Systolic Blood Pressure Amplification Research Articles

Central-to-peripheral blood pressure amplification: role of the recording site, technology, analysis approach, and calibration scheme in invasive and non-invasive data agreement.

Systolic blood pressure amplification (SBPA) and pulse pressure amplification (PPA) can independently predict cardiovascular damage and mortality. A wide range of methods are used for the non-invasive estimation of SBPA and PPA. The most accurate non-invasive method for obtaining SBPA and/or PPA remains unknown. This study aims to evaluate the agreement between the SBPA and PPA values that are invasively and non-invasively obtained using different (1) measurement sites (radial, brachial, carotid), (2) measuring techniques (tonometry, oscillometry/plethysmography, ultrasound), (3) pulse waveform analysis approaches, and (4) calibration methods [systo-diastolic vs. approaches using brachial diastolic and mean blood pressure (BP)], with the latter calculated using different equations or measured by oscillometry. Invasive aortic and brachial pressure (catheterism) and non-invasive aortic and peripheral (brachial, radial) BP were simultaneously obtained from 34 subjects using different methodologies, analysis methods, measuring sites, and calibration methods. SBPA and PPA were quantified. Concordance correlation and the Bland-Altman analysis were performed. (1) In general, SBPA and PPA levels obtained with non-invasive approaches were not associated with those recorded invasively. (2) The different non-invasive approaches led to (extremely) dissimilar results. In general, non-invasive measurements underestimated SBPA and PPA; the higher the invasive SBPA (or PPA), the greater the underestimation. (3) None of the calibration schemes, which considered non-invasive brachial BP to estimate SBPA or PPA, were better than the others. (4) SBPA and PPA levels obtained from radial artery waveform analysis (tonometry) (5) and common carotid artery ultrasound recordings and brachial artery waveform analysis, respectively, minimized the mean errors. Overall, the findings showed that (i) SBPA and PPA indices are not "synonymous" and (ii) non-invasive approaches would fail to accurately determine invasive SBPA or PPA levels, regardless of the recording site, analysis, and calibration methods. Non-invasive measurements generally underestimated SBPA and PPA, and the higher the invasive SBPA or PPA, the higher the underestimation. There was not a calibration scheme better than the others. Consequently, our study emphasizes the strong need to be critical of measurement techniques, to have methodological transparency, and to have expert consensus for non-invasive assessment of SBPA and PPA.

Divergent effects of systolic blood pressure amplification on accuracy and precision of cuff blood pressure measurement.

Divergent effects of systolic blood pressure amplification on accuracy and precision of cuff blood pressure measurement.

Accuracy of cuff blood pressure and systolic blood pressure amplification

Automated cuff measured blood pressure (BP) is the global standard used for diagnosing hypertension, but there are concerns regarding the accuracy of the method. Individual variability in systolic BP (SBP) amplification from central (aorta) to peripheral (brachial) arteries could be related to the accuracy of cuff BP, but this has never been determined and was the aim of this study. Automated cuff BP and invasive brachial BP were recorded in 795 participants (74% male, aged 64 ± 11 years) receiving coronary angiography at five independent research sites (using seven different automated cuff BP devices). SBP amplification was recorded invasively by catheter and defined as brachial SBP minus aortic SBP. Compared with invasive brachial SBP, cuff SBP was significantly underestimated (130 ± 18 mmHg vs. 138 ± 22 mmHg, p < 0.001). The level of SBP amplification varied significantly among individuals (mean ± SD, 7.3 ± 9.1 mmHg) and was similar to level of difference between cuff and invasive brachial SBP (mean difference –7.6 ± 11.9 mmHg). SBP amplification explained most of the variance in accuracy of cuff SBP (R2 = 19%). The accuracy of cuff SBP was greatest among participants with the lowest SBP amplification (ptrend < 0.001). After cuff BP values were corrected for SBP amplification, there was a significant improvement in the mean difference from the intra-arterial standard (p < 0.0001) and in the accuracy of hypertension classification according to 2017 ACC/AHA guideline thresholds (p = 0.005). The level of SBP amplification is a critical factor associated with the accuracy of conventional automated cuff measured BP.

