![]() The main culprit in this disease seems to be the TGF-B1 signaling mechanism that is responsible for activating matrix degradation through increased production of plasminogen activators and release of matrix metalloproteinases. The different conditions that cause TAAs either affect structural components of the aortic wall or alter the intracellular signaling cascade that maintains vascular wall integrity. Recent developments have helped better explain the cellular changes that lead to aneurysmal ascending aortas. In addition, according to Laplace's law, the dilation of the aorta increases wall tension, triggering vascular wall remodeling and even further aortic dilatation. With aging, there is fragmentation of elastic fiber, smooth muscle dropout and replacement by amorphous material (known as cystic medial degeneration), which leads to increased stiffness and weakening of the aortic wall which predisposes to dilatation of the ascending aorta. In diastole, recoil of the aorta transforms the stored potential energy back to kinetic energy, propelling the blood distally into the arterial bed. During systole, expansion of the aorta allows kinetic energy from left ventricular contraction to be stored as potential energy in the aortic wall. The internal elastic lamina separates the intima from the media.Įlastic fiber in the medial layer of the aorta allows continuous forward flow during the whole cardiac cycle. The aorta is an elastic vessel composed of three main layers: the tunica intima, the tunica media and the tunica adventitia. Women and men have similar incidences of thoracic aortic aneurysm but the age at diagnosis is a decade higher in women (70s) than in men (60s). According to the CDC, the incidence of ascending TAA is estimated to be around 10 per 100,000 person-years. The incidence of TAA has been reported to be only 5.9 cases per 100,000 person-years in the early 1980s, however recent advances in imaging modalities, aging of the population, increased use of transthoracic echocardiography and routine screening have resulted in a twofold increase in the incidence. pointed out, the prognosis of patients with TAA is indeed improved if they are treated before complications occur. Unfortunately, the mortality rate of patients presenting with complications of TAA has remained relatively stable in the last two decades, in contrast to the improved survival observed in patients presenting with complications of coronary artery disease (CAD). ![]() Thoracic aortic aneurysms (TAA) and its associated complications are life threatening clinical entities that rank in the top 20 leading causes of mortality in the United States (15th leading cause of death in people over 65 years old) ( CDC, ). In addition, some authors suggest using the aortic size index which takes into account the body surface area, thus minimizing classification of normal aorta as pathologically dilated and vice versa. Aneurysm should be distinguished from ectasia, which represents a diffuse dilation of the aorta less than 50% of normal aorta diameter.Īn official cutoff for the definition of aortic dilatation has not been determined because of the variability of this measure, but most experts agree that ascending aorta size should be correlated to size and gender. In contrast, an aneurysm is defined as a localized dilation of the aorta that is more than 50% of predicted (ratio of observed to expected diameter ≥ 1.5). Nevertheless, by common convention, aortic dilatation refers to a dimension that is greater than the 95th percentile for the normal person age, sex and body size. Published data on arteries diameter in healthy population are often scant or variable because of different imaging modalities used for measurement. ![]()
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