Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3720_Библиотеки_им_академика_М_И_Перельмана

thrombus vigorously accumulates, blood flow at and distal to the thrombotic lesion turns slow and turbulent. Clinically, the accompanying vasoconstriction further impairs myocardial perfusion, adversely affects the hemodynamics, and enhances development of ischemic coronary events [29]. Moreover, during PCIs, operators frequently are challenged by the marked friability of the thrombus at the targeted lesion. Yet, at times, an opposite reaction of the thrombus is encountered, with marked resistance to removal attempts by extraction techniques. Such structural instability and rigidity occurs while the

thrombus may loosely or firmly adhere to the underlying atherosclerotic plaque and vessel wall. This duality of response and seemingly contradictory characteristics of thrombus, i.e., eith er marked friability or a resistance, stem from cumulative effects, which are generated by an assortment of thrombus components. Structurally, the thrombus is supported by a framework made of fibrin fibers [30], which anchor platelets and red blood cells as shown in Fig. 12.2. Two distinct types of branching fibrin fibers are organized in a three-dimensional network. Thin fibers are more dense and exhibit resistance to degradation due to higher elastic modulus (i.e., expression of resistance). Thus, thin fibers demonstrate more resistance to deformation by mechanical tools and pharmacologic agents. The opposite holds true for thick fibrin fibers, which are more rapidly dissolved by fibrinolytic agents, exert lower elastic modulus, and are more easily deformed by external forces (e.g., guidewires, balloons, stents, etc.). There are numerous causes behind the formation of thin versus thick fibrin fibers. There are genetic causes, such as Dusart’s disease (autosomal dominant disorder of qualitatively abnormal fibrinogens), which causes formation of thin fibers with increased resistance to degradation and a hypercoagulable state. In addition, acquired etiologies such as diabetes mellitus may cause hyperglycosylation of fibrinogen leading to formation of thinner fibers capable of increased resistance to degradation. Ionic causes, such as pH shifts, ionic strength changes, or calcium concentrations can also affect fiber size. Kinetic causes, including rapid assembly, will also create thinner fibers. Platelets, red blood cells, procoagulants, and vasoconstrictors are anchored to the matrix of the crisscrossing fibers. Abnormalities in platelet function can persist and also predict adverse clinical events following PCI [31,32]. In patients presenting with acute coronary syndromes, the platelets that adhere to the thrombus exert a significant increase in contractile force. This leads to increased platelet aggregation and the entire thrombotic structure exhibits increased elastic modulus [23,24]. The platelets sustain and amplify the coagulant response at the plaque site and further release procoagulant platelet-derived micro­particles [33]. Prominent factors accounting for the formation of a high-grade thrombus burden are displayed in Table 12.1. Two factors, which have drawn recent attention, are hyperglycemia and an increased white blood cell count [29]. Both factors additionally portend the lack of ST-segment resolution in AMI and are associated with worse PCI outcome [34].

angiographically evident intracoronary thrombi [35]. Relying on visual assessment of cineangiographic views of the thrombus size compared with the diameter of the host vessel, this original TIMI thrombus classification was defined as follows: in TIMI thrombus grade 0, no cineangiogr aphic characteristics of thrombus are present; in TIMI thrombus grade 1, possible thrombus is present as determined by such angiography characteristics as reduced contrast density, hazine ss, irregular lesion contour, or a smooth convex “meniscus” at the site of total occlusion suggestive but not diagnostic of thrombus; in TIMI thrombus grade 2, there is definite thrombus, with greatest dimensions <1/2 the vessel diameter; in TIMI thrombus grade 3, there is definite thrombus but with greatest linear dimension >1/2 but <2 vessel diameters; in TIMI thrombus grade 4, there is definite thrombus, with the largest dimension >2 vessel diameters; and in TIMI thrombus grade 5, there is total occlusion. While this classification is user friendly and universally accepted, the accuracy of both the score’s lowest level, i.e., grade 0, and the score’s highest level, i.e., grade 5, can be questioned. With its hallmark characteristic of TIMI 0 flow, the ischemic vessel that contains a thrombus grade 5 is totally occluded. Consequently, the actual ratio between the volume of the underlying plaque and the associated thrombus volume is unknown, yet the assumption of the TIMI scale is that this grade represents the highest thrombus burden. Fig. 12.3AeK presents the different TIMI grades.

In a development intent on overcoming the limitation of the original TIMI grade 5, an important modification was introduced in 2007 by the Thoraxcenter investigators from Rotterdam, the Netherlands [36]. They added a critical step to the recognition and management of this specific grade consisting of a restratification process as shown in Table 12.4. The restratification method incorporates insertion of a thin PCI guidewire or a 1.5-mm balloon for crossing and recanalization of the occlusive grade 5 thrombus. This significantly improves the determination of an underlying occlusive thrombus because in most instances this intervention restores at least some measure of antegrade flow. The next step is angiographic stratification of the “exposed” thrombus within the recanalized artery. Accordingly, a small thrombus burden is represented by grades 1e3 and a large thrombus burden is referred to as grade 4. Then the optimal revascularization tool can be selected for application. From a practical standpoint, the stratified small residual thrombus can be managed with an aspiration catheter followed by implantation of any stent. Adjunct pharmacotherapy can be tailored as well to the target’s needs. For efficient removal, the large-size residual thrombus, especially when resisting standard aspiration, requires application of a powe r-based mechanical thrombectomy device [37]. Among the prominent devices for this task are rheolytic thrombectomy, excimer laser, and the X-Sizer [38e40], with subsequent post-thrombus-removal utilization of