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Atherosclerosis: Difference between revisions
→1.3 Complications of atherosclerosis
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The concept of ‘vulnerable plaque’ has developed into a new concept of ‘vulnerable patient’ as the recent evidence shows that a person’s susceptibility to coagulation and thus vascular events can be influenced by many other factors such as genetics (e.g. procoagulant prothombin gene mutation), coexisting condition (e.g. diabetes), and lifestyle factors (e.g. smoking, obsesity). | The concept of ‘vulnerable plaque’ has developed into a new concept of ‘vulnerable patient’ as the recent evidence shows that a person’s susceptibility to coagulation and thus vascular events can be influenced by many other factors such as genetics (e.g. procoagulant prothombin gene mutation), coexisting condition (e.g. diabetes), and lifestyle factors (e.g. smoking, obsesity). | ||
= | =Complications of atherosclerosis = | ||
Developing of atherosclerotic plaques is not homogenous throughout the vasculature. The following anatomical structures are the most common areas where atherosclerosis takes place, starting from the most common region: dorsal section of the abdominal aorta, proximal coronary arteries, the popliteal arteries, descending thoracic aorta, internal carotid arteries, and renal arteries. It is needless to say that the areas perfused by these vessels are most frequently impaired by the consequences of atherosclerosis. Clinically, this can lead to thromboembolism resulting in major cardiovascular diseases such as stroke and myocardial infarction. | Developing of atherosclerotic plaques is not homogenous throughout the vasculature. The following anatomical structures are the most common areas where atherosclerosis takes place, starting from the most common region: dorsal section of the abdominal aorta, proximal coronary arteries, the popliteal arteries, descending thoracic aorta, internal carotid arteries, and renal arteries. It is needless to say that the areas perfused by these vessels are most frequently impaired by the consequences of atherosclerosis. Clinically, this can lead to thromboembolism resulting in major cardiovascular diseases such as stroke and myocardial infarction. | ||
There are several major complications, such as calcification, rupture, hemorrhage, embolization and weakening of the vessel wall that can lead to serious clinical consequences by acute restriction of blood flow or alterations in arterial wall integrity. Clinically, atherosclerosis can lead to major cardiovascular disease: | |||
* 1.Atherosclerotic plaque can be calcified, which leads to higher rigidity of the vessel wall and therefore favor its fragility. | |||
* 2.When the plaque ruptures, it will release its pro-coagulants to blood and that will lead to the formation of thrombus at the rupture site. This thrombus may cause a complete occlusion of the vessel and result in acute infarction of the involved organ. Or, the thrombus is incorporated into another plaque and continues the process of atherogenesis. | |||
* 3.Fibrous cap or micro vessels, which are formed within the plaque can rupture and cause hemorrhage within the plaque. This hemorrhage results in intramural hematoma and may contribute to the occlusion of the vessel. | |||
* 4.Embolization is the transfer of the fragments of disrupted atheroma to distal vascular sites, which results into occlusion of those sites. | |||
* 5.After a chronic period, fibrous plaque can increase the pressure of the medial layer, which results into atrophy and loss of elastic tissue, forming dilatation and weakness of the artery, causing aneurysm. | |||