Author + information
- Michael F. O’Rourke, MD, DSc∗ (, )
- Cameron Holloway, DPhil and
- John O’Rourke, MBBS
- Victor Chang Cardiac Research Institute, St. Vincent’s Hospital and Clinic, University of New South Wales, Sydney, Australia
- ↵∗Reprint requests and correspondence:
Dr. Michael O’Rourke, Victor Chang Cardiac Research Institute, St. Vincent’s Clinic, University of New South Wales, Suite 810, 438 Victoria Street, Darlinghurst, Sydney NSW 2010, Australia.
The proximal thoracic aorta—composed of the ascending aorta, aortic arch, and upper descending aorta—plays the major role in accepting blood from the left ventricle (LV), cushioning flow pulsations and passing blood to the body’s tissues and organs with minimal energy loss (1). The load presented to the LV is best characterized as input impedance to the systemic circulation, measurable from pulsatile pressure and flow waves in the ascending aorta (1,2).
To understand arterial function as measurable by highly sophisticated cardiac magnetic resonance (CMR) imaging, we need to apply equally sophisticated theory to the pulsations of pressure, flow, and diameter (2). Pulses of pressure travel with finite velocity along the aortic wall and the walls of its arterial branches to the brain, arms, and torso; these waves are reflected at arterial terminations and return to the ascending aorta (1,2), where they continue into the oppositely running vessels (1,3,4) (i.e., from descending aorta into carotid and subclavian arteries). This is expected because the arterial system, top to bottom, is just 1 to 2 meters long, and pulse wave velocity (PWV) varies between 4 and 15 m/s in the proximal aorta and peripheral arteries, respectively.
The ejecting LV produces 1 spurt of flow per heartbeat. Because the arteries do not contract, other pulsations in the cardiac cycle must be caused by pressure wave reflection (1,5) (Figure 1). In contrast to pressure impulses, which travel in the arterial wall, blood flow occurs within the arterial lumen, and velocity of travel is much slower, <1 m/s peak and a mean of approximately 0.2 m/s in major arteries.
Pressure wave reflection arises from the junction of conduit, low-resistance arteries with high-resistance arterioles (1,5). With far more such junctions in the lower than the upper body, most reflection returning from the periphery comes from the lower body up into the proximal thoracic aorta. Arterial/arteriolar junctions in the brain produce far less reflection than elsewhere because high cerebral flow encounters very low cerebrovascular resistance (1,3,6). Peripheral wave reflection from the arms greatly amplifies the pressure wave entering the subclavian arteries; this may be up to twice as high as in the proximal aorta.
These principles underscore the proximal aorta as a keystone for receipt of pulsatile blood flow from the LV (1–7). Optimal function is indeed apparent in the interaction of the arterial tree with the LV and with timing of wave reflection in relation to the period of systole and diastole (1). In younger subjects, wave reflection returns to the proximal aorta just as ejection ceases (1). It does not add pressure to the LV when ejecting but does boost and maintain coronary pressure during diastole as the coronary arteries open after being squeezed shut during ventricular contraction (1,8). During diastole, passage of the reflected wave up from the descending aorta into the carotid arteries helps maintain a steadier perfusion pressure and flow over the whole cardiac cycle, through the low-resistance brain vessels (1–4,6).
Favorable function and vascular/ventricular interaction depend on arterial wall elasticity. Low aortic PWV (4 to 5 m/s) in young humans depends on low elastic modulus, with the relationship given by the Moens-Korteweg equation:
in which PWV is proportional to the square root of the incremental elastic modulus (Einc), h equals wall thickness, r is internal radius, and ρ represents blood density (usually taken as 1.05) (1).
The proximal aorta’s “Achilles’ heel” is an unfortunate consequence of its keystone role in youth: it pulsates passively to a greater degree than any other artery, by approximately 15% in youth with each heartbeat (1). Osler (9) described the “wear and tear” from multiple pulsations as causing “physiological arteriosclerosis” through breakdown of “vital rubber” in the aortic media (Figure 2). Based on modern engineering principles quantifying “wear and tear,” rubber, distended by 15%, will begin to fracture at approximately 1 billion cycles, corresponding to some 30 years at a heart rate of 70 beats/min (1). Thus, the body’s “vital rubber” of natural elastin will begin to fracture at around 30 years of age, leading to dilation of the aorta, with stresses transferred to stiffer collagenous materials in the disorganized media, with elastin lamellae that are frayed and fractured (Figure 2) (1,8). As aging continues, the elastic modulus increases progressively up to 4 to 10 times its value in youth, leading to a 2- to 3-fold increase in aortic PWV. This causes wave reflection to return during systole, adds to LV load, reduces coronary perfusion pressure, increases systolic pulsation in carotid and cerebral arteries relative to the aorta (1–3,5,8), and predisposes to small cerebral artery thrombosis and rupture (10).
The paper by Redheuil et al. (11) in this issue of the Journal describes change in aortic distention and distensibility in middle-aged to older adults in the MESA (Multi-Ethnic Study of Atherosclerosis) study. They showed that measures of distensibility were inversely related to cardiovascular events, independently of blood pressure and risk factors of atherosclerotic disease. The MESA trial was designed before the implications of wave travel and reflection in the upper limb were appreciated as causing (variable) differences in systolic and pulse pressure between the aorta and arteries in the upper limb (brachial and radial); consensus groups (12,13) stress measuring hemodynamic parameters at the same site. Redheuil et al. (11) demonstrated positive outcome results despite having to relate very accurate measures of aortic distension via CMR imaging with highly inaccurate measures of aortic pressure using an unsophisticated, century-old technique. It is probable that their outcome results would have been more strongly positive if they had determined central pressure (from the radial artery waveform) as is now used in the U.S. National Institute of Aging (14) and other outcome studies (1,15). In young subjects with distensible aortas, the central pulse pressure can be almost half that in the brachial and radial arteries; therefore, use of brachial pressure will give falsely low values of distensibility (1,8,12).
CMR imaging offers possibilities for future trials (and in life insurance), with PWV measured from rate of travel of the wavefoot around the aortic arch or by relating aortic pulsatile flow to central pressure as ascending aortic input impedance (1,16). It remains expensive, but costs are decreasing, and the time for taking flow and pressure for impedance (<1 min) makes that incremental cost reasonable in persons undergoing magnetic resonance imaging for another purpose.
Perhaps the best professional outcome from an article such as this is to urge reflection (mental, in this case) regarding the aorta’s Achilles’ heel—its degeneration with repeated pulsation—to the principles that determine optimal function in youth, and then to maintain such lifestyle and therapy to maintain the aorta as its keystone.
↵∗ Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology.
Dr. Michael O’Rourke is a founding director of AtCor Medical and Aortic Wrap; and has acted as a consultant to Novartis and Merck. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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