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EFFECTS OF EXERCISE ON BRACHIAL SYSTOLIC BLOOD PRESSURE VERSUS CENTRAL AORTIC SYSTOLIC PRESSURE IN PATIENTS WITH HYPERTENSION
E564 JACC April 5, 2011 Volume 57, Issue 14
GENERAL CARDIOLOGY: HYPERTENSION, PREVENTION AND LIPIDS EFFECTS OF EXERCISE ON BRACHIAL SYSTOLIC BLOOD PRESSURE VERSUS CENTRAL AORTIC SYSTOLIC PRESSURE IN PATIENTS WITH HYPERTENSION ACC Poster Contributions Ernest N. Morial Convention Center, Hall F Monday, April 04, 2011, 9:30 a.m.-10:45 a.m.
Session Title: Arterial Stiffness in Hypertension Abstract Category: 16. Hypertension Session-Poster Board Number: 1080-284 Authors: Bryan Williams, Fabio Baschiera, Peter S. Lacy, Cheraz Cherif Papst, Patrick Brunel, Department of Cardiovascular Sciences, University of Leicester, Leicester, United Kingdom, Novartis Pharma AG, Basel, Switzerland Background: Exercise increases brachial systolic blood pressure (BrSBP), often to alarming levels. It is unknown to what extent exercise-induced rises in BrSBP accurately reflect changes in central aortic systolic pressures (CASP), or whether exercise enhances pressure amplification from the aortic root to the peripheral circulation. It is now feasible to measure the effect of exercise on CASP due to the development of non-invasive techniques. Methods: Untreated hypertensive patients (n = 68, mean age 59 years, 68% male) underwent treadmill exercise testing (Bruce protocol) to peak exercise (85% predicted max. heart rate). Standing BrSBP and CASP were measured at rest, peak exercise and during recovery. CASP was measured non-invasively using tonometric radial pulse wave analysis calibrated to BrBP (BPro™, Healthstats, Singapore). Results: At rest, mean CASP was lower than mean BrSBP (137.6 ± 14.4 vs 153.9 ± 15.0 mmHg) with a systolic amplification ratio of 1.1 ± 0.1. Mean CASP and BrSBP both increased during exercise; however, the rise in CASP was markedly attenuated and approximately half the increase in BrSBP (22.2 ± 20.6 vs 41.3 ± 19.8 mmHg). CASP and BrSBP quickly recovered to below baseline levels within 10 min of recovery (Table). Conclusions: During exercise, BrSBP is markedly amplified from the aorta and exaggerates the rise in aortic pressures. Thus, BrSBP:CASP amplification is not a fixed ratio and may vary as a consequence of exercise, aortic age and efficiency of ventricular:vascular coupling. Time point Rest Peak exercisea Recovery,b 10 minutes Recovery,b 20 minutes Recovery,b 30 minutes Change from rest to peak exercise Data are presented as mean ± SD. a85% of predicted maximum heart rate. bTime shown is time after peak exercise was reached.
BrSBP, mmHg 153.9 ± 15.0 196.6 ± 22.9 150.0 ± 17.6 143.1 ± 14.7 144.7 ± 15.5 41.3 ± 19.8
CASP, mmHg 137.6 ± 14.4 162.7 ± 20.9 133.3 ± 13.8 128.8 ± 12.9 130.7 ± 12.9 22.2 ± 20.6
GENERAL CARDIOLOGY: HYPERTENSION, PREVENTION AND LIPIDS EFFECTS OF EXERCISE ON BRACHIAL SYSTOLIC BLOOD PRESSURE VERSUS CENTRAL AORTIC SYSTOLIC PRESSURE IN PATIENTS WITH HYPERTENSION ACC Poster Contributions Ernest N. Morial Convention Center, Hall F Monday, April 04, 2011, 9:30 a.m.-10:45 a.m.
Session Title: Arterial Stiffness in Hypertension Abstract Category: 16. Hypertension Session-Poster Board Number: 1080-284 Authors: Bryan Williams, Fabio Baschiera, Peter S. Lacy, Cheraz Cherif Papst, Patrick Brunel, Department of Cardiovascular Sciences, University of Leicester, Leicester, United Kingdom, Novartis Pharma AG, Basel, Switzerland Background: Exercise increases brachial systolic blood pressure (BrSBP), often to alarming levels. It is unknown to what extent exercise-induced rises in BrSBP accurately reflect changes in central aortic systolic pressures (CASP), or whether exercise enhances pressure amplification from the aortic root to the peripheral circulation. It is now feasible to measure the effect of exercise on CASP due to the development of non-invasive techniques. Methods: Untreated hypertensive patients (n = 68, mean age 59 years, 68% male) underwent treadmill exercise testing (Bruce protocol) to peak exercise (85% predicted max. heart rate). Standing BrSBP and CASP were measured at rest, peak exercise and during recovery. CASP was measured non-invasively using tonometric radial pulse wave analysis calibrated to BrBP (BPro™, Healthstats, Singapore). Results: At rest, mean CASP was lower than mean BrSBP (137.6 ± 14.4 vs 153.9 ± 15.0 mmHg) with a systolic amplification ratio of 1.1 ± 0.1. Mean CASP and BrSBP both increased during exercise; however, the rise in CASP was markedly attenuated and approximately half the increase in BrSBP (22.2 ± 20.6 vs 41.3 ± 19.8 mmHg). CASP and BrSBP quickly recovered to below baseline levels within 10 min of recovery (Table). Conclusions: During exercise, BrSBP is markedly amplified from the aorta and exaggerates the rise in aortic pressures. Thus, BrSBP:CASP amplification is not a fixed ratio and may vary as a consequence of exercise, aortic age and efficiency of ventricular:vascular coupling. Time point Rest Peak exercisea Recovery,b 10 minutes Recovery,b 20 minutes Recovery,b 30 minutes Change from rest to peak exercise Data are presented as mean ± SD. a85% of predicted maximum heart rate. bTime shown is time after peak exercise was reached.
BrSBP, mmHg 153.9 ± 15.0 196.6 ± 22.9 150.0 ± 17.6 143.1 ± 14.7 144.7 ± 15.5 41.3 ± 19.8
CASP, mmHg 137.6 ± 14.4 162.7 ± 20.9 133.3 ± 13.8 128.8 ± 12.9 130.7 ± 12.9 22.2 ± 20.6