PS-C08-1: ACCURACY OF CUFF BLOOD PRESSURE AND SYSTOLIC BLOOD PRESSURE AMPLIFICATION

Objective: Automated cuff measured blood pressure (BP) is the global standard used for diagnosing hypertension, but there are concerns regarding the accuracy of the method. Individual variability in systolic BP (SBP) amplification from central (aorta) to peripheral (brachial) arteries could be related to the accuracy of cuff BP, but this has never been determined and was the aim of this study. Methods: Cuff BP and invasive brachial BP were recorded in 755 participants (73% male, aged 64 ± 11 years) receiving coronary angiography at six independent research sites (using seven different automated cuff BP devices). SBP amplification was recorded invasively by catheter and defined as brachial SBP minus aortic SBP. Results: Compared with invasive brachial SBP, cuff SBP was significantly underestimated (130 ± 18 mmHg vs. 138 ± 22 mmHg, p &lt; 0.001). The level of SBP amplification varied significantly among individuals (mean ± SD, 7.3 ± 9.1 mmHg; interquartile range, -2.4 to 12.3 mmHg) and was similar to level of difference between cuff and invasive brachial SBP (mean difference -7.6 ± 11.9 mmHg). SBP amplification explained most of the variance in accuracy of cuff SBP (R2 = 19%). The accuracy of cuff SBP was greatest among those participants in the lowest SBP amplification quintiles (ptrend&lt; 0.001). After cuff BP values were corrected for SBP amplification, there was a significant improvement in the mean difference from the intra-arterial standard (p &lt; 0.0001) and in the accuracy of hypertension classification according to 2017 ACC/AHA guideline thresholds (p = 0.005). Conclusions: The accuracy of automated cuff BP is markedly influenced by individual variability in SBP amplification. This knowledge can help improve the accuracy of cuff BP.

PS-C07-11: COMPARISON BETWEEN CUFF-BASED AND INVASIVE SYSTOLIC BLOOD PRESSURE AMPLIFICATION

Objective: Accurate measurement of central blood pressure (BP) using upper arm cuff-based methods is associated with several factors, including determining the level of systolic BP (SBP) amplification. This study aimed to determine the agreement between cuff-based and invasively measured SBP amplification. Methods: Patients undergoing coronary angiography had invasive SBP amplification (brachial SBP minus central SBP) measured simultaneously with cuff-based SBP amplification using a commercially available central BP device (device 1: Sphygmocor Xcel; n = 171, 70% men, 60 ± 10 years) and a now superseded model of a central BP device (device 2: Uscom BP+; n = 52, 83% men, 62 ± 10 years). Results: Mean difference (±2SD, limits of agreement) between cuff-based and invasive SBP amplification was 4 mmHg (−12, + 20 mmHg, p &lt; 0.001) for device 1 and -2 mmHg (−14, + 10 mmHg, p = 0.10) for device 2. Both devices systematically overestimated SBP amplification at lower levels and underestimated at higher levels of invasive SBP amplification, but with stronger bias for device 1 (r = −0.68 vs. r = −0.52; Z = 2.72; p = 0.008). Concordance of cuff-based and invasive SBP amplification across quartiles of invasive SBP amplification was low, particularly in the lowest and highest quartiles. The root mean square errors from regression between cuff-based central SBP and brachial SBP were significantly lower (indicating less variability) than from invasive regression models (p &lt; 0.001). Conclusions: Irrespective of the difference from invasive measurements, cuff-based estimates of SBP amplification showed evidence of proportional systematic bias and had less individual variability. These observations could provide insights on how to improve the performance of cuff-based central BP.

Comparison between cuff-based and invasive systolic blood pressure amplification.

