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The central aorta constitutes the main trunk of the systemic arterial tree. It dilates passively with cardiac ejection during systole and then constricts with its recoil function during diastole, thereby regulating blood pressure and blood flow. The central pulsatile hemodynamics affects local hemodynamics within as well as downstream of the aorta (e.g., end organs).

The aorta progressively stiffens and dilates with advancing age, and such age-dependent change is accelerated by hypertension. According to the law of Laplace, wall stress depends on the diameter and pressure of the blood vessel. This has been confirmed by substantial studies which have associated baseline aortic diameter with subsequent development of aortic dissection and progressive dilatation of aortic lumen. This law can also imply potential importance of local pressure within the aorta (i.e., the central pressure) in predicting the development and progression of aortic aneurysms.

Several previous studies have shown that hypertension (together with age and obesity) is related to dilatation of the proximal ascending aorta (rather than of the aortic root). In addition, aortic blood flow abnormality may also be importantly related to aortic dilatation because of strong positive association between the diastole flow reversal and lumen diameter in the proximal thoracic aorta. As for the abdominal (infrarenal) aorta, aneurysmal development and progression have been attributed to aortic segmental stiffening (of the bifurcational versus infrarenal segment) and aortic pressure elevation, respectively.

Central pulsatile pressure not only represents aortic wall stress but also determines cardiac afterload and microvascular wall stress in the brain and kidney. Central pulsatile flow (in both directions) could also affect the flow distribution into the upper and lower parts of the body and control end-organ function. Aortic structural change (including segmental stiffening and aneurysmal formation) causes central hemodynamic abnormalities and may thus lead to systemic organ damage and dysfunction.

In this session, clinical implications of central hemodynamics will be discussed in terms of aortic and end-organ diseases.

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