1 - JACC

JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
VOL. 64, NO. 24, 2014
ª 2014 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION
ISSN 0735-1097/$36.00
PUBLISHED BY ELSEVIER INC.
http://dx.doi.org/10.1016/j.jacc.2014.10.010
EDITORIAL COMMENT
The Proximal Thoracic Aorta
Keystone or Achilles’ Heel?*
Michael F. O’Rourke, MD, DSC, Cameron Holloway, DPHIL, John O’Rourke, MBBS
T
he proximal thoracic aorta—composed of the
pressure impulses, which travel in the arterial wall,
ascending aorta, aortic arch, and upper
blood flow occurs within the arterial lumen, and
descending aorta—plays the major role in
velocity of travel is much slower, <1 m/s peak and a
accepting blood from the left ventricle (LV), cush-
mean of approximately 0.2 m/s in major arteries.
ioning flow pulsations and passing blood to the
Pressure wave reflection arises from the junction of
body’s tissues and organs with minimal energy loss
conduit, low-resistance arteries with high-resistance
(1). The load presented to the LV is best characterized
arterioles (1,5). With far more such junctions in the
as input impedance to the systemic circulation,
lower than the upper body, most reflection returning
measurable from pulsatile pressure and flow waves
from the periphery comes from the lower body up
in the ascending aorta (1,2).
into the proximal thoracic aorta. Arterial/arteriolar
To understand arterial function as measurable by
junctions in the brain produce far less reflection than
highly sophisticated cardiac magnetic resonance
elsewhere because high cerebral flow encounters
(CMR) imaging, we need to apply equally sophisti-
very low cerebrovascular resistance (1,3,6). Peripheral
cated theory to the pulsations of pressure, flow, and
wave reflection from the arms greatly amplifies the
diameter (2). Pulses of pressure travel with finite
pressure wave entering the subclavian arteries; this
velocity along the aortic wall and the walls of its
may be up to twice as high as in the proximal aorta.
arterial branches to the brain, arms, and torso; these
These principles underscore the proximal aorta as a
waves are reflected at arterial terminations and return
keystone for receipt of pulsatile blood flow from the
to the ascending aorta (1,2), where they continue into
LV (1–7). Optimal function is indeed apparent in the
the oppositely running vessels (1,3,4) (i.e., from
interaction of the arterial tree with the LV and with
descending aorta into carotid and subclavian arteries).
timing of wave reflection in relation to the period of
This is expected because the arterial system, top to
systole and diastole (1). In younger subjects, wave
bottom, is just 1 to 2 meters long, and pulse wave
reflection returns to the proximal aorta just as ejec-
velocity (PWV) varies between 4 and 15 m/s in the
tion ceases (1). It does not add pressure to the LV
proximal aorta and peripheral arteries, respectively.
when ejecting but does boost and maintain coronary
The ejecting LV produces 1 spurt of flow per
pressure during diastole as the coronary arteries
heartbeat. Because the arteries do not contract, other
open after being squeezed shut during ventricular
pulsations in the cardiac cycle must be caused by
contraction (1,8). During diastole, passage of the
pressure wave reflection (1,5) (Figure 1). In contrast to
reflected wave up from the descending aorta into the
carotid arteries helps maintain a steadier perfusion
pressure and flow over the whole cardiac cycle,
*Editorials published in the Journal of the American College of Cardiology
reflect the views of the authors and do not necessarily represent the
through the low-resistance brain vessels (1–4,6).
Favorable function and vascular/ventricular inter-
views of JACC or the American College of Cardiology.
action depend on arterial wall elasticity. Low aortic
From Victor Chang Cardiac Research Institute, St. Vincent’s Hospital and
PWV (4 to 5 m/s) in young humans depends on low
Clinic, University of New South Wales, Sydney, Australia. Dr. Michael
elastic modulus, with the relationship given by the
O’Rourke is a founding director of AtCor Medical and Aortic Wrap; and
reported that they have no relationships relevant to the contents of this
Moens-Korteweg
qffiffiffiffiffiffiffiffiffiffi equation:
$h
PWV ¼ Einc
2rr in which PWV is proportional to the
paper to disclose.
square root of the incremental elastic modulus
has acted as a consultant to Novartis and Merck. All other authors have
O’Rourke et al.
JACC VOL. 64, NO. 24, 2014
DECEMBER 23, 2014:2630–2
2631
Keystone Or Achilles Heel?
F I G U R E 1 Elementary Effects of Lower Body Wave Reflection
on Pressure Waves in the Ascending Aorta
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
OLD
YOUNG
MESA (Multi-Ethnic Study of Atherosclerosis) study.
SEE PAGE 2619
Pressure
They showed that measures of distensibility were
Pressure
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
Flow
Flow
upper limb were appreciated as causing (variable)
differences in systolic and pulse pressure between
the aorta and arteries in the upper limb (brachial and
AORTA
radial); consensus groups (12,13) stress measuring
hemodynamic parameters at the same site. Redheuil
In both young (left) and old (right) subjects, flow waves
et al. (11) demonstrated positive outcome results
(bottom) generated in the aorta by left ventricular ejection are
despite having to relate very accurate measures of
identical. The pressure waveforms (top) characteristically are
aortic distension via CMR imaging with highly inac-
quite different, although each shows 2 localized peaks, whereas
curate measures of aortic pressure using an unso-
the aortic flow wave shows just 1. The second localized peak is
attributable to wave reflection from the periphery. Differences
between “young” and “old” pressure waves are due to earlier
phisticated, century-old technique. It is probable that
their outcome results would have been more strongly
return of wave reflection in the older subject, caused by
positive if they had determined central pressure
increased aortic pulse wave velocity from aortic stiffening.
