the optimal timing of bnp measurement after exercise

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ABSTRACTS Heart, Lung and Circulation Abstracts S65 2007;16:S1–S201 Conclusion: CR-BNP NT-proBNP measurements are tightly correlated with laboratory immunoassay E-BNP but systematic differences exist. doi:10.1016/j.hlc.2007.06.166 162 The Optimal Timing of BNP Measurement after Exercise J. Harris , M.P. Feneley, C.S. Hayward Cardiac Investigations and Echocardiography, St Vincent’s Clinic, Sydney, NSW, Australia Background: B-type Natriuretic Peptide (BNP) is released by cardiac myocytes in response to increased left ventric- ular end diastolic pressure (LVEDP). Upregulation of BNP production has been postulated to be the major determi- nant of BNP levels, however a small amount of BNP stored in cardiac myocytes may be released acutely. The opti- mal timing of BNP measurement post exercise is yet to be identified. Methods: 19 patients (pts) underwent a Bruce protocol exercise test. Point of care NT-proBNP (Roche Diagnostics) was assayed at rest, and 5, 20, and 60 min post-exercise. Results: NTproBNP (pg/mL) was below reading threshold (<60) in 7 pts. In the 11 pts in whom BNP increased, eleva- tion was evident 5 min. BNP decreased in 1. In the 12 pts with valid results mean BNP (±SEM, heavy line) peaked at 5 min, p = 0.07 figure, (Rest 270 ± 86, 5 min 354 ± 128, 20 min 345 ± 127, 60 min 341 ± 130). Conclusion: An acute rise in BNP was detected in 11 of 12 patients post-exercise, evident at 5 min. This suggests secretion of preformed stored NTproBNP. This informa- tion will be used in studies designed to detect a rise in LVEDP after exercise in an attempt to identify patients with impaired diastolic function. doi:10.1016/j.hlc.2007.06.167 163 Monitoring of Antihypertensive Treatment for Left Ven- tricular Mass Regression J. Hashimoto , Y. Imai, M.F. O’Rourke Tohoku University, Sendai, Japan; and St. Vincent’s Clinic, Dar- linghurst, New South Wales, Australia Background: Pressure pulse waveform features may pre- dict treatment-induced regression of left ventricular (LV) mass better than casual brachial blood pressure (BP). We compared predictive power for LV mass reduction between the putative optimal pulse waveform feature (pulse amplification) and the putative optimal brachial cuff measurement (home BP measurement). Methods: Brachial BP was self-monitored at home in 43 untreated patients with hypertension. Radial pressure waveforms were recorded with tonometry in the clinic and transformed to aortic waveforms, and pulse amplifica- tion (upper-limb pulse pressure ÷ central pulse pressure) was calculated. LV mass index (LVMI) was determined by echocardiography. Examinations were repeated before and after 1 year of standard medical treatment. Results: Antihypertensive treatment significantly (p < 0.001) reduced LV load, manifest by decrease in home BP and by increase in pulse amplification. These changes were accompanied by reduction in LVMI. However, for individual patients, treatment-induced LVMI change did not correlate with change in home BP (r < 0.05), but closely correlated with change in amplification (r = 0.54, p < 0.001). Amplification was a strong determinant of LVMI reduction, independent of age, gender and home BP. Estimated subject numbers required for predicting a significant LVMI reduction were far less when the pulse waves were used rather than home BP; for α = 0.05 and β = 0.20, numbers were 25 subjects for amplification but over 1000 for home BP. Conclusion: Regression of LV mass is closely associated with reduction in wave reflection, and can be assessed more precisely and easily from radial tonometry than from the brachial cuff measurement, even in the home setting. doi:10.1016/j.hlc.2007.06.168

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Page 1: The Optimal Timing of BNP Measurement after Exercise

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Heart, Lung and Circulation Abstracts S652007;16:S1–S201

Conclusion: CR-BNP NT-proBNP measurements aretightly correlated with laboratory immunoassay E-BNPbut systematic differences exist.

doi:10.1016/j.hlc.2007.06.166

162The Optimal Timing of BNP Measurement after Exercise

J. Harris ∗, M.P. Feneley, C.S. Hayward

Cardiac Investigations and Echocardiography, St Vincent’sClinic, Sydney, NSW, Australia

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Conclusion: An acute rise in BNP was detected in 11 of12 patients post-exercise, evident at 5 min. This suggestssecretion of preformed stored NTproBNP. This informa-tion will be used in studies designed to detect a rise inLVEDP after exercise in an attempt to identify patientswith impaired diastolic function.

doi:10.1016/j.hlc.2007.06.167

163Monitoring of Antihypertensive Treatment for Left Ven-tricular Mass Regression

J. Hashimoto ∗, Y. Imai, M.F. O’Rourke

Tohoku University, Sendai, Japan; and St. Vincent’s Clinic, Dar-linghurst, New South Wales, Australia

Background: Pressure pulse waveform features may pre-dict treatment-induced regression of left ventricular (LV)mass better than casual brachial blood pressure (BP).We compared predictive power for LV mass reductionbetween the putative optimal pulse waveform feature(pulse amplification) and the putative optimal brachialcuff measurement (home BP measurement).Methods: Brachial BP was self-monitored at home in 43untreated patients with hypertension. Radial pressurewaveforms were recorded with tonometry in the clinicand transformed to aortic waveforms, and pulse amplifica-twbaR(BwidcpLBswβ

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ackground: B-type Natriuretic Peptide (BNP) is releasedy cardiac myocytes in response to increased left ventric-lar end diastolic pressure (LVEDP). Upregulation of BNProduction has been postulated to be the major determi-ant of BNP levels, however a small amount of BNP stored

n cardiac myocytes may be released acutely. The opti-al timing of BNP measurement post exercise is yet to

e identified.ethods: 19 patients (pts) underwent a Bruce protocol

xercise test. Point of care NT-proBNP (Roche Diagnostics)as assayed at rest, and 5, 20, and 60 min post-exercise.esults: NTproBNP (pg/mL) was below reading threshold

<60) in 7 pts. In the 11 pts in whom BNP increased, eleva-ion was evident 5 min. BNP decreased in 1. In the 12 ptsith valid results mean BNP (±SEM, heavy line) peaked atmin, p = 0.07 figure, (Rest 270 ± 86, 5 min 354 ± 128, 20 min45 ± 127, 60 min 341 ± 130).

ion (upper-limb pulse pressure ÷ central pulse pressure)as calculated. LV mass index (LVMI) was determinedy echocardiography. Examinations were repeated beforend after 1 year of standard medical treatment.esults: Antihypertensive treatment significantly

p < 0.001) reduced LV load, manifest by decrease in homeP and by increase in pulse amplification. These changesere accompanied by reduction in LVMI. However, for

ndividual patients, treatment-induced LVMI changeid not correlate with change in home BP (r < 0.05), butlosely correlated with change in amplification (r = 0.54,< 0.001). Amplification was a strong determinant ofVMI reduction, independent of age, gender and homeP. Estimated subject numbers required for predicting aignificant LVMI reduction were far less when the pulseaves were used rather than home BP; for α = 0.05 and= 0.20, numbers were 25 subjects for amplification butver 1000 for home BP.onclusion: Regression of LV mass is closely associatedith reduction in wave reflection, and can be assessedore precisely and easily from radial tonometry than from

he brachial cuff measurement, even in the home setting.

oi:10.1016/j.hlc.2007.06.168