Article

Laser-assisted Angioplasty - A Promising Therapy for Critical Limb Ischemia

Register or Login to View PDF Permissions
Permissions× For commercial reprint enquiries please contact Springer Healthcare: ReprintsWarehouse@springernature.com.

For permissions and non-commercial reprint enquiries, please visit Copyright.com to start a request.

For author reprints, please email rob.barclay@radcliffe-group.com.
Average (ratings)
No ratings
Your rating
Copyright Statement:

The copyright in this work belongs to Radcliffe Medical Media. Only articles clearly marked with the CC BY-NC logo are published with the Creative Commons by Attribution Licence. The CC BY-NC option was not available for Radcliffe journals before 1 January 2019. Articles marked ‘Open Access’ but not marked ‘CC BY-NC’ are made freely accessible at the time of publication but are subject to standard copyright law regarding reproduction and distribution. Permission is required for reuse of this content.

Critical limb ischaemia (CLI) is defined as ischaemic rest pain requiring opiate analgesics, and ulceration or gangrene of the foot or toes attributable to arterial occlusive disease.1 In contrast to patients with claudication, those with CLI have resting arterial perfusion that is inadequate to sustain the metabolic demands of the distal bed. CLI has been formally graded within the current Rutherford system (grades 4-6), and is usually a consequence of multi-level lower extremity atherosclerotic disease.2 Early clinical consequences of untreated CLI include limb loss with amputation, gangrene, sepsis, myocardial infarction, stroke and death.3,4 In 2005, over 200,000 lower extremity amputations were performed in the US, highlighting the prevalence of this clinical entity. The periprocedural mortality rate for amputation in patients with CLI has been reported at 5-17%, and as many as 37% of CLI patients are considered poor surgical candidates.5,6 While surgical bypass can be an effective strategy for limb salvage and quality of life improvement, it is nonetheless associated with prolonged recovery, potential loss of saphenous vein conduit, myocardial infarction, wound infection and death.7,8 Therefore, in treating CLI, the therapeutic goals for the endovascular specialist should be limb preservation, quality of life improvement and a reduction in the morbidity and mortality associated with traditional revascularisation.

Patients with CLI require aggressive medical therapy and local wound care. Defining the lower extremity arterial circulation by either invasive (angiography) or noninvasive (vascular duplex, magnetic resonance angiography or computed tomography angiography) methods is imperative. Restoration of pulsatile, 'straight-line' blood flow to the pedal arch via one or more tibial arteries is necessary for clinical success.9 Whereas percutaneous transluminal angioplasty (PTA) has been shown to be effective for focal or short segment occlusions; long segment arterial occlusions have traditionally responded poorly.10-12 Numerous innovative technologies are currently being utilised for limb salvage including laser atherectomy, excisional atherectomy, cryoplasty, cutting balloon angioplasty, balloon-expandable and self-expanding stents. The recently reported phase II Laser-Assisted Angioplasty for Critical Limb Ischemia (LACI) trial, which employed the excimer laser in population of patients with CLI, deemed poor surgical candidates, has demonstrated promising acute and intermediate outcomes in this clinically challenging population.13

Recent advances in the design and performance of laser catheters have led to promising improvements in the treatment of complex peripheral arterial disease.14,15

The LACI multi-centre trial was designed to evaluate the effectiveness of excimer laser angioplasty for patients with lower extremity CLI who were poor candidates for surgical revascularisation.13 145 patients with 155 critically ischaemic limbs were prospectively enrolled, and the diagnosis of CLI was based on ischaemic rest pain or by non-healing ulcers or gangrene. Tissue loss was present in 69% of enrolled patients. Inclusion criteria included at least one angiographically identifiable tibial artery in poor candidates for surgical bypass due to 1. absence of suitable autologous vein; 2. lack of undiseased distal targets >1mm in diameter; and/or 3. high-risk of surgical mortality. The procedural objective of the LACI trial was to achieve pulsatile 'straight-line' blood flow to the foot through at least one tibial artery. For occlusions resistant to guidewire penetration, the 'step-by-step' technique was utilized; the guidewire was advanced just proximal to the lesion, and the excimer laser catheter was brought into contact with the occlusion. The laser catheter was gently advanced and activated for five to ten seconds in an attempt to penetrate the fibrous cap. The guidewire was then used to probe antegrade to find a channel through the lesion. If this could not be found, the laser was reactivated and the above technique repeated. After the lesion was crossed with the guidewire, the laser catheter was used to debulk the entire lesion (Figure 1). Procedural success was defined as <50% residual stenosis in the treated limb, and the primary endpoint was avoidance of major amputation above the level of the ankle at six months. Secondary endpoints included all-cause mortality, need for surgical intervention, stroke or myocardial infarction.

