The aorta is not only a simple conduit but also a functional reservoir. Figure 3.2 explains the reservoir function of the aorta [2]. During systole, the systemic ventricle ejects the blood into the aorta. However, the blood volume that runs off to organs during systole is less than half of the ejected blood. More than half of the ejected blood from the systemic ventricle is stored in the aorta during systole and runs off to the organs during diastole (Fig. 3.2a). When the reservoir function is damaged, the blood flow runoff during diastole is diminished, and the systolic blood pressure elevates, which is called isolated systolic hypertension (Fig. 3.2b). One of the most important organs that is mainly circulated during diastole is the heart. Therefore, the damage of the reservoir function is disadvantageous for the coronary circulation.

As with the other functions of the human body, the aortic reservoir function is deteriorating with aging. Therefore, we could study the aortic reservoir function by comparing the conditions of the function in young and old. With aging, degeneration of elastin fibers in the aortic wall occurs, and collagenous material increases. Calcium deposition also occurs. The progression of the processes results in cystic medial necrosis, which is also well known as the histological characteristic of aortopathy. As a matter of course, the histological changes, the decrease of elastin fibers, and the increase of collagen cause damage to the elastic properties of the aorta. Figure 3.3 demonstrates the decreased aortic distensibility in the aging process [3]. As a result of the loss of the elasticity, the pulse wave velocity elevates with aging (Fig. 3.4) [4]. Because the ejection to the stiff aorta augments the cardiac workload, the myocardial blood flow increases (Fig. 3.5a). However, the stiff aorta, it means the damage for the reservoir function, could not increase the pooling of the blood in the aorta during systole. As a result, the myocardial flow reserve decreases with aging (Fig. 3.5b) [5].

Interestingly, it is well known that the aortic diameter enlarges with aging process (Fig. 3.6) [6]. Aortopathy is usually defined as a dilatation of the aorta. However, many reports demonstrated that the aortic root expansion and the stiffening of the aorta occur together in many clinical settings [7–10]. Moreover, it is reported that the pulse wave velocity of the dilated aorta is elevated in patients with aortopathy [11], although the increase of the diameter means the decreased pulse wave velocity based on physical laws. Therefore, it is possible that the damaged aortic distensibility precedes the dilatation of the aorta in the aortopathy. The reason why the aorta with the decreased distensibility dilates has not been fully elucidated. One of the possible mechanisms of the phenomenon is a compensation for the cardiac demand-coronary supply balance [12–14].

Several theories are proposed in order to explain the phenomenon.

One of the theories is that the enhanced aortic pressure augmentation caused by pressure wave reflection results in the localization of the abnormal aortic property. Aortic pressure waveform is composed of two pressure waveforms: the forward pressure wave and the reflected pressure wave. The forward pressure wave is generated by the systemic ventricular ejection, and the backward pressure is the sum of the pressure wave reflections. The pressure wave reflections arise from any discontinuity in elastic properties along the arterial tree in which there is a change (or mismatch) in impedance [15]. In young people, the reflected pressure wave returns to the heart during diastole, it means after closure of the aortic valve, because the pulse wave velocity in young is slow. Therefore, it enhances the coronary perfusion by pushing the aortic blood stored during systole. With aging, the pulse wave velocity gradually increases. It means the early return of the reflected pressure wave (in systole) impairs arterial and ventricular function. The opposite directional reflected pressure wave that returns to the heart during systole interferes with the systemic ventricular ejection and increases the workload of the systemic ventricle (Fig. 3.7).