Accurate measurement of central blood pressure (BP) using upper arm cuff-based methods is associated with several factors, including determining the level of systolic BP (SBP) amplification. This study aimed to determine the agreement between cuff-based and invasively measured SBP amplification. Patients undergoing coronary angiography had invasive SBP amplification (brachial SBP - central SBP) measured simultaneously with cuff-based SBP amplification using a commercially available central BP device (device 1: Sphygmocor Xcel; n = 171, 70% men, 60 ± 10 years) and a now superseded model of a central BP device (device 2: Uscom BP+; n = 52, 83% men, 62 ± 10 years). Mean difference (±2SD, limits of agreement) between cuff-based and invasive SBP amplification was 4 mmHg (-12, +20 mmHg, P < 0.001) for device 1 and -2 mmHg (-14, +10 mmHg, P = 0.10) for device 2. Both devices systematically overestimated SBP amplification at lower levels and underestimated at higher levels of invasive SBP amplification, but with stronger bias for device 1 (r = -0.68 vs. r = -0.52; Z = 2.72; P = 0.008). Concordance of cuff-based and invasive SBP amplification across quartiles of invasive SBP amplification was low, particularly in the lowest and highest quartiles. The root mean square errors from regression between cuff-based central SBP and brachial SBP were significantly lower (indicating less variability) than from invasive regression models (P < 0.001). Irrespective of the difference from invasive measurements, cuff-based estimates of SBP amplification showed evidence of proportional systematic bias and had less individual variability. These observations could provide insights on how to improve the performance of cuff-based central BP.

Validation Study to Determine the Accuracy of Central Blood Pressure Measurement Using the Sphygmocor Xcel Cuff Device

Numerous devices purport to measure central (aortic) blood pressure (BP) as distinct from conventional brachial BP. This validation study aimed to determine the accuracy of the Sphygmocor Xcel cuff device (AtCor Medical, CardieX, Sydney, Australia) for measuring central BP. 296 patients (mean age 61±12 years) undergoing coronary angiography had simultaneous measurement of invasive central BP and noninvasive cuff-derived central BP using the Xcel cuff device (total n=558 individual comparisons). A subsample (n=151) also had invasive brachial BP measured. Methods were undertaken according to the Artery Society recommendations, and several calibration techniques to derive central systolic BP (SBP) were examined. Minimum acceptable error was ≤5±≤8 mm Hg. Central SBP was significantly underestimated, and with wide variability, when using the default calibration of brachial-cuff SBP and diastolic BP (DBP; mean difference±SD, -7.7±11.0 mm Hg). Similar variability was observed using other calibration methods (cuff 33% form-factor mean arterial pressure and DBP, -4.4±11.5 mm Hg; cuff 40% form-factor mean arterial pressure and DBP, 4.7±11.9 mm Hg; cuff oscillometric mean arterial pressure and DBP, -18.2±12.1 mm Hg). Only calibration with invasive central integrated mean arterial pressure and DBP was within minimal acceptable error (3.3±7.5 mm Hg). The difference between brachial-cuff SBP and invasive central SBP was 3.3±10.7 mm Hg. A subsample analysis to determine the accuracy of central-to-brachial SBP amplification showed this to be overestimated by the Xcel cuff device (mean difference 4.3±9.1 mm Hg, P=0.02). Irrespective of cuff calibration technique, the Sphygmocor Xcel cuff device does not meet the Artery Society accuracy criteria for noninvasive measurement of central BP.

Atenolol's Inferior Ability to Reduce Central vs Peripheral Blood Pressure Can Be Explained by the Combination of Its Heart Rate-Dependent and Heart Rate-Independent Effects.

