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Hypertension. 2001;37:e23

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(Hypertension. 2001;37:e23.)
© 2001 American Heart Association, Inc.


In Memoriam

Ray Kelly

Michael O’Rourke; David A. Kass

*    Introduction
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*Introduction
down arrowReferences
 
Raymond Kelly, who died at age 43, on October 5, 2000, was one of a small group of young cardiovascular researchers in Sydney who have made major contributions to their field over the past 15 years. Kelly’s work extended that of Stephen MacMahon on epidemiology of hypertension and complemented that of David Celermajer on arterial function, both working in the Olympic city.

Kelly’s major contributions related to the interpretation of the arterial pulse in humans. As a doctoral student in a department with strength in arterial hemodynamics, he was presented with a new tonometer that had been specially developed by Huntly Millar of Houston. Kelly validated this instrument against invasive recordings for clinical use in recording the radial and carotid pressure waveforms.1 He then conducted a study in >1000 normal subjects to establish aging changes in the arterial pulse at the 2 anatomic sites. He showed there was a progressive rise with age in the second systolic pressure peak caused by progressive medial degeneration of the aorta and elastic arteries, and he emphasized that changes in the radial pulse paralleled those in the carotid pulse but followed several decades behind. He showed that increase in amplitude of the second systolic pressure peak in central arteries was due to early wave reflection, consequent on aortic stiffening, and that this could be reduced by vasodilator drug therapy.2 An important corollary of this work, subsequently confirmed by colleagues Takazawa (Japan),3 and Fitchett (Canada),4 was that beneficial effects of vasodilator drugs on left ventricular load and central arterial pressures are underestimated by conventional recordings of systolic brachial pressure. All this work showed a consistency between pulse contour in central and upper limb arteries, leading torecent development of systems designed to generate aortic pressure from the radial pulse.

Kelly’s next contribution in Baltimore and Montreal was to confirm in animal studies how arterial stiffening (as seen with aging in humans) compromises ventricular function and energetics at rest and especially during simulated exercise.5 Extending human work on the arterial pulse, he showed how this could be used with dimensional and flow ultrasound to characterize ventricular/vascular interaction, as well as the hydraulic properties of the systemic circulation (as systemic vascular impedance).6

Returning home to Sydney in 1993, Kelly initiated further clinical studies, including 1 in a large group of twins in order to separate genetic and acquired contributions to arterial stiffness as interpreted from the arterial pulse. He was able to establish the different effects of body height, of gender,7 of other genetic influences, and of hypertension, atherosclerosis, smoking, and drug therapy. Papers on these topics are still in press, and 2 abstracts were presented at the AHA meeting 1 month after his death by his pupil Chris Hayward.

Ray Kelly’s death took many by surprise. His continuing scientific productivity was matched by a busy career in cardiovascular medicine. He did not want his colleagues or patients to know of his illness (renal cell carcinoma). He bore his illness stoically, with optimism and strong faith in his creator. He leaves his beloved wife, Louise, and 4 young sons: Thomas, Stephen, Peter, and Matthew, ages 3 to 12. He was deeply committed to his family and wished his life and his passing to be of some inspiration to them. It was, and it is, to the larger family of medical scientists throughout the world.


*    References
up arrowTop
up arrowIntroduction
*References
 

  1. Kelly R, Hayward C, Avolio A, O’Rourke M. Noninvasive determination of age-related changes in the human arterial pulse. Circulation.. 1989;80:1652–1659.[Abstract/Free Full Text]
  2. Kelly RP, Gibbs HH, O’Rourke MF, Daley JE, Mang K, Morgan JJ, Avolio AP. Nitroglycerin has more favourable effects on left ventricle overload than apparent from measurement of pressure in a peripheral artery. Eur Heart J. 1990;11:138–144.[Abstract/Free Full Text]
  3. Takazawa K, Tanaka N, Takeda K, Kurosu F, Ibukiyama C. Underestimation of vasodilator effects of nitroglycerin by upper limb blood pressure. Hypertension. 1995;26:520–523.[Abstract/Free Full Text]
  4. Fitchett DH, Simkus GJ, Beaudry JP, Marpole DG. Reflected pressure waves in the ascending aorta: effect of glycerol trinitrate. Cardiovasc Res. 1988;22:494–500.[Medline] [Order article via Infotrieve]
  5. Kelly RP, Tunin R, Kass DA. Effect of reduced aortic compliance on cardiac efficiency and contractile function of in situ left ventricle. Circ Res. 1992;71:490–502.[Abstract/Free Full Text]
  6. Kelly R, Fitchett D. Noninvasive determination of aortic input impedance and external left ventricular power output: a validation and repeatability study of a new technique. J Am Coll Cardiol. 1992;20:952–963.[Abstract]
  7. Hayward CS, Kelly RP. Gender-related differences in the central arterial pressure waveform. J Am Coll Cardiol. 1997;30:1863–1871. [Abstract]




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