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Pressure-dependent amplification of the pressure pulse along the aorta in normotensive and spontaneously hypertensive rats
Abstracts
Table 1. BP lowering Antiplatelet
BP lowering All three + statin therapies
Prior MI 85% 83% 75% 67% Prior ischaemic 56% 42% 36% 26% stroke OR (95% CI)a 5.7 (3.8–8.4) 6.2 (4.3–9.1) 5.3 (3.8–7.4) 6.2 (4.4–8.7) a
MI vs. stroke, adjusted for age and sex.
doi:10.1016/j.hlc.2009.05.689 644 PRESSURE-DEPENDENT AMPLIFICATION OF THE PRESSURE PULSE ALONG THE AORTA IN NORMOTENSIVE AND SPONTANEOUSLY HYPERTENSIVE RATS K. Ng, M. Butlin, Y.-Y. Liu, I. Tan, K. Xu, A. Avolio The Australian School of Advanced Medicine, Macquarie University, Sydney, Australia Background: Pulse pressure (PP) increases with distance from central to peripheral arteries; PP amplification (PPA) depends on arterial properties, which are affected by the distending pressure. This haemodynamic pattern has not been quantified, particularly in hypertensive rats over a wide range of physiological blood pressure (BP). The aim of this study was to characterize the amplification of the pressure pulse between proximal and distal aorta over a range of BP in normotensive Wistar-Kyoto and spontaneously hypertensive rats (SHR). Methods: The intra-arterial beat-to-beat BP of adult normotensive and SHR at 24 weeks of age was measured with two high fidelity 1.4 F catheter-tipped pressure sensors inserted in the carotid and femoral arteries and positioned in the thoracic and abdominal aorta at known sites. Mean aortic pressure (MP) was increased and decreased by 30 s infusions of phenylephrine (50 g/min) and sodium nitroprusside (10 g/min) respectively. Aortic pulse amplification was defined as the ratio of abdominal to thoracic aortic PP. Results: MP was significantly higher in untreated SHR than in normotensive rats (n = 8 per group, P = <0.001). In the MP range of 70–140 mmHg, SHR had a lower average PPA (1.1025 ± 0.0963) than normotensive rats (1.6394 ± 0.1473) (P < 0.001) with a lower MP dependent increase (SHR: 0.0050 mmHg, normotensive: 0.0165 mmHg, R2 = 0.991) and decrease (SHR: 0.0031 mmHg; normotensive: 0.0106 mmHg, (R2 = 0.965). Maximum PPA occurred at 90 (normotensive) and 132 (SHR), respectively. Conclusions: PPA in both tnormotensive rats and SHR show a biphasic relationship with MP and isobaric PPA is reduced for SHR. Maximum PPA occurred at high MP for untreated SHR indicating a possible vascular adaptive mechanism to the sustained higher MP in the SHR. doi:10.1016/j.hlc.2009.05.690
S281
645 PREVALENCE OF PERIPHERAL ARTERY DISEASE IN AT RISK INDIVIDUALS IN THE COMMUNITY: RESULTS FROM A MOBILE CARDIOVASCULAR RISK ASSESSMENT PROGRAM S. Nagendirarajah, M. Carrington, S. Stewart Baker IDI Heart and Diabetes Research Institute, Melbourne, Australia Background: There are few community-based studies of the underlying prevalence of previously diagnosed and undetected peripheral arterial disease (PAD). Methods: As part of community-based risk screening program (Healthy Hearts—Beyond City Limits) participants from 2 regional communities in Victoria, were profiled via a mobile cardiovascular (CV) risk screening unit and their absolute CV risk (ACVR) and Edinburgh Claudication Score (ECS) calculated. Those at mediumto-high risk of a CV event within 5 years (ACVR ≥5% according to latest Australian guidelines) were targeted for PAD screening via ankle-brachial index (ABI) estimations via a standardised protocol using a Doppler ultrasound and an automatic blood pressure monitor. Results: Of 1058 community participants subject to CV risk screening, 797 (75%) had ACVR score ≥5%. Of these, ABI estimates were obtained for 221 (28%) participants (53% male, mean age 62 ± 12 years versus 40% male and mean age 57 ± 15 years for the total cohort: p < 0.001 for both comparisons). A total of 38 cases of PAD (ABI < 0.9) were identified. The prevalence of undetected PAD in these at risk individuals was, therefore, 17% (95% CI 12.6–21.4%); a minimum PAD prevalence of 3.6% among study participants. The ECS showed a sensitivity and specificity of 3% and 97% to the presence of underlying PAD. On an adjusted basis, a positive response to the Arroll tool for potential depression (38 of those screened [17%]) was associated with 2.58-fold increased probability (95% CI 1.18–5.66; p = 0.018) of underlying PAD. Moreover, within this group of participants with elevated CV risk, an increasingly elevated score was still associated (borderline significance) with underlying PAD (OR 1.06 per unit, 95% CI 1.00–1.13; p = 0.053). Conclusion: The prevalence of PAD in an at risk group of adults subject to advanced CV screening in 2 regional communities was 17%. Most were asymptomatic and asymptomatic supporting the need for such screening programs. doi:10.1016/j.hlc.2009.05.691
ABSTRACTS
Heart, Lung and Circulation 2009;18S:S1–S286
Table 1. BP lowering Antiplatelet
BP lowering All three + statin therapies
Prior MI 85% 83% 75% 67% Prior ischaemic 56% 42% 36% 26% stroke OR (95% CI)a 5.7 (3.8–8.4) 6.2 (4.3–9.1) 5.3 (3.8–7.4) 6.2 (4.4–8.7) a
MI vs. stroke, adjusted for age and sex.