Objective Whether the inferior ability of atenolol to reduce central (aortic) compared to peripheral (brachial) blood pressure (BP) is related to its heart rate (HR)-dependent or -independent effects, or their combination, remains unclear. To provide further mechanistic insight into this topic, we studied the acute effects of atenolol versus nebivolol and ivabradine on systolic blood pressure amplification (SBPA; peripheral systolic BP minus central systolic BP) in a model of sick sinus syndrome patients with a permanent dual-chamber cardiac pacemaker in a nonrandomized single-blind single-group clinical trial. Methods We determined hemodynamic indices noninvasively (Sphygmocor XCEL) before and at least 3 h after administration of oral atenolol 50 or 100 mg, nebivolol 5 mg, or ivabradine 5 or 7.5 mg during atrial pacing at a low (40 bpm), middle (60 bpm), and high (90 bpm) HR level in 25 participants (mean age 65.5 years, 12 men). Results At the low HR level, i.e., when the drugs could exert their HR-dependent and HR-independent effects on central BP, only atenolol produced a significant decrease in SBPA (mean change 0.74 ± 1.58 mmHg (95% CI, 0.09–1.40; P = 0.028)), indicating inferior central vs peripheral systolic BP change. However, we observed no significant change in SBPA with atenolol at the middle and high HR levels, i.e., when HR-dependent mechanisms had been eliminated by pacing. Conclusion The findings of our trial with a mechanistic approach to the topic imply that the inferior ability of atenolol to reduce central vs peripheral BP can be explained by the combination of its heart rate-dependent and -independent effects. This trial is registered with NCT03245996.

Central-to-peripheral systolic blood pressure different phenotypes and relation to accuracy of daily used cuff devices

Background. Cuff blood pressure (BP) measurement has been the standard method for taking BP in routine daily practice for more than a century. However, some concerns were raised about the accuracy of this method which could lead to misclassification of BP in many situations. We aimed primarily to confirm a recent major discovery that distinct BP phenotypes based on central-to-peripheral systolic blood pressure (SBP) amplification do exist, and whether application of a validated cuff BP method (e.g. oscillometric) could accurately discriminate these differences. Material and methods. Among 106 participants (mean age 62 ± 11; 58% males) undergoing coronary angiography, intra-arterial BP was measured at 3 points (ascending aorta, brachial and radial arteries). Central-to-peripheral SBP amplification (SBPamp) was defined as ≥ 5 mm Hg SBP increased from aorta-to-brachial and/or from brachial-to-radial arteries. A validated cuff BP device (oscillometric) was used to measure BP at 4 different time points. Results. Four different BP phenotypes were confirmed based on the magnitude of SBPamp; phenotype-I, both aortic-to brachial and brachial-to radial SBPamp; phenotype-II, only aortic-to-brachial SBPamp; phenotype-III, only brachial-to-radial SBPamp; and phenotype-IV, no SBPamp at all. Aortic SBP was significantly higher in phenotypes-III and IV compared to phenotypes-I and II (p = 0.001). This was not discriminated using a validated cuff BP device measurement (p = 0.996). Results for the pulse pressure (PP) followed the same pattern. Conclusion. Distinct BP phenotypes do exist based on SBPamp. A validated cuff BP method failed to discriminate this. Improving quality of BP measurements in daily practice is a priority.

P86 Can Central Blood Pressure be Accurately Estimated in Individuals with and Without Systolic Blood Pressure Amplification?

