures this high thermally scar intimal tissue and significantly alter the architecture of atherosclerotic plaque. 21-23 Denser lesions of total or near total occlusion would be able to absorb this high temperature with little damage to the healthy tissue below, while shallow subcritical stenoses are less able to insulate the intima from damage. We have recently conducted thermistor studies of probe temperature, and we have seen the evidence of this temperature variation in relation to plaque density. It may well be that glazing after the plaque's density has been reduced may be deleterious, at least at high temperatures. Another area of concern, unrelated to the issue of thermal injury but relevant to outcome, was the incidence of thrombosis. As a complication, thrombosis was rare (4%) and usually easy to treat with thrombolytic therapy (urokinase or streptokinase) or mechanical thrombectomy and relasing. However, dealing with the cause of this problem has not proven as simple. In most of these patients, the anticoagulation therapy was limited to use of antiplatelet drugs pre- and postoperatively and intraoperative heparinisation. However, in an effort to reduce early thrombosis and restenosis, the therapy was enhanced to include a 1000 unit/h

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heparin drip initiated postoperatively after sheath removal andadjusted to maintain the activated coagulation time above 200 s for 48 h. This has diminished the incidence of acute postoperative thrombosis, but it will be some time before its impact on restenosis is determined. Finally, we need to look at the issue of safety. The impression we first had that the closed beam probe was not harmful to the artery may well be an error, and an ironic one considering the evolution of this probe. Indeed, evidence is mounting that there are several instances in which the laser may do more harm than good. For one, the high temperature of the metal-tipped probe is definitely injurious to normal tissue; nondiseased intima should never be subjected to laser energy. Further, laser energy should not be delivered longer than is necessary for plaque ablation. Research now suggests that the potential for tissue damage is directly related to the temperature of the probe and length of time it is in contact with the tissue. 2~'22'24 Moreover, at a constant energy/time dosage, the degree of damage is dependent on the ratio of the probe's diameter to that of the artery. 24 Given all these factors, patient selection at this point can best be addressed on the basis of lesion pathology. Obviously, a non-calcified plaque stands a much better chance of being successfully lased than its calcified counterpart. Total occlusions appear to do better in the SFA than the iliacs, but in general, stenoses respond somewhat more favourably. In terms of length, short, discrete lesions are more amenable to lasing than long occluded segments. In the lengthy blockages, the probe is more likely to produce multiple false lumens which ultimately create an inadequate central channel. Lastly, larger vessels and the proximal arteries are more suitable to lasing. Here, the greater diameter ratio of probe to artery lessens the potential for thermal injury, although it leaves more plaque in need of displacement by the balloon. In summary, this assessment of data from 206 patients treated in the first year in our multi-year protocol has raised technical problems, some of which have been addressed, and generated questions yet to be resolved. Definitely, laser-assisted angioplasty with the currently available technology appears less innocuous and, at the same time, less effective than had originally been hoped. Serious considerations exist for the ultimate safety of the closed beam probe and "hot" lasers; further research is needed to clarify the ramifications of thermal injury. There are limitations to the use of the probes now available. Even the partial open beam Spectraprobe cannot deal effectively with all calcified plaques, and other aspects of lesion architecture (fibrous components, Eur J VascSurg Vol 3, February 1989

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length, density, etc.) currently make lasing less effective. However, these m a y no longer be restrictive once the technology advances. W h a t is quite clear at this point is that laser angioplasty is in a state of flux, perhaps greater than it has ever been before. There is considerably basic histopathologic research which is needed now to help us resolve the questions of tissue interaction. Follow-up data is just now becoming available for analysis, and the incidence and causes of restenosis m a y spark further alterations in technique and instrumentation.

References 1 ABELAGS, SEEC,ER IM, BARBIERIE, FRANZINI D, FENECHA, PEPINE Cl, CONTI CR. Laser angioplasty with angioscopic guidance in h u m a n s . ] Am Coll Cardiol 1986 ; 8 : 1 8 4 - 1 9 2 . 2 CUMBERLANDDC, SANBORN T, TAYLORDI, RYAN TI. Percutaneous laser thermal angioplasty: clinical experience in peripheral artery occlusions. J Am Coll Cardiol 1986 ;2 : 211 A. 3 CUMBERLANDDC, SANBORN TA, TAYLORDI, MOORE Di, WELSH CL, GREENFIELD Al, GUBEN JK, RYAN TJ. Percutaneous laser thermal angioplasty: initial clinical results with a laser probe in total peripheral artery occlusions. Lancet 1986; 1 : 1 4 5 7 - 1 4 5 9 . 4 CUMBERLANDDC, TAYLORDI, PROCTORAE. Laser-assisted percutaneous angioplasty: initial clinical experience in peripheral arteries. Clin Radiol 1986: 37: 4 2 3 - 4 2 8 . 5 CUMBERLANDDC, TAYLERDI, PROCTERAE. Pereutaneous laser angioplasty. Initial clinical experience. Ann Radiol (Paris) 1986 ;29 : 215 218. 6 GESCHWINDH], BOUSSIGNACG, TEISSEIRE B, BENHAIEMN, BITTOUNR, LAURENT D. Conditions for effective Nd-YAG laser angioplasty. Br Heart J 1984; 52:484M~89. 7 GESCHWINDH, FABRE M, CHAITMAN BR, LEFEBVRE-VILLARDEBOM, LADoucH A, BOUSSIGNACG, BLAIR JD, KENNEDYHL. Histopathology after Nd:YAG laser percutaneous transluminal angioplasty of the peripheral arteries. ] Am Coil Cardiol 1986: 8 : 1 0 8 9 - 1 0 9 5 . 8 GINSBURGR, KIM DS, GUTHANBRD, TOTHJ, MITCHELLRS. Salvage of an ischemic limb by laser angioplasty: description of a new technique. Clin Cardiol 1984: 7 : 54-58. 9 GINSBERG R, WEXLER L, MITCHELL KS, PROFITT D. Percutaneous transluminal laser angioplasty for treatment of peripheral vascular disease: clinical experience with sixteen patients. Radiology 1985; 1 5 6 : 6 1 9 624.