Results

The lesion characteristics and major outcomes from the LACI trial are summarised in Table 1. The mean number of treated lesions was 2.7 per limb, with a mean lesion length of 6.0cm and a total lesion length of 16.0cm per limb. Excimer laser atherectomy was successfully delivered in all but two limbs. Adjunctive balloon angioplasty was performed in 149 (96%) limbs, and stent implantation, at the operator's discretion, in 70 (45%). Stent implantation was most commonly employed in the superficial femoral artery.

Procedural success was achieved in 85% of treated limbs, with pre- and post- angiographic stenosis severities of 92% and 18%. Procedural complications occurred in 12% of treated limbs and included major dissection, acute thrombus formation, distal embolisation and perforation. However, in-hospital-adjudicated serious adverse advents were low, affecting only 2% of patients (one haematoma requiring surgery, two major amputations). At six-month follow-up, patient survival was 92%, with nine (7%) major amputations for a limb salvage rate of 93%. This compares favourably with prior trials which used angioplasty alone and reported amputation rates of 21-35%.10,17 The only risk factor associated with major amputation was Rutherford category 6 at the time of presentation, and there was no significant difference in the stented versus non-stented groups with regard to limb salvage.

Conclusions

Since <30% of patients with CLI have focal lesions favourable for PTA, new endovascular approaches for the treatment of diffuse arterial occlusive disease are needed. The LACI trial treated patients who were poor surgical candidates with an endovascular strategy consisting of 'cool' excimer laser angioplasty followed by adjunctive PTA and/or stenting. The excimer laser has the ability to remove plaque and thrombus by photoacoustic ablation, theoretically reducing the incidence of clinical embolisation.18 An additional advantage of this laser technology is its ability to facilitate guidewire passage in lesions not typically negotiable by standard techniques. Despite the burden of atherosclerotic lesions in these patients, a remarkably high salvage rate of 93% was achieved at six months in surviving patients. Finally, as patients with CLI carry high mortality rates at baseline (up to 21% at 12 months), long-term patency is a less relevant issue, and amputation-free survival and relief of ischaemic symptoms should remain the clinician's primary focus.

References

  1. Eur J Vasc Endovasc Surg (2000);19 Suppl A:S144-243.
    PubMed
  2. Rutherford RB, Baker JD, Ernst C, et al., J Vasc Surg (1997);26: pp. 517-538.
    Crossref | PubMed
  3. ICAI, Eur J Vasc Endovasc Surg (1997);14: pp. 91-95.
    PubMed
  4. Weitz JI, Byrne J, Clagett GP, et al., Circulation (1996);94: pp. 3026-3049.
    Crossref | PubMed
  5. Faglia E, Clerici G, Clerissi J, et al., Eur J Vasc Endovasc Surg (2006);in press.
    Crossref | PubMed
  6. Ann Intern Med (1999);130: pp. 412-421.
    Crossref | PubMed
  7. Albers M, Fratezi AC, De Luccia N, J Vasc Surg (1992);16: pp. 54-59.
    Crossref | PubMed
  8. Treiman GS, Copland S, Yellin AE, et al., J Vasc Surg (2001);33: pp. 948-954.
    Crossref | PubMed
  9. Rastogi S, Stavropoulos SW, Tech Vasc Interv Radiol (2004);7: pp. 33-39.
    Crossref | PubMed
  10. Matsi PJ, Manninen HI, Suhonen MT, et al., Radiology (1993);188: pp. 381-387.
    Crossref | PubMed
  11. Molloy KJ, Nasim A, London NJ, et al., J Endovasc Ther (2003);10: pp. 298-303.
    Crossref | PubMed
  12. Saab MH, Smith DC, Aka PK, et al., Cardiovasc Intervent Radiol (1992);15: pp. 211-216.
    Crossref | PubMed
  13. Laird JR, Zeller T, Gray BH, et al., J Endovasc Ther (2006);13: pp. 1-11.
    Crossref | PubMed
  14. Scheinert D, Laird JR, Jr., Schroder M, et al., J Endovasc Ther (2001);8: pp. 156-166.
    Crossref | PubMed
  15. Visona A, Perissinotto C, Lusiani L, et al., Angiology (1998);49: pp. 91-98.
    Crossref | PubMed
  16. Wollenek G, Laufer G, Thorac Cardiovasc Surg (1988);36 Suppl 2: pp. 126-132.
    Crossref | PubMed
  17. Parsons RE, Suggs WD, Lee JJ, et al., J Vasc Surg (1998);28: pp. 1066-1071.
    Crossref | PubMed
  18. Topaz O, Bernardo NL, Shah R, et al., Am J Cardiol (2001);87: pp. 849-855.
    Crossref | PubMed