IntroductionSystolic blood pressure (SBP) does not always amplify from central to peripheral arteries. Individuals without SBP amplification (SBPamp) have higher aortic blood pressure (BP) despite similar brachial cuff SBP. To circumvent this discrepancy, the aim of this study was to determine if aortic SBP can be accurately estimated non-invasively in patients with and without SBPamp.MethodsPatients undergoing percutaneous coronary intervention were recruited. Individuals with atrial fibrillation, ≥10 mmHg between-arm SBP difference or severe aortic stenosis were excluded. Aortic and brachial intra-arterial BP were measured using a fluid-filled catheter. Simultaneously, brachial and central cuff BP were measured in triplicate (Mobil-o-Graph, IEM, Germany). Central BP was estimated by pulse wave analysis with Type I (SBP and diastolic BP) and Type II (mean and diastolic BP) calibrations. Aortic-to-brachial SBPamp was defined as ≥5 mmHg increase between intra-arterial aortic and brachial SBP.ResultsOf the 151 patients recruited, only 85 had SBPamp. SBPamp+ and SBPamp- patients had similar brachial cuff SBP (126 +/− 15 vs 126 +/− 16 mmHg, p = 0.8) and clinical characteristics, apart from lower augmentation index in SBPamp+ (18 +/− 10 vs 22 +/− 11, p = 0.03). Central BP estimated with Type I or Type II calibration could not accurately determine aortic SBPs in both phenotypes (Table 1). Using the mean of both estimates only provided a slightly better accuracy.ConclusionCentral BP measurements cannot accurately identify the different aortic BP of the SBPamp phenotypes. A new central BP calibration may be needed to circumvent this problem.Table 1Baseline characteristicsSBPamp+ (n = 85)SBPamp− (n = 66)p-valueMale sex74%74%1.0Age66 ± 1165 ± 90.6Height (cm)171 ± 10170 ± 100.6BMI (kg/m2)29 ± 630 ± 100.3Active smoking28%27%0.9Diabetes19%17%0.7Hypertension59%55%0.6Dyslipidemia55%55%0.9Prior cardiovascular disease39%52%0.1eGFR (mL/min/1.73 m2)80 ± 1881 ± 180.7Brachial cuff SBP126 ± 15126 ± 160.8Brachial cuff diastolic blood pressure78 ± 978 ± 120.9Heart rate (bpm)67 ± 1165 ± 110.3Augmentation index @ 75 bmp18 ± 1022 ± 110.03Pulse wave velocity (m/s)10 ± 29 ± 20.09SBPamp+ and SBPamp− denotes individuals with and without SBP amplification, defined as ≥5 mmHg increase between intra-arterial aortic and brachial SBP. Values are expressed as mean ± standard deviation. All blood pressure measures are expressed in mmHg. p-values are calculated using Pearson’s chi-square and Student t-tests. SBP, systolic blood pressure.

Abstract 104: Amplification of Systolic Blood Pressure and Pulse Pressure is Higher in Resistant Hypertensive Patients Irrespective of Blood Pressure Control

Background: Systolic blood pressure (SBP) is higher in peripheral than in central arteries, a phenomenon referred to as BP amplification. A greater amplification of SBP and pulse pressure (PP) is associated with increased cardiovascular disease (CVD). The objective of this study is to investigate whether BP amplification is different in patients with uncontrolled resistant hypertension (uRHTN) when compared to those with controlled RHTN (cRHTN) and controlled non-RHTN (cnRHTN). Methods: In this prospective study, 149 patients were recruited from The University of Alabama at Birmingham’s HTN clinic. Brachial BP was measured using in-office BpTRU. Aortic BP was determined using pulse wave analysis by SpygmoCor. BP amplification was calculated as the difference between brachial and aortic BP. Results: The cohort comprised 50.0% women and 53.6% African Americans. Mean baseline values were: age 58.6 ± 10.3 years, BMI 34.2 ± 6.7 Kg/m 2 , SBP amplification 11.0 ± 4.4 mmHg and PP amplification 12.0 ± 4.7 mmHg. Multiple regression analysis showed a significant correlation of gender and increasing BMI with amplification of SBP (p&lt;0.0001 and 0.003, respectively) and PP (p=0.001 and 0.007, respectively). Amplification of SBP and PP were significantly higher in patients with uRHTN compared to patients with cRHTN and similarly, patients with cRHTN had higher amplification than those with cnRHTN (p=0.046 and 0.021, respectively). Conclusion: This prospective study showed that the amplification of SBP and PP remains high in patients with RHTN regardless of BP control, indicating that patients with RHTN retain a higher risk of CVD morbidity and mortality in spite of successful BP control.

