Hypertension: Sharman JE

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A digest of articles written 1999 and later, on the topic "Hypertension," originating from Planet Earth —» Sharman JE.  Display:  All Citations ·  All Abstracts
1 Guideline Australian association for exercise and sports science position statement on exercise and hypertension. 2009

Sharman JE, Stowasser M. · School of Human Movement Studies, The University of Queensland, St. Lucia, Australia. · J Sci Med Sport. · Pubmed #19147407 No free full text.

Abstract: Hypertension (high blood pressure; BP) is a leading contributor to premature death and disability from cardiovascular disease. Lifestyle modification that includes regular physical activity is often recommended to patients with hypertension as one of the first line treatments for lowering BP, as well as improving overall risk for cardiovascular events. It is recognised that allied health care professionals play an important role in helping patients to achieve BP control by influencing and reinforcing appropriate lifestyle behavior. The minimum amount of exercise that is recommended in patients with hypertension comprises a mix of moderate to vigorous aerobic (endurance) activity (up to 5 days/week) in addition to resistance (strength) training (on 2 or more non-consecutive days/week). However, due to the dose-response relationship between physical activity and health, exercise levels performed beyond the minimum recommendations are expected to confer additional health benefits. Vigorous exercise training is generally safe and well tolerated by most people, including those with hypertension, although some special considerations are required and these are discussed in this review.

2 Clinical Conference Nitric oxide does not significantly contribute to changes in pulse pressure amplification during light aerobic exercise. free! 2008

Sharman JE, McEniery CM, Campbell R, Pusalkar P, Wilkinson IB, Coombes JS, Cockcroft JR. · Department of Medicine, University of Queensland, Brisbane, Australia. · Hypertension. · Pubmed #18285615 links to  free full text

Abstract: NO modulates resting blood pressure and wave reflection. The effect of NO on exercise central hemodynamics is unknown but has important implications relating to cardiovascular risk. The aim of this study was to determine the contribution of NO to pulse pressure (PP) amplification and wave reflection during exercise. Twelve healthy men aged 29+/-1 years (mean+/-SEM) undertook cycle exercise at 60% of their maximal heart rate. Noninvasive measures of central blood pressure, estimated aortic pulse wave velocity, and wave reflection (augmentation index) were obtained by pulse wave analysis during intravenous infusion of saline (control), N(G)-monomethyl-l-arginine (a NO-synthase inhibitor), or noradrenaline (control vasoconstrictor). PP amplification was defined as the ratio of peripheral to central PP. Cardiac output and stroke volume were determined by electric bioimpedance. Both N(G)-monomethyl-l-arginine and noradrenaline caused a significant increase in mean arterial pressure (P<0.01) and augmentation index (P<0.01), as well as reduced ratio of peripheral to central PP (P<0.05) at baseline. Exercise caused a significant increase in the ratio of peripheral to central PP (P<0.001), whereas augmentation index and estimated aortic pulse wave velocity declined (for both P<0.05) during all 3 of the infusion protocols. However, no significant differences were observed in augmentation index, ratio of peripheral to central PP, or estimated aortic pulse wave velocity between infusion procedures (P>0.50) during exercise. Also, heart rate, peripheral vascular resistance, and cardiac output did not differ during exercise between saline, N(G)-monomethyl-l-arginine, or noradrenaline. Although we cannot rule out other vasodilator mechanisms having adjusted for NO blockade, our results indicate that NO does not solely contribute to systemic arterial stiffness or altered blood pressure amplification during light exercise.

3 Article Pulse pressure amplification during exercise is significantly reduced with age and hypercholesterolemia. 2007

Sharman JE, McEniery CM, Dhakam ZR, Coombes JS, Wilkinson IB, Cockcroft JR. · The University of Queensland, Department of Medicine, Princess Alexandra Hospital, Woolloongabba, Brisbane, Australia. · J Hypertens. · Pubmed #17563538 No free full text.

Abstract: OBJECTIVES: Exercise brachial blood pressure (BP) is predictive of cardiovascular events. As a result of the amplification of pulse pressure, central BP (a stronger cardiovascular risk factor) differs significantly from peripheral measures. Pulse pressure amplification is reduced with increasing age and hypercholesterolemia at rest, but the effect of exercise on central pressure in these populations is unknown. This study aimed to assess the central and peripheral BP response to exercise with aging and hypercholesterolemia. METHODS: Twenty healthy younger (aged 29 +/- 5 years; mean +/- SD), 20 healthy older (aged 57 +/- 5 years) and 12 matched older (aged 59 +/- 7 years) men with hypercholesterolemia exercised (bicycle ergometer) at 60% of their predicted maximal heart rate. Central BP and augmentation index (AIx), a marker of systemic arterial stiffness, were obtained non-invasively using pulse wave analysis. Pulse pressure amplification was defined as the ratio of peripheral to central pulse pressure. RESULTS: The resting haemodynamics of the older men were not significantly different from those with hypercholesterolemia. During exercise, amplification was significantly lower (P < 0.001), and the augmentation index significantly higher (P < 0.001) in the hypercholesterolemic individuals. Younger men had significantly increased amplification (P < 0.01) and reduced AIx (P < 0.001) at rest and during exercise compared with older men. In multiple regression analysis, exercise pulse pressure amplification was independently predicted by age (beta = -0.48; P < 0.001) and total cholesterol (beta = -0.28; P = 0.03). CONCLUSION: With increasing age, exercise pulse pressure amplification is significantly attenuated because of increased wave reflection. These effects are exacerbated by hypercholesterolemia and may contribute to cardiovascular risk by mechanisms associated with central hypertension.

