The circulatory system is a closed system. The heart and the vascular system interact to provide adequate blood flow throughout the body. This interaction of properties of the systolic ventricle, as a pump, and the vascular system, as a load, plays a critical role in determining cardiac output. Therefore, arterial-cardiac interaction, also known as ventricular-vascular interaction or ventricular-vascular coupling, is considered a central deteminant of net cardiovascular performance.1-3) There has been much interest in the relationship among vascular stiffness, cardiac function, and cardiovascular diseases. The concept of arterial-cardiac interaction is important to understanding the pathophysiologies of heart failure, especially in patients with preserved ejection fraction. This review will focus on the concept and implications of arterial-cardiac interaction and the non-invasive methods available for its clinical assessment.

Vascular stiffening of the large arteries is a common feature of human aging and is exacerbated by many common disorders such as hypertension, diabetes mellitus, and renal disease.4-6) The normal aorta delivers blood from the heart to the capillaries and cushions pulsations.5) The arterial system in youth is a very effective conduit and a very efficient cushion.5)6) In young subjects, the wave travels slowly in the distensible tube so that the reflected wave from the resistance artery boosts pressure during diastole. As the aorta ages and stiffens, blood travels faster, returns earlier, and boosts pressure in late systole. Therefore, vascular stiffening results in widening of the arterial pulse pressure (PP), high augmentation pressure, high augmentation index (AIx) and high pulse wave velocities (PWV). Because young subjects have good pressure amplification from the central to the peripheral, and elderly subjects do not, their central blood pressures (BP) differ even when they have the same peripheral BPs.7-9) Elderly subjects have higher central BPs in similar peripheral BPs with younger sujects, that can cause pulsatile stress on the left ventricle (LV). There are several different methods of assessing arterial stiffness, some of which are more widely applicable than others.10) The representative indices and surrogates of arterial stiffness are summerized in Table 1 and shown on Fig. 1. PWV is the speed at which the forward pressure wave is transmitted from the aorta through the vascular tree.11) It is calculated by measuring the time taken for the arterial waveform to pass between two points a measured distance apart. The PWV has been validated and is reproducible, and has been widely applied as the gold standard of arterial stiffness measurement.11) Pulse waveform analysis permits measurement of central systolic BP, central PP and AIx.11)12) The arterial pressure waveform is a composite of the forward wave created by LV contraction and a reflected wave generated in the periphery, returning towards the heart. AIx is calculated as the ratio between augmentation pressure and central PP and is expressed as a percentage.11) It is a complex composite measurement, derived from many important dynamic variables. It is influenced by PWV, the reflectance point, and LV ejection characteristics.10) The age-related changes in central AIx and aortic PWV follow different patterns.9) AIx might provide a more sensitive marker of arterial aging in younger individuals, whereas aortic PWV might be a more sensitive marker in older individuals.9) Recently, PP amplification has been suggested as a mechanical biomarker of cardiovascular diesase and risk, together with global arterial properties.13) Normally, differences in vessel stiffness and reflection of pressure waves within the arterial tree result in considerable amplification of PP between the aorta and brachial artery. This so-called PP amplification is a well-established hemodynamic phenomenon and reduced PP amplification is related to increased cardiovascular risks and poor outcomes superior to the values of brachial or central arteries alone.13)14)

Ultrasound-based measurements of arterial stiffness are also in use. It is necessary to simultaneously measure BP. The stiffness index β is less affected by arterial pressure changes and could be more useful than other parameters, being easily determined using ultrasound.10) Carotid stiffness index β has been used to assess arterial stiffness in various cardiovascular diseases.10)15)

The pathophysiological and clinical implications of arterial stiffness should be considered together with LV function. Several possible pathways exist whereby aortic stiffening may contribute to pathological changes in the LV, which can be the substrate of diastolic dysfunction.16) Aortic stiffening leads to augmentation of the central aortic systolic BP, thus increasing LV afterload. Increased afterload may promote myocyte hypertrophy and slow LV relaxation. Concomitant reduction in central aortic diastolic BP may compromise coronary perfusion and aggravate subendocardial ischemia. This can further impair myocardial relaxation and promote myocardial fibrosis leading to diastolic dysfunction. Fig. 2 illustrates the mechanisms that predispose the LV to ischemia and to dysfunction with aortic stiffening.16)17) A vicious cycle becomes relevant in the development of heart failure with preserved ejection fraction, probably the most common form of heart failure in the elderly.5) In a recent study, we demonstrated the gender differences in the association between the indices of arterial stiffness and LV diastolic functional parameters in age-matched men and women with preserved LV ejection fraction.18) In women, despite similar peripheral pressures to those of men, there were significant differences in central pressures and indices of wave reflections.18)19) LV diastolic function significantly correlated with parameters representing arterial stiffness in women but not in men.18) The effect of earlier wave reflection on central pressure and stronger relation to LV diastolic function could be a possible contributor of hemodynamic liability prone to heart failure in women.