THE ACCURACY OF FORM-FACTOR DERIVED MEAN ARTERIAL PRESSURE IS DEPENDENT ON SYSTOLIC BLOOD PRESSURE AMPLIFICATION

Objective: Accurate assessment of mean arterial pressure (MAP) is crucial in clinical and research settings. Measurement of MAP requires pressure waveform integration, but for convenience the standard approach is via form-factor (FF) equations incorporating systolic blood pressure (SBP) measured at a peripheral artery. SBP undergoes variable central-to-peripheral amplification and may therefore influence accuracy of FF-derived MAP, which we aimed to determine in this study. Design and method: 188 patients (age 60 ± 10 years) undergoing coronary angiography had intra-arterial pressure measured in the ascending aorta, brachial and radial arteries by sequential catheter pull-back. MAP was measured at each location by integration of ensembled pressure waveforms and derived using standard 0.33 and 0.40 FFs. Results: Integrated MAP decreased on average from the aorta to the brachial (−0.7 ± 4.2 mmHg) and radial artery (−1.7 ± 4.8 mmHg), whilst FF-derived MAP increased (0.33FF 1.1 ± 4.2 and 1.7 ± 4.7 mmHg; 0.40FF 0.9 ± 4.8 and 1.4 ± 5.4 mmHg respectively). FF-derived MAP did not accurately represent integrated aortic MAP (0.33FF −2.5 ± 4.6 and −1.6 ± 5.8; 0.40FF 2.5 ± 5.0 and 3.9 ± 6.4 mmHg, brachial and radial arteries respectively), with significant variation in FF required to generate MAP equivalent to integrated aortic MAP (FF range 0.20–0.57 brachial; 0.17–0.74 radial). Aortic-to-brachial SBP amplification was strongly related to the brachial FF required to generate MAP equivalent to integrated aortic MAP (r = −0.695, p < 0.001). The standard 0.33FF was most accurate in those with high SBP amplification (difference in estimated MAP vs. integrated aortic MAP 0.06 ± 3.93 mmHg) but substantially overestimated integrated aortic MAP in those with low SBP amplification (difference in estimated MAP vs. integrated aortic MAP 5.8 ± 4.6 mmHg). The opposite was observed for the 0.40FF. Conclusions: The standard approach of estimating MAP using peripheral FFs should not be used because it is non-physiological and inaccurate due to the influence of central-to-peripheral SBP amplification. These findings have implications for accurate assessment of MAP in clinical and research settings.

Central-to-brachial blood pressure amplification in type 2 diabetes: a systematic review and meta-analysis.

Due to systolic blood pressure (SBP) amplification, brachial SBP may not accurately reflect central SBP, the pressure the organs are exposed to. Patients with type 2 diabetes (T2D) have vascular irregularities that may affect blood pressure (BP) amplification and central BP indices (i.e. augmentation index [AIx] and augmentation pressure [AP]). By systematic review and meta-analysis, this study aimed firstly to determine the magnitude of central-to-brachial SBP and pulse pressure (PP) amplification in T2D compared to healthy controls and secondly, the difference in AIx and AP between the groups. Online databases were searched for published studies reporting invasive or non-invasive central and brachial SBP in T2D and healthy controls up to the 20th of February 2018. Random effects meta-analyses and meta-regression were used to analyze the studies. Eighteen studies (all non-invasive: 17 radial tonometry, 1 carotid tonometry, 2 brachial oscillometry) with a total of 2758 patients with T2D and 10,561 healthy controls were identified. There was no significant difference in SBP amplification between groups (T2D = 9.9 ± 4.7, healthy controls = 9.6 ± 4.5 mmHg, p = 0.84; pooled difference = 0.64 mmHg, 95%CI -0.27 1.54, p = 0.17) or PP amplification ratio (p = 0.16). However, among these studies, central BP indices (AIx corrected for heart rate and AP) were significantly higher in T2D (p < 0.05 for both). Despite a similar magnitude of central-to-brachial SBP amplification, patients with T2D have increased central systolic loading (AIx and AP) that cannot be discerned from brachial BP alone.