4 Article Validation of a generalized transfer function to noninvasively derive central blood pressure during exercise. free! 2006

Sharman JE, Lim R, Qasem AM, Coombes JS, Burgess MI, Franco J, Garrahy P, Wilkinson IB, Marwick TH. · Department of Medicine, School of Human Movement Studies, University of Queensland, Princess Alexandra Hospital, Queensland, Australia. · Hypertension. · Pubmed #16651459 links to  free full text

Abstract: Exercise brachial blood pressure (BP) predicts mortality, but because of wave reflection, central (ascending aortic) pressure differs from brachial pressure. Exercise central BP may be clinically important, and a noninvasive means to derive it would be useful. The purpose of this study was to test the validity of a noninvasive technique to derive exercise central BP. Ascending aortic pressure waveforms were recorded using a micromanometer-tipped 6F Millar catheter in 30 patients (56+/-9 years; 21 men) undergoing diagnostic coronary angiography. Simultaneous recordings of the derived central pressure waveform were acquired using servocontrolled radial tonometry at rest and during supine cycling. Pulse wave analysis of the direct and derived pressure signals was performed offline (SphygmoCor 7.01). From rest to exercise, mean arterial pressure and heart rate were increased by 20+/-10 mm Hg and 15+/-7 bpm, respectively, and central systolic BP ranged from 77 to 229 mm Hg. There was good agreement and high correlation between invasive and noninvasive techniques with a mean difference (+/-SD) for central systolic BP of -1.3+/-3.2 mm Hg at rest and -4.7+/-3.3 mm Hg at peak exercise (for both r=0.995; P<0.001). Conversely, systolic BP was significantly higher peripherally than centrally at rest (155+/-33 versus 138+/-32 mm Hg; mean difference, -16.3+/-9.4 mm Hg) and during exercise (180+/-34 versus 164+/-33 mm Hg; mean difference, -15.5+/-10.4 mm Hg; for both P<0.001). True myocardial afterload is not reliably estimated by peripheral systolic BP. Radial tonometry and pulse wave analysis is an accurate technique for the noninvasive determination of central BP at rest and during exercise.

5 Article Increased stroke volume and aortic stiffness contribute to isolated systolic hypertension in young adults. free! 2005

McEniery CM, Yasmin, Wallace S, Maki-Petaja K, McDonnell B, Sharman JE, Retallick C, Franklin SS, Brown MJ, Lloyd RC, Cockcroft JR, Wilkinson IB, Anonymous00340. · Clinical Pharmacology Unit, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK. · Hypertension. · Pubmed #15867140 links to  free full text

Abstract: Isolated systolic hypertension is a common condition in individuals aged older than 60 years. However, isolated systolic hypertension has also been described in young individuals, although the mechanisms are poorly understood. We hypothesized that in young adults, isolated systolic hypertension and essential hypertension have different hemodynamic mechanisms and the aim of this study was to test this hypothesis in a cohort of subjects from The ENIGMA Study. Peripheral and central blood pressure, aortic pulse wave velocity, cardiac output, stroke volume, and peripheral vascular resistance were determined in 1008 subjects, aged 17 to 27 years. Compared with normotensive subjects, those with isolated systolic hypertension had significantly higher peripheral, central, and mean blood pressure, aortic pulse wave velocity, cardiac output, and stroke volume (P<0.001 for all comparisons). However, there were no differences in pulse pressure amplification, heart rate, or peripheral vascular resistance between the two groups. Compared with subjects with essential hypertension, mean pressure, heart rate, and peripheral vascular resistance were all significantly lower in isolated systolic hypertensive subjects, but pulse pressure amplification, aortic pulse wave velocity, cardiac output, and stroke volume were higher (P<0.001 for all comparisons). We have demonstrated that in young adults, isolated systolic hypertension and essential hypertension arise from different hemodynamic mechanisms. Isolated systolic hypertension appears to result from an increased stroke volume and/or aortic stiffness, whereas the major hemodynamic abnormality underlying essential hypertension is an increased peripheral vascular resistance. Long-term follow-up of these individuals is now required to determine whether they are at increased risk compared with age-matched normotensive individuals.

6 Minor Cardiac syndrome X: relevance of arterial pressure waveform analysis to patients with chest pain and normal coronary arteries. 2006

Sharman JE, Lim R, Marwick TH. · No affiliation provided · J Hum Hypertens. · Pubmed #16554844 No free full text.

This publication has no abstract.