T.P. Wróbel et al.
508
[27, 28]. Immobilized foam cells, lipids, debris, crystals of cholesterol (lipid core)
surrounded by vascular smooth muscle cells, connective tissue t-lymphocytes and
other elements accumulated in subendothelial space form assymetrical focal thickening of tunica media—atherosclerotic plaque [29–31, 35].
Further activation of inflammatory processes in atherosclerotic plaque results in
matrix metalloproteinases (mmPs), cysteine proteases and mast cell- derived chymase secretion. this may lead to thinning of cap of atherosclerotic plaque, which is
prone to rupture [36–39] and form so called vulnerable atherosclerotic plaque. thin
cap surrounding the whole lesion structure contains a smaller amount of smooth
muscle cells, extracellular matrix components and is highly infiltrated by activated
macrophages Fig. 17.1b. A plaque rupture can be defined as a disruption of the
fibrous cap accompanied by intrusion of erythrocytes into the plaque itself [40].
Plague rupture leads to intravascular thrombus formation and partial or total artery
occlusion. Plaque ruptures do not always result in ischemic symptoms and are often
clinically silent. In advanced plaque angiogenesis is actived but new vessels are
susceptible for rupture. Intraplaque haemorrhage occurring during plaque rupture
may be detected in healed lesion by the presence of erythrocytes surrounded by
lipid core components [41]. the majority of unstable plaque structure is composed
of large “necrotic core”, occupying approximately 1/3 to ½ of the total plaque area,
whereas in unruptured vulnerable plaques it occupies usually less than ¼ of the lesion [42]. typical for this structure is large free cholesterol content (including cholesterol crystals) and spotty calcifications, whereas in contrast to early plaques cholesterol esters compartment is significantly smaller. Necrotic core is a major part of
plaque in advanced atherosclerosis. massive necrosis within atherosclerotic plaque
leads to the accumulation of cellular remnants in necrotic core area, which becomes
“the graveyard of dead macrophages” [43] and the major pro-inflammatory stimuli
that promotes vascular inflammation. the model of plaque’s features important in
atherosclerotic plaque progression (described above) and detectable with the use of
vibrational spectroscopies is presented in Fig. 17.1b.
17.2.3 Techniques in the Diagnosis of Atherosclerosis
there are numerous amounts of imaging techniques in vascular biology and medicine that could by applied for atherosclerotic plaque imaging. A list of the most
common imaging techniques includes: integrated backscatter intravascular ultrasound (IB-IvuS), virtual histology intravascular ultrasound (vh-IvuS), optical
coherence topography (oCt), magnetic resonance imaging (mRI), angiography,
thermography, angioscopy, elastography, positron emission topography (PEt) and
electron-beam computed topography (EBCt).
one of the most interesting trends is the use of laser spectroscopy for identification of atherosclerotic plaques. An example of this is the use of fluorescence
spectroscopy (IFS) in the identification and diagnosis of atherosclerotic lesions [44,
45] and guidance for laser angioplasty systems [46]. other optical diagnostics techniques, which can be used are reflectance spectroscopy (dRS) [45] and light scat-
508
[27, 28]. Immobilized foam cells, lipids, debris, crystals of cholesterol (lipid core)
surrounded by vascular smooth muscle cells, connective tissue t-lymphocytes and
other elements accumulated in subendothelial space form assymetrical focal thickening of tunica media—atherosclerotic plaque [29–31, 35].
Further activation of inflammatory processes in atherosclerotic plaque results in
matrix metalloproteinases (mmPs), cysteine proteases and mast cell- derived chymase secretion. this may lead to thinning of cap of atherosclerotic plaque, which is
prone to rupture [36–39] and form so called vulnerable atherosclerotic plaque. thin
cap surrounding the whole lesion structure contains a smaller amount of smooth
muscle cells, extracellular matrix components and is highly infiltrated by activated
macrophages Fig. 17.1b. A plaque rupture can be defined as a disruption of the
fibrous cap accompanied by intrusion of erythrocytes into the plaque itself [40].
Plague rupture leads to intravascular thrombus formation and partial or total artery
occlusion. Plaque ruptures do not always result in ischemic symptoms and are often
clinically silent. In advanced plaque angiogenesis is actived but new vessels are
susceptible for rupture. Intraplaque haemorrhage occurring during plaque rupture
may be detected in healed lesion by the presence of erythrocytes surrounded by
lipid core components [41]. the majority of unstable plaque structure is composed
of large “necrotic core”, occupying approximately 1/3 to ½ of the total plaque area,
whereas in unruptured vulnerable plaques it occupies usually less than ¼ of the lesion [42]. typical for this structure is large free cholesterol content (including cholesterol crystals) and spotty calcifications, whereas in contrast to early plaques cholesterol esters compartment is significantly smaller. Necrotic core is a major part of
plaque in advanced atherosclerosis. massive necrosis within atherosclerotic plaque
leads to the accumulation of cellular remnants in necrotic core area, which becomes
“the graveyard of dead macrophages” [43] and the major pro-inflammatory stimuli
that promotes vascular inflammation. the model of plaque’s features important in
atherosclerotic plaque progression (described above) and detectable with the use of
vibrational spectroscopies is presented in Fig. 17.1b.
17.2.3 Techniques in the Diagnosis of Atherosclerosis
there are numerous amounts of imaging techniques in vascular biology and medicine that could by applied for atherosclerotic plaque imaging. A list of the most
common imaging techniques includes: integrated backscatter intravascular ultrasound (IB-IvuS), virtual histology intravascular ultrasound (vh-IvuS), optical
coherence topography (oCt), magnetic resonance imaging (mRI), angiography,
thermography, angioscopy, elastography, positron emission topography (PEt) and
electron-beam computed topography (EBCt).
one of the most interesting trends is the use of laser spectroscopy for identification of atherosclerotic plaques. An example of this is the use of fluorescence
spectroscopy (IFS) in the identification and diagnosis of atherosclerotic lesions [44,
45] and guidance for laser angioplasty systems [46]. other optical diagnostics techniques, which can be used are reflectance spectroscopy (dRS) [45] and light scat-