Isolated systolic hypertension of the young and its association with central blood pressure in a large multi-ethnic population. The HELIUS study.

BackgroundIsolated systolic hypertension (ISH) of the young has been associated with both normal and increased cardiovascular risk, which has been attributed to differences in central systolic blood pressure and arterial stiffness.MethodsWe assessed the prevalence of ISH of the young and compared differences in central systolic blood pressure and arterial stiffness between ISH and other hypertensive phenotypes in a multi-ethnic population of 3744 subjects (44% men), aged <40 years, participating in the HELIUS study.ResultsThe overall prevalence of ISH was 2.7% (5.2% in men and 1.0% in women) with the highest prevalence in individuals of African descent. Subjects with ISH had lower central systolic blood pressure and pulse wave velocity compared with those with isolated diastolic or systolic-diastolic hypertension, resembling central systolic blood pressure and pulse wave velocity values observed in subjects with high-normal blood pressure. In addition, they had a lower augmentation index and larger stroke volume compared with all other hypertensive phenotypes. In subjects with ISH, increased systolic blood pressure amplification was associated with male gender, Dutch origin, lower age, taller stature, lower augmentation index and larger stroke volume.ConclusionISH of the young is a heterogeneous condition with average central systolic blood pressure values comparable to individuals with high-normal blood pressure. On an individual level ISH was associated with both normal and raised central systolic blood pressure. In subjects with ISH of the young, measurement of central systolic blood pressure may aid in discriminating high from low cardiovascular risk.

Discovery of New Blood Pressure Phenotypes and Relation to Accuracy of Cuff Devices Used in Daily Clinical Practice.

Cuff blood pressure (BP) is the reference standard for management of high BP, but the method is inaccurate and can lead to BP misclassification. The aims of this study were to determine whether distinctive BP phenotypes exist based on BP transmission (amplification) variability from central-to-peripheral arteries and whether applying one standard cuff BP measurement approach (eg, oscillometry) to all people could discriminate the BP phenotypes. Intra-arterial BP was measured at the ascending aorta and brachial and radial arteries in 126 participants (61±10 years; 69% male) after coronary angiography. Central-to-peripheral systolic BP (SBP) transmission (SBP amplification) was defined by ≥5 mm Hg SBP increase between the aorta-to-brachial or brachial-to-radial arteries. Standard cuff BP was measured 4 different times using 3 different devices. Three independent investigators also provided data (n=255 from 4 studies) using another 3 separate cuff BP devices. Four distinct BP phenotypes were discovered based on variability in SBP amplification: phenotype 1, both aortic-to-brachial and brachial-to-radial SBP amplification; phenotype 2, only aortic-to-brachial SBP amplification; phenotype 3, only brachial-to-radial SBP amplification; and phenotype 4, neither aortic-to-brachial nor brachial-to-radial SBP amplification. Aortic SBP was significantly higher among phenotypes 3 and 4 compared with phenotypes 1 and 2 (P=0.00074), but this was not discriminated using any standard cuff BP measures (P=0.31). Data from independent investigators confirmed the key findings. This is the first-in-human discovery of BP phenotypes that have significantly different BPs, but which are not discriminated by standard cuff BP devices used in daily clinical practice. Improved BP device accuracy may be achieved by considering individual phenotypic BP differences.

