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The Nature of Dissections in Infrapopliteal Arteries: Insights from Intravascular Ultrasound Imaging
Abstract: Treatment of infrapopliteal (IP) arteries can be challenging due to the presence of medial calcinosis and fibrotic rings. Adequate balloon sizing is important and angiography seems to underestimate the true size of the vessel by about 30% when compared with intravascular ultrasound. Dissection post angioplasty is a key mechanism that yields a larger minimal luminal area within the vessel. In this case report, we illustrate a pattern of dissection in an IP artery that appears different from dissections seen in atherosclerotic plaques. The dissection is a focal break within the fibrotic ring but can lead to subintimal flow/hematoma and possibly vessel recoil. We discuss the implications of this dissection pattern on treatment.
Key words: critical limb ischemia, chronic total occlusion, intravascular ultrasound, infrapopliteal
Reprinted with permission from VASCULAR DISEASE MANAGEMENT 2019;16(3):E38-E40.
We present a case of critical limb ischemia (CLI) with chronic total occlusion of the anterior tibialis artery (AT) treated under intravascular ultrasound (IVUS) guidance to illustrate the nature of dissections in the infrapopliteal (IP) territory and how this may be different from the femoropopliteal artery. Precise imaging with intravascular ultrasound (IVUS) was carried on to evaluate accurately vessel size and to define the nature of dissections post angioplasty.1-5
Case presentation
A 78-year old man with history of diabetes mellitus, coronary artery disease, and peripheral arterial disease (PAD) developed a non-healing ulcer in the left heel and was brought for intervention to treat critical limb ischemia (CLI). Angiography revealed total occlusion of the tibial arteries with only the AT seen reconstituted by collaterals to the foot (Figure 1A). Severe 90% in-stent restenosis of the distal left femoropopliteal artery was also observed.
After achieving contralateral access, antegrade crossing of the left AT could not be achieved. Pedal access was then obtained via micropuncture technique with a 4 Fr sheath (Cook), and intraluminal crossing was accomplished under ultrasound guidance. IVUS was then performed via the retrograde approach. Using IVUS, the distance from the internal elastic lamina (IEL) to IEL was measured, and the vessel diameter was quantitated at 4.0 mm. Extensive 360° medial calcinosis and fibrosis in the AT were appreciated (Figure 2A).
Dilatation of the diseased segment of the left AT into the left popliteal was then done with an Armada 4.0 mm in diameter (Abbott) up to 16 atm. This high pressure was needed for full balloon expansion. Following percutaneous transluminal angioplasty (PTA), IVUS revealed a focal dissection in the AT fibrotic/calcified ring not identified on the angiogram. Based on the iDissection grading of dissections, this was classified as C2 (Figure 2B).6
Via the pedal access, a Xience drug-eluting stent (DES) 4 × 38 mm was used to treat the proximal AT and post dilated to 20 atm, followed by another 4 × 33 mm Xience DES placed in tandem fashion and post dilated to 22 mm Hg. This was followed by stenting via the contralateral approach to the distal left superficial femoral artery (SFA) into the popliteal to the bifurcation with the AT using the Eluvia 6.0 × 120 mm DES (Boston Scientific). The remainder of the diseased distal left SFA that was not covered by the Eluvia stent was treated with a 6.0 mm IN.PACT drug coated balloon (Medtronic). Excellent flow was seen across the left femoropopliteal segment into the left AT (Figure 1B). The pedal sheath was removed, and hemostasis was achieved manually. Patency of the dorsalis pedis at the site of the pedal access was verified for integrity by an antegrade injection of contrast via the contralateral sheath.
Images were analyzed by the quantitative vascular lab (QVL) at the Midwest Cardiovascular Research Foundation using Echoplaque software (INDEC Systems) for IVUS analysis and CAAS software (Pie Medical Imaging) for angiographic analysis. The AT diameter was quantitated at 2.75 mm by angiography, whereas it was 4.0 mm on IVUS. This represents an underestimation of the true size of the vessel by ~ 31%, similar to what we have previously reported.7
Discussion
This cases illustrates the gross underestimation of the size of the IP vessels by angiography1,2 and the need for precise imaging with IVUS for optimal balloon dilatation and stent sizing.4-6 Of particular importance is the pattern of dissection that was seen, which appeared to behave differently from femoropopliteal dissections. IP disease is generally characterized with rings of fibrosis and medial calcinosis restricting lumen expansion with percutaneous transluminal angioplasty (PTA) alone. Intentional dissections with PTA are part of the process to gain luminal area after treatment. However, dissections carry with them the risk of deeper injury and restenosis, or a wider circumference of injury and subsequent acute or subacute vessel closure. Several methods have been proposed to improve vessel compliance in IP disease and reduce the risk of severe dissections, including atherectomy6 and scoring devices. Although angiographically these devices appear to reduce dissections and bailout stenting, IVUS reveals that angiography is suboptimal in defining the presence and severity of dissections left within the vessel after the use of these devices. In fact, angiography missed approximately 6 to 1 dissections when compared with IVUS in femoropopliteal arteries. Additionally, IVUS identified medial and adventitial injury in almost 40% of cases after atherectomy.5 Therefore, dissections are an inevitable process needed to achieve better luminal gain when treating PAD. Pretreatment of the vessel using compliance-modifying devices to avoid wider or deeper dissections, and repair of such dissections when they occur, may prove to be an important strategy to accomplish optimal luminal gain with minimal vessel disruption.
Femoropopliteal dissections involve significant intimal/subintimal dissection planes that can be of narrow or wide circumference and of varying depth involving the intima to the adventitia.5,6 In cases below the knee, the fibrotic rings and calcinosis resist stretching and therefore can easily recoil after PTA. Unless a break in these rings occur, the likelihood of expanding the vessel is reduced. When sizing the balloon to match the internal elastic lamina (IEL) to IEL, PTA resulted in a focal break in these rings which subsequently allowed dissections and flow behind the fibrotic/calcified ring at various depth. The fibrotic tear does not result in a wide flap that falls back into the lumen. Therefore, an expanding circumferential hematoma/flow around the fibrotic ring may become more important in vessel recoil and lumen loss after IP PTA. Managing these types of dissections below the knee may therefore be different than managing those from above the knee. The placement of a scaffold (Stent or Endotack, Investigational in the US, Intact Vascular) proximal and distal to the entry point may become important in stabilizing these types of dissections. A full characterization of this finding is being studied in the iDissection below the knee following PTA and orbital atherectomy and currently is ongoing in our laboratory.
In conclusion, precise imaging is critical to characterize vessel size and lesion morphology with significant implications on IP arterial interventions.
Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr Shammas receives educational and research grants from Intact Vascular, Phillips, Boston Scientific, VentureMed Group and Bard. Dr Armstrong reports consulting for Abbott Vascular, Boston Scientific, Medtronic, Philips, and Intact Vascular. John Shammas, Dr Radaidah, and Gail A Shammas report no conflicts of interest regarding the content herein.
Manuscript submitted February 7, 2019; accepted February 9, 2019.
Address for correspondence: Nicolas W. Shammas, MD, MS, EJD, FACC, FSCAI, FSVM, Midwest Cardiovascular Research Foundation, 1622 E. Lombard Street, Davenport, IA 52803. Email: shammas@mchsi.com
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