Page 4 - Carotid and peripheral vascular interventions textbook
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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.
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