PP.11.19] SYSTOLIC BLOOD PRESSURE AND PULSE PRESSURE AMPLIFICATION IN SMOKERS

Objective: To assess blood pressure (BP) and pulse pressure (PP) amplification in smokers and their relationship with arterial stiffness, coronary perfusion indices, arterial age and data related to smoking. Design and method: A total of 147 smokers, aged 37 ± 15 years, 48% male (71) were investigated using an Arteriograph. Blood pressure variables, pulse wave velocity (PWV), augmentation indices, arterial age (AA) and coronary perfusion indices (DRA, DAI) were assessed. Data about smoking habits, such as number of cigarettes smoked/day and number of years as smokers (NYS) were self-reported. Smoking pack years (SPY), systolic blood pressure (SBPAo/SBP) and pulse pressure amplification (PPAo/PP) were calculated. Results: PWV, AA, PPAo/PP, SBPAo/SBP, DRA, DAI were, as follows: 8.96 ± 4.93 m/s, 41.16 ± 17.22 years, 0.82 ± 0.13, 0.92 ± 0.06, 51.52 ± 11.78 and 51.37 ± 4.51%. Significant correlations and associations were obtained between PPAo/PP, SBPAo/SBP and DRA, AA, SPY and NYS, respectively. SPY and NYS were significantly associated with PPAo/PP, considering results of linear regression analysis (multiple R = 0.36 and 0.43, respectively and p < 0.01). SBPAo/SBP was significantly associated with DRA (multiple R = 0.34, p < 0.01). PP amplification > 0.8 and systolic blood pressure amplification > 0.9 were sensitive predictors of increased PWV (sensitivity: 0.86, 95% CI: 0.68–0.95 and 0.88, 95% CI: 0.72–0.96, respectively). SPY > 12 was a specific predictor of increased PP amplification (specificity: 0.85, 95% CI: 0.75–0.91) and a sensitive predictor of systolic BP amplification (sensitivity: 0.88, 95% CI: 0.72–0.96). Conclusions: The study provides evidence that SPY, PP and SBP amplification are useful tools in smokers, in predicting increased arterial stiffness, early arterial ageing and impaired coronary perfusion.

Systolic blood pressure amplification and waveform calibration.

Systolic blood pressure amplification and waveform calibration.

PP.28.12] 24-HOUR PATTERNS OF CENTRAL AORTIC AND BRACHIAL SYSTOLIC BLOOD PRESSURE IN THE VERY ELDERLY

Objective: The aim of current study was to investigate and compare 24-hour profiles of central and peripheral blood pressures in the very elderly via their simultaneous ambulatory monitoring. Design and method: Parallel 24-h ambulatory aortic and brachial blood pressure monitoring was performed in 67 treated hypertensive subjects older than 80 years (mean age 84,1 ± 3,1 years, 25,5% male, mean clinic brachial SBP 134,8 ± 23,2 mmHg) with an oscillometric cuff-based device BPLab Vasotens («Petr Telegin», Russia). Patients with ejection fraction < 40%, atrial fibrillation and severe comorbidities were not included. 24-h, awake and sleep-time systolic, diastolic and pulse blood pressure in aorta and brachial artery were compared in subgroups divided according to the diurnal pattern of brachial systolic blood pressure (SBP). Results: The diurnal profiles of central systolic and pulse BPs run in parallel with those of peripheral BPs in patients with all types of diurnal pattern and SBP amplification at night did not change significantly comparing to day-time values. Non-dipping or reverse-dipping SBP patterns appeared to be typical and were observed in 82,1% patients, while 50,7% participants had inadequate DBP dip < 10%. The proportionality of night-time SBP and DBP changes varied in different types of SBP diurnal profile. SBP and DBP decreased proportionally in dippers (ratio of DBP/SBP night-time reduction was 1,18) and disproportionately in non-dippers (the ratio was 2,6). In those patients with reverse-dipping pattern SBP and DBP changed in opposite directions at night. This disproportion in SBP and DBP night-time changes resulted in different intensity of PP night-time rise that was most evident in reverse-dippers. Relative nocturnal reduction of PP was 9,3 ± 4,72% in dippers, whereas non-dippers and reverse-dippers had relative PP increase of 6,2 ± 8,6 and 22,9 ± 12,3 %, respectively. Conclusions: The diurnal patterns of central and brachial BPs observed in very elderly treated hypertensives were almost parallel. PP amplification is similar in the day- and nighttime and this finding is different from previously described diurnal PP amplification behavior in younger subjects. Proportionality of SBP and DBP sleep-time changes depends on dipping status and results in nocturnal PP increase in non- and reverse-