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10 McCowAN TC, FERRIS E], BAKER ML, et al. H u m a n percutaneous laser angioplasty, ] Ark Med Soc 1 9 8 6 : 8 2 : 5 9 4 - 5 9 6 . 1 ] LEE G, REIS RL, BOGGANMD. CHAN MC, LEE MH, LOW RI, HANNAHH, MASON DT. Laser reeanalisation in severe end-stage peripheral vascular disease. Am ] Cardiol 1987; 59: 3 8 6 - 3 8 7 , 12 SANBORNTA, HAUDENSCHILDCC, GABBER GR, RYAN TJ, FAXON DP, Angiographic and histologic consequences of laser thermal angioplasty: comparison with balloon angioplasty. Circulation 1987; 75: 1281-1286. 13 SANBORNTA, GREENFIELDAJ, GUBENJK, MENSOIAN JO, LOGERFOFW, H u m a n percutaneous and intraoperative laser thermal angioplasty: initial clinical results as an adjunct to balloon angioplasty. ] Vase Surg 1 9 8 7 : 5 : 8 3 - 9 0 . 14 ABELAGS. Laser arterial recanalization: a current perspective. ] Anl Coil Cardiol 1988 : 12 : 103-1 () 5. 15 DIETHKICH EB, TIMBADIA E, BAHADIR I. Hydrophilic guidewire for laser-assisted angioplasty (letter). ] Vase Surg 1988 : 8 : 201 202, 16 DIETHRICH ~B, ROZACIJ, TIMBADIAE, BAIIAI/IR 1, COBURNK, ZENZEN S. Laser angioplasty--a surgical perspective. Medicamundi 1987: 32:127-132. 17 DIETtfKICHEB, ROZACl], T~MBAmAE, BAHADIRI, COBURNK, ZENZEN S. Argon laser-assisted peripheral angioplasty. Vase Surg 1988;22: 77-87. 18 DIETHRICH EB, TIMBADIA E, BAHADIR 1. Peripheral laser-assisted angioplasty. In: Proceedings of the XXVI World Congress of the International College of Surgeons, Montorsi W.. ed., Monduzzi Editorc, Milan, Italy, 1988, pp 4 3 3 - 6 . 19 DIETHRICHEB, TIMBADIAE, BAHADIRI. Peripheral laser angioplasty. In: Advances in Angioplasty, Proceedings of the First German Symposium on Laser Angioplasty, Muller GJ, Biamino G, eds., Ecomed Verlagsgesellschaft, Berlin, West Germany, 1988, pp. 2 1 7 - 2 2 6 . 20 DIETHRICH LB. Surgical laser recanalization techniques. In: Laser Angioplasty, Sanborn TA, ed,, Alan R. Liss, New York. 1989 (in press). 21 JENKINSRD, SINCLAIRIN, ANANDR, KALII, AG, SCHOENF], SPEARSJR. Laser balloon angioplasty: effect of tissue temperature on weld strength of h u m a n postmortem intima-media separations. Lasers Surg Med 1988 ; 8 : 30-3% 22 ANANDRK, SINCLAIRIN, JENKINSRD, HIEHLE l F, lAMES L, SPEARSJR. Laser balloon angioplasty: effect of constant temperature versus constant power on tissue weld strength. Lasers Surg Med 1988;8: 40-44. 23 WELCH AJ, BRADLEY AB, TORBES JH, MOTAMEDI M, GHIDONI JJ, PEARCEJA, HUSSEINH, O'ROURKERA. Laser probe ablation of normal and atherosclerotic h u m a n aorta in vitro: a first thermographic and histologic analysis. Circulation 1987 ; 5 : 1 3 5 3 - 1 3 6 3 . 24 STRIKWERDA S, BOTT-SILVERMANC, RATLIFF NB, GOOKMAST1CM, COTHREN RM, COSTELLOB, KITTRELLC, ]~ELDMS, KRAMERJR. Effects of varying argon ion laser intenstiy and exposure time on ablation of atherosclerotic plaque. Lasers Surg Med 1988 ; 8 : 6 6 - 7 1 .

Received 4 October 1988