Arterial thrombus formation, mechanism

Dissection of the internal carotid and vertebral arteries is a common cause of stroke, particularly in young patients. Although many occur due to trauma, it is estimated that over half occur spontaneously. The mechanism of stroke following arterial dissection is either by artery-to-artery embolism, by thrombosis in situ, or by dissection-induced lumenal stenosis with secondary cerebral hypoperfusion and low-flow watershed infarction. Occasionally, dissection may lead to the formation of a pseudoaneurysm as a source of thrombus formation. Vertebrobasilar dissections that extend intracranially have a higher risk of rupture leading to subarachnoid hemorrhage (SAH). ° ... 

Goto S. Understanding the mechanism and prevention of arterial occlusive thrombus formation by antiplatelet agents. Curr Med Chem Cardiovasc Hematol Agents. 2004 2 149-156. 

Protocol 4 Stenosis+PAF Infusion The LCX is stenosed without prior mechanical wall injury. This preparation does not lead to thrombus formation (subcritical stenosis). For the induction of CFRs, in addition PAF (C16-PAF, Bachem) (0.2 nmol/kg/min) is infused into one cannulated lateral branch of the coronary artery. 

Fig. 4. Technique for monitoring platelet aggregation in the partially obstructed left circumflex coronary artery of the dog. Electromagnetic flow probes measure blood flow. Partial obstruction of the coronary artery with a plastic Lexan cylinder results in episodic cyclical reductions in coronary blood flow that are due to platelet-dependent thrombus formation. Every 2-3 mm the thrombus must be mechanically shaken loose to restore blood. For detailed application of the Folts model, see Sullivan et al. (1992) Folts, Rowe (1974, 1988) and Folts et al. (1976, 1982).

Harbauer (1984) first described a venous model of thrombosis induced by mechanical injury and stenosis of the jugular vein. In a modification, both arterial and venous thrombosis is produced in rabbits by stenosis of the carotid artery and the jugular vein with simultaneous mechanical damage of the endothelium. This activates platelets and the coagulation system and leads to changes in the bloodstream pattern. As a consequence, occluding thrombi are formed as detected by blood flow measurement. The dominant role of platelets in this model is shown by the inhibitory effect of an antiplatelet serum in both types of vessels (Just 1986). The test is used to evaluate the antithrombotic capacity of compounds in an in vivo model of arterial and venous thrombosis where thrombus formation is highly dependent on platelet activation. 

Peripheral arterial occlusion can be the initial manifestation of cardiac or systemic disease. At times, patients with chronic stable claudication may experience abrupt shortening of the distance at which claudication occurs, and this may be the only symptomatic evidence of an acute arterial occlusion either by embolization of by thrombus formation on a pre-existing arterial stenosis. The situation is not chronic and stable any more, but acute and unstable. As ischemia becomes more severe, the patient with chronic peripheral arterial disease develops ischemic pain at rest. The pathophysiologic mechanisms and the clinical presentation parallel the evolution of chronic stable angina pectoris to unstable angina and acute coronary syndromes. 

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