(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
(E inc), h equals wall thickness, r is internal radius, and
distensible aortas, the central pulse pressure can be
r represents blood density (usually taken as 1.05) (1).
almost half that in the brachial and radial arteries;
The proximal aorta’s “Achilles’ heel” is an unfor-
therefore, use of brachial pressure will give falsely
tunate consequence of its keystone role in youth: it
low values of distensibility (1,8,12).
pulsates passively to a greater degree than any other
CMR imaging offers possibilities for future trials
artery, by approximately 15% in youth with each
(and in life insurance), with PWV measured from rate
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 en-
F I G U R E 2 Section of Aorta and Components of the Aortic Wall
gineering principles quantifying “wear and tear,”
<30 years of age
>30 years of age
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
Section
of aorta
collagenous materials in the disorganized media,
Section
of aorta
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
Proximal thoracic
aorta
aortic PWV. This causes wave reflection to return
during systole, adds to LV load, reduces coronary
perfusion pressure, increases systolic pulsation in
The wall of the younger (left) versus the older (right) human aorta is disorganized as
a consequence of fraying and fracture of the elastic lamellae and loss of muscle
carotid and cerebral arteries relative to the aorta
attachments, together with increase in collagen fibers and mucoid material, and with
(1–3,5,8), and predisposes to small cerebral artery
foci of “medionecrosis.”
thrombosis and rupture (10).
2632
O’Rourke et al.
JACC VOL. 64, NO. 24, 2014
DECEMBER 23, 2014:2630–2
Keystone Or Achilles Heel?
of travel of the wavefoot around the aortic arch or by
degeneration with repeated pulsation—to the princi-
relating aortic pulsatile flow to central pressure as
ples that determine optimal function in youth, and
ascending aortic input impedance (1,16). It remains
then to maintain such lifestyle and therapy to main-
expensive, but costs are decreasing, and the time for
tain the aorta as its keystone.
taking flow and pressure for impedance (<1 min)
makes that incremental cost reasonable in persons
REPRINT REQUESTS AND CORRESPONDENCE: Dr.
undergoing magnetic resonance imaging for another
Michael O’Rourke, Victor Chang Cardiac Research
purpose.
Institute, St. Vincent’s Clinic, University of New
Perhaps the best professional outcome from an
South Wales, Suite 810, 438 Victoria Street, Dar-
article such as this is to urge reflection (mental, in
linghurst, Sydney NSW 2010, Australia. E-mail:
this case) regarding the aorta’s Achilles’ heel—its
[email protected].
REFERENCES
1. Nichols WW, O’Rourke MF, Vlachopoulos C.
McDonald’s Blood Flow in Arteries. 6th ed.
London, United Kingdom: Hodder Arnold, 2011.
apparently normal humans. J Hypertens 2013;
31(e-SupplA):e23.
methodological issues and clinical applications.
Eur Heart J 2006;27:2588–605.
7. Karamanoglu M, Gallagher D, Avolio AP,
2. O’Rourke MF. Vascular impedance in studies of
arterial and cardiac function. Physiol Rev 1982;62:
570–623.
O’Rourke MF. Pressure wave propagation in a
multi-branched model of the human upper limb.
Am J Physiol 1995;269:H1363–9.
3. Hirata K, Yaginuma T, O’Rourke MF,
Kawakami M. Age-related change in the carotid
artery flow and pressure pulses: implications to
8. O’Rourke MF, Hashimoto J. Mechanical factors
in arterial aging: a clinical perspective. J Am Coll
Cardiol 2007;50:1–13.
13. The Reference Values for Arterial Stiffness’
Collaboration. Determinants of pulse wave velocity in healthy people and in the presence of cardiovascular risk factors: “establishing normal and
reference values.” Eur Heart J 2010;31:2338–50.
cerebral microvascular disease. Stroke 2006;37:
2552–6.
9. Osler W. The Principles and Practices of Medicine. 3rd ed. New York, NY: Appleton, 1898:770.
4. Hashimoto J, Ito S. Aortic stiffness determines
diastolic blood flow reversal in the descending
10. O’Rourke MF, Safar ME. Relationship between
aortic stiffening and microvascular disease in brain
and kidney: cause and logic of therapy. Hypertension 2005;46:200–4.
thoracic aorta: potential implication for retrograde
embolic stroke in hypertension. Hypertension
2013;62:542–9.
5. Hamilton WF, Dow P. An experimental study of
the standing waves in the pulse propagated
through the aorta. Am J Physiol 1938;125:48–59.
6. Kim MO, Li Y, Wei F, Wang J, O’Rourke M,
Avolio A. Influence of wave reflection and lower
body arterial properties on cerebral perfusion in
11. Redheuil A, Wu CO, Kachenoura N, et al.
Proximal aortic distensibility is an independent
predictor of all-cause mortality and incident CV
events: the MESA study. J Am Coll Cardiol 2014;
64:2619–29.
12. Laurent S, Cockcroft J, Van Bortel L, et al.
Expert consensus document on arterial stiffness:
14. Wang KL, Cheng HM, Sung SH, et al. Wave
reflection and arterial stiffness in the prediction of
15-year all-cause and cardiovascular mortalities: a
community-based study. Hypertension 2010;55:
799–805.
15. Roman MJ, Devereux RB. Association of central
and peripheral blood pressures with intermediate
cardiovascular phenotypes. Hypertension 2014;
63:1148–53.
16. O’Rourke MF, Clubb J. Guidelines for assessment of cardiovascular disease in life insurance.
J Am Coll Cardiol 2011;57:1570–1.
KEY WORDS aorta, impedance, reflection,
stiffness