Page 4 - Carotid and peripheral vascular interventions textbook
P. 4
CAROTID AND PERIPHERAL VASCULAR INTERVENTIONS: STEP-BY-STEP
PATHOGENESIS to f brosis development and calcif cation of atheromatous
plaque that results in CTO which has negative impact on
Atherosclerosis is the most common pathology the long-term outcomes of any endovascular procedure.
of femoropopliteal occlusive disease. Inf ammation is Crossing femoropopliteal CTO is still a problematic
important in causing and progression of PAD. Diabetes endovascular procedure. A normal CTO plaque comprises
mellitus and smoking produce oxidative stress, which calcium, extracellular matrix, smooth muscle cells, as well
indirectly and directly induce inf ammatory pathways. as extracellular and intracellular lipids. A rigid f brous cap
These two risk factors are related to atherosclerosis in is normally present at both CTO ends with loose or soft
the femoropopliteal segment. Haltmayer et al. discovered lipid tissue, thrombus, and extracellular matrix within
no-site specif c relationship between cholesterol and the core. CTO lesions frequently show endothelialized
hypertension and prevalent PAD, but triglyceride level was microchannels, produced via neovascularization, which
only signif cantly related to PAD for the femoropopliteal cover the blocked segment from proximal to distal cap.
segment (8). The marked vulnerability of the femoropopliteal The presence of microchannels within the CTO facilitates
segment for atherosclerosis remains poorly understood. guide wire passage across occlusion. However, more
Many factors make this area susceptible to disease. The frequently, there is a compact homogenous f brous core,
femoropopliteal segment is f xed between the knee and hip which blocks guide wire crossing and subsequent balloon
joints, and the SFA endures complex external mechanical inf ation diff cult.
stress comprising torsion, bending, compression and Another uncommon etiology of femoropopliteal
f exion (Fig. 12-2). Its distal segment also crosses the occlusive disease is popliteal artery entrapment syndrome
adductor canal that additionally magnif es compression (PAES), in which an abnormally located or enlarged
with thigh contraction. In addition, the adductor canal is calf muscle compresses the main artery at the back of
a region with low wall shear stress, which is associated the knee (popliteal artery) (10). The incidence of PAES
with atherogenesis (9). Repeated injury at this area leads is around 0.17%-3.5% of the Unites States general
Contraction
Torsion
Kink
332 Compression
Fixed
Kink
Compression
Flexion
Figure 12-2. Unique mechanical forces on the superf cial femoral and popliteal artery cause negatively impact on the long-term outcomes
of endovascular intervention.