doi:10.1016/j.hlc.2009.05.689 644 PRESSURE-DEPENDENT AMPLIFICATION OF THE PRESSURE PULSE ALONG THE AORTA IN NORMOTENSIVE AND SPONTANEOUSLY HYPERTENSIVE RATS K. Ng, M. Butlin, Y.-Y. Liu, I. Tan, K. Xu, A. Avolio The Australian School of Advanced Medicine, Macquarie University, Sydney, Australia Background: Pulse pressure (PP) increases with distance from central to peripheral arteries; PP amplification (PPA) depends on arterial properties, which are affected by the distending pressure. This haemodynamic pattern has not been quantified, particularly in hypertensive rats over a wide range of physiological blood pressure (BP). The aim of this study was to characterize the amplification of the pressure pulse between proximal and distal aorta over a range of BP in normotensive Wistar-Kyoto and spontaneously hypertensive rats (SHR). Methods: The intra-arterial beat-to-beat BP of adult normotensive and SHR at 24 weeks of age was measured with two high fidelity 1.4 F catheter-tipped pressure sensors inserted in the carotid and femoral arteries and positioned in the thoracic and abdominal aorta at known sites. Mean aortic pressure (MP) was increased and decreased by 30 s infusions of phenylephrine (50 g/min) and sodium nitroprusside (10 g/min) respectively. Aortic pulse amplification was defined as the ratio of abdominal to thoracic aortic PP. Results: MP was significantly higher in untreated SHR than in normotensive rats (n = 8 per group, P = <0.001). In the MP range of 70–140 mmHg, SHR had a lower average PPA (1.1025 ± 0.0963) than normotensive rats (1.6394 ± 0.1473) (P < 0.001) with a lower MP dependent increase (SHR: 0.0050 mmHg, normotensive: 0.0165 mmHg, R2 = 0.991) and decrease (SHR: 0.0031 mmHg; normotensive: 0.0106 mmHg, (R2 = 0.965). Maximum PPA occurred at 90 (normotensive) and 132 (SHR), respectively. Conclusions: PPA in both tnormotensive rats and SHR show a biphasic relationship with MP and isobaric PPA is reduced for SHR. Maximum PPA occurred at high MP for untreated SHR indicating a possible vascular adaptive mechanism to the sustained higher MP in the SHR. doi:10.1016/j.hlc.2009.05.690
S281
645 PREVALENCE OF PERIPHERAL ARTERY DISEASE IN AT RISK INDIVIDUALS IN THE COMMUNITY: RESULTS FROM A MOBILE CARDIOVASCULAR RISK ASSESSMENT PROGRAM S. Nagendirarajah, M. Carrington, S. Stewart Baker IDI Heart and Diabetes Research Institute, Melbourne, Australia Background: There are few community-based studies of the underlying prevalence of previously diagnosed and undetected peripheral arterial disease (PAD). Methods: As part of community-based risk screening program (Healthy Hearts—Beyond City Limits) participants from 2 regional communities in Victoria, were profiled via a mobile cardiovascular (CV) risk screening unit and their absolute CV risk (ACVR) and Edinburgh Claudication Score (ECS) calculated. Those at mediumto-high risk of a CV event within 5 years (ACVR ≥5% according to latest Australian guidelines) were targeted for PAD screening via ankle-brachial index (ABI) estimations via a standardised protocol using a Doppler ultrasound and an automatic blood pressure monitor. Results: Of 1058 community participants subject to CV risk screening, 797 (75%) had ACVR score ≥5%. Of these, ABI estimates were obtained for 221 (28%) participants (53% male, mean age 62 ± 12 years versus 40% male and mean age 57 ± 15 years for the total cohort: p < 0.001 for both comparisons). A total of 38 cases of PAD (ABI < 0.9) were identified. The prevalence of undetected PAD in these at risk individuals was, therefore, 17% (95% CI 12.6–21.4%); a minimum PAD prevalence of 3.6% among study participants. The ECS showed a sensitivity and specificity of 3% and 97% to the presence of underlying PAD. On an adjusted basis, a positive response to the Arroll tool for potential depression (38 of those screened [17%]) was associated with 2.58-fold increased probability (95% CI 1.18–5.66; p = 0.018) of underlying PAD. Moreover, within this group of participants with elevated CV risk, an increasingly elevated score was still associated (borderline significance) with underlying PAD (OR 1.06 per unit, 95% CI 1.00–1.13; p = 0.053). Conclusion: The prevalence of PAD in an at risk group of adults subject to advanced CV screening in 2 regional communities was 17%. Most were asymptomatic and asymptomatic supporting the need for such screening programs. doi:10.1016/j.hlc.2009.05.691
ABSTRACTS
Heart, Lung and Circulation 2009;18S:S1–S286