The most comprehensive and precise definition of the arterial load is the time-resolved aortic input impedance measurements, which describes the relationship between pulsatile pressure and flow in the frequency domain, and has dimensions of amplitude and phase . However, the complex nature and interpretation of time-varying aortic input impedance make it unfeasible for daily clinical practice and usual hemodynamic monitoring . Fortunately, noninvasive assessment of arterial load can provide important physiological and prognostic information .
3.1 Sex Differences in Arterial Load
The sex differences in arterial load are noninvasively investigated in 460 healthy adults, and the primary finding is that with or without adjustment for the cuff-measured blood pressure; women have higher EaI and pulsatile load, and lower TACI, and shorter Tau-W than men. The arterial load describes all the extracardiac factors opposing ventricular ejection . The SVR, which is mostly dependent on the distal resistive arterioles, modulates the steady component of arterial load . The TAC, which is mostly dependent on the proximal elastic large arteries, modulates the pulsatile component of arterial load . A lower TAC indicates a higher arterial stiffness, which leads to a higher pulsatile load . The Ea is a measure of the net arterial load imposed on the left ventricle that integrates the effects of the SVR, TAC, aortic characteristic impedance, heart rate, and systolic and diastolic time intervals [12, 13]. The allometrically scaled EaI, SVRI and TACI are used for comparative purposes because arterial load is heavily dependent on body size . According to the widely used Windkessel model, the Tau-W represents the time constant of the exponential decay of diastolic aortic pressure . A shorter Tau-W indicates a stiffer aortic wall. In summary, our results demonstrate that healthy women have higher integrated and pulsatile arterial load than their male counterparts for any given cuff-measured blood pressure.
By integrating arterial tonometry with echocardiography, Coutinho et al. found that in 461 participants (189 men and 272 women) without heart failure, women had higher aortic characteristic impedance and lower TAC than men, and the SVRI was similar between sexes . In another paper, Coutinho et al. reported that in 600 non-Hispanic whites belonging to hypertensive sibships (249 men and 351 women), women had higher aortic characteristic impedance and SVR than men, and the SVRI was similar between sexes . Using invasive hemodynamic parameters and direct Fick cardiac output, Lau et al. found that in 190 adults (83 men and 107 women) with heart failure with preserved ejection fraction, the arterial stiffness in women was greater than in men . The evidence from these studies [14,15,16] also indicate that women have a higher arterial load than their male counterparts.
A higher resting EaI increases the myocardial energetic costs for a given SVI . We find that the SV is larger in men than in women, but the SVI is similar between sexes; which is entirely consistent with the strong heart study . Moreover, we find that women have a higher EaI than men. Haider et al. find that both baseline and hyperaemic myocardial blood flow are typically higher in women as compared to men , which implies that women have higher myocardial energy consumption than their male counterparts. The evidence indicates that the myocardial energetic costs are higher in women than in men, and which is closely associated with the relatively higher arterial load in women.
3.2 Clinical Relevance
The arterial load is a key determinant of LV systolic and diastolic function [7, 9]. For example, arterial stiffness, a major contributor to pulsatile load, is the result of a complex interplay of endothelial and smooth muscle cell function, extracellular matrix composition, genetics, hemodynamic factors, and vasoactive properties . A lower arterial compliance indicates a higher arterial stiffness or a greater pulsatile load, which has been shown to be central to the pathogenesis of heart failure with preserved ejection fraction, impairing ventricular-arterial coupling, LV diastolic and sub-clinical systolic dysfunction . In the presence of a normal aortic valve, LV afterload corresponds to the mechanical load imposed by the systemic arterial tree (arterial load). The arterial load is the external opposition that must be overcome by the left ventricle during ejection, which gathers all extracardiac factors opposing the movement of blood out of the heart into the aorta, compromising different arterial properties, blood viscosity, and the effects of arterial wave reflections . In a large-sample investigation; where 27 542 participants (54% women) without baseline cardiovascular disease are followed over 28 ± 12 years, and 4081 subjects develop heart failure . Then the researchers divide the blood pressure into eight categories, and find that the risk of heart failure is higher in women than in men for any level of blood pressure . It has been confirmed that the underlying reasons for heart failure may not always be a primary cardiac pathology but a mechanical inefficiency of myocardium against an excessive afterload . We find that for any given blood pressure, the integrated and pulsatile arterial load are higher in women than in men. Thus, our results lay the mechanical groundwork for the explanation of why the risk of heart failure is higher in women than in men for the same level of blood pressure.
3.3 Limitations and Perspectives
The arterial load compromises not only mechanical properties of the arterial system, such as compliance or arterial resistance, but also the effects of arterial wave reflections . The arterial wave reflections could not be determined here because we used brachial artery blood pressure to calculate aortic pressure instead of quantifying central hemodynamics with arterial tonometry. Thus, although it does not affect our results, the arterial load indexes investigated in this study can only partially represent the comprehensive definition of arterial load. Moreover, notwithstanding the accuracy of the calculated aortic blood pressure is validated with invasive intra-arterial measurements in large groups of adult population [22, 23], the calculated aortic pressure might still slightly differ from the true values due to the individual differences.
Through adequate calibration of aortic and brachial distension waveforms with arterial tonometry or meticulous ultrasonography, the aortic pressure can be noninvasively quantified using cuff-measured brachial blood pressure combined with the form factor calibration [24, 25]. However, our study was limited by the original design, and the arterial distension waveforms were not acquired. Thus, we could not validate the consistency in aortic pressure measurement between the method proposed by Van Bortel et al. [24, 25] and that used in our study. Further studies focusing on this topic have potentially important clinical relevance, and which are clearly warranted.