Clinical Images

Location of Dissections Post Balloon Angioplasty in Patients With Femoropopliteal Arterial Disease as Seen on Intravascular Ultrasound

Nicolas W. Shammas, MD, MS1;  W. John Shammas, BS1;  James T. Torey, PA2;  Andrew N. Shammas, BS, OMS1

Nicolas W. Shammas, MD, MS1;  W. John Shammas, BS1;  James T. Torey, PA2;  Andrew N. Shammas, BS, OMS1

J INVASIVE CARDIOL 2019;31(7):E230-E231.

Key words: angioplasty, calcium, deep injury, dissections, femoropopliteal artery, intima, IVUS


Dissections following balloon angioplasty of femoropopliteal arterial disease are under-appreciated on angiography and their extent and depth are not characterized. The location of dissections post angioplasty in relationship to plaque morphology may give insight to appropriate therapeutic interventions. Dissections in the coronaries have been reported to occur adjacent to calcium deposits within the plaque and are more likely to occur with eccentric lesions. Recent data indicate that the presence of deeper dissections or subintimal tears correlates with higher target-lesion revascularization. Also, it is likely that wider dissections may lead to acute or subacute lumen compromise.  We have reviewed images from our intravascular ultrasound (IVUS) core lab to define the various locations of dissections in femoropopliteal arteries post angioplasty in relation to plaque morphology. It has been anticipated that dissections would occur at the interface of two different plaque densities.

The following dissection patterns emerge:

(1) At edges of superficial calcium within the plaque (Figure 1). This type of dissection tends to have flow behind the plaque. They can be extensive and dissect deep into the media and adventitia, and on occasion create intramural hematoma. Also, calcified plaques are less likely to detach from the intima toward the lumen. One mechanism of narrowing at the site of these dissections may be the result of expanding hematoma within the vessel wall. Debulking superficial calcium will likely improve vessel compliance and may reduce deeper dissections behind these plaques.

(2) At the interface of fibrous, non-calcified plaque and the internal elastic lamina (Figure 2). This type of dissection seems to involve mostly the intima and leads to detachment of the plaque from the internal external lamina. They tend to be superficial and can be extensive post angioplasty. Although not deep, these dissections can have large flaps (≥180°) that may cause more of an acute or subacute flow impairment. We believe, however, that when these flaps become more extensive, a scaffold becomes necessary to prevent acute or subacute loss of patency.

(3) At areas within ulcerated plaque (Figure 3). When plaque integrity is compromised, angioplasty creates or worsens intimal dissections with larger detachment of these plaques from the internal elastic lamina.

(4) At areas of eccentric plaques (Figure 4). After angioplasty, edge dissections with intraplaque flow are noted. These plaques are likely to be at high risk of embolization with atherectomy and may be an indication to consider embolic filter protection with debulking.

The use of IVUS generates information about plaque morphology that predicts where dissections are likely to occur, allows appropriate sizing of balloons to avoid excessive vessel over-stretching and tears, and defines the potential mechanism of lumen loss post angioplasty, eg, whether it is an expanding hematoma or wide detached flaps from intima.  Similar to coronary interventions, precision imaging with IVUS in peripheral interventions may yield better outcomes. Registries and randomized trials evaluating IVUS as the primary imaging technique to guide peripheral arterial interventions are needed.


From the 1Midwest Cardiovascular Research Foundation, Davenport, Iowa; and 2St. John Hospital and Medical Center, Detroit, Michigan.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr N. Shammas reports research grants from Phillips, Boston Scientific, Intact Vascular, and Bard. The remaining authors report no conflicts of interest regarding the content herein.

The authors report that patient consent was provided for publication of the images used herein.

Manuscript accepted December 11, 2018.

Address for correspondence: Nicolas W. Shammas, MD, MS, FACC, FSCAI, FSVM, Research Director, Midwest Cardiovascular Research Foundation, 1622 E. Lombard Street, Davenport, IA 52803. Email: shammas@mchsi.com

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