What is the difference between thrombus and plaque




















Carotid artery disease refers to the blockage of carotid arteries, which can give rise to complications such as stroke. Peripheral artery disease can occur due to narrowing and thereby result in a reduced perfusion of upper limbs, lower limbs, and pelvis. Major risk factors for the development of atherosclerosis include smoking, obesity, alcohol, reduced physical activity, family history and an unhealthy diet rich in cholesterol and fat components.

Most patients will not experience any sign or symptom until a major disastrous condition like a stroke or a myocardial infarction takes place. The diagnosis of atherosclerosis mainly includes the lipid profile which will reveal increased levels of total cholesterol levels, triglycerides, LDL and VLDL along with a reduced HDL level. Moreover, it is important to diagnose other comorbid conditions like hypertension and diabetes mellitus by making regular visits to the clinic.

However, major treatments for atherosclerosis includes lifestyle modifications such as quitting smoking and alcohol, a healthy diet, exercise, reducing weight and avoiding stressful conditions.

This is the formation of a blood clot inside a blood vessel which mainly consists of a platelet plug made out of aggregated platelets and a mesh of cross-linked fibrin proteins. A thrombus is usually a healthy response to a blood vessel wall injury, but the danger occurs when it tends to get detached from the wall, traveling to distant sites, obstructing the major blood vessels of important organs like lungs, heart, and brain.

Thrombosis can result in strokes, heart attacks, and pulmonary embolism. Fissuring commonly promotes thrombosis also in the lumen of the artery and may be followed by thrombus fragmentation and embolization. Mural thrombi may wax and wane, causing intermittent occlusions and fleeting, minor clinical symptoms. Further episodes of thrombosis increase the mass of the mural thrombus in the already restricted lumen and may herald the onset of ischemic symptoms, abruptly aggravate a stable clinical state and produce the crescendo type of unstable angina, dysrhythmias, myocardial infarction or sudden coronary death.

Palabras clave:. Full Text. Figure 1. Table 3. TCFA, thin-cap fibroatheroma. Figure 2. Maseri, S. Severi, M. Nes, et al. Pathogenetic mechanisms, estimated incidence and clinical and coronary arteriographic findings in patients. Am J Cardiol. Finn, M. Nakano, J. Narula, et al. Arterioscler Thromb Vasc Biol. Kramer, S. Rittersma, R. De Winter, et al. Relationship of thrombus healing to underlying plaque morphology in sudden coronary death. J Am Coll Cardiol. Richardson, M.

Davies, G. Influence of plaque configuration and stress distribution on fissuring of coronary atherosclerotic plaques. Lin, P.

Penha, F. Zak, et al. Morphodynamic interpretation of acute coronary thrombosis, with special reference to volcano-like eruption of atheromatous plaque caused by coronary artery spasm. Maseri, A. Baroldi, et al. Coronary vasospasm as a possible cause of myocardial infarction.

N Engl J Med. Gertz, G. Uretsky, R. Wajnberg, et al. Endothelial cell damage and thrombus formation after partial arterial constriction: Relevance to the role of coronary artery spasm in the pathogenesis of myocardial infarction.

Shin, S. Ann, G. Singh, et al. OCT—defined morphological characteristics of coronary artery spasm aides in vasospastic angina. Guidelines for diagnosis and treatment of patients with vasospastic angina coronary spastic angina JCS : Digest version. Circ J. Philipp, D. Bose, W. Wijns, et al. Do systemic risk factors impact invasive findings from virtual histology? Insights from the international virtual histology registry.

Eur Heart J. Kume, T. Akasaka, T. Kawamoto, et al. Assessment of coronary arterial thrombus by optical coherence tomography. Jia, F. Abtahian, A.

Aguirre, et al. In vivo diagnosis of plaque erosion and calcified nodule in patients with acute coronary syndrome by intravascular optical coherence tomography. Yabushita, B. Bouma, S. Houser, et al. Characterization of human atherosclerosis by optical coherence tomography. Sumi, A. Yamashita, S.

Matsuda, et al. Disturbed blood flow induces erosive injury to smooth muscle cell-rich neointima and promotes thrombus formation in rabbit femoral arteries. J Thromb Haemost. Shiomi, T. Ishida, T. Kobayashi, et al. Vasospasm of atherosclerotic coronary arteries precipitates acute ischemic myocardial damage in myocardial infarction-prone strain of the Watanabe heritable hyperlipidemic rabbits. Acute vascular endothelial changes associated with increased blood velocity gradients.

Circ Res. Koskinas, C. Feldman, Y. Chatzizisis, et al. Natural history of experimental coronary atherosclerosis and vascular remodeling in relation to endothelial shear stress: A serial, in vivo intravascular ultrasound study. Para, D. Bark, A. Lin, et al.

Rapid platelet accumulation leading to thrombotic occlusion. Ann Biomed Eng. Yamashita, Y. Asada, H. Sugimura, et al.

Contribution of von Willebrand factor to thrombus formation on neointima of rabbit stenotic iliac artery under high blood-flow velocity. B2 Medline. Bentzon, F. Otsuka, R. Virmani, et al.

Virmani, A. Burke, A. Farb, et al. Farb, A. Tang, et al. Coronary plaque erosion without rupture into a lipid core. A frequent cause of coronary thrombosis in sudden coronary death.

Van der Wal, A. Becker, C. Van der Loos, et al. Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology. Yoo, S. Song, J. Lee, et al.



0コメント

  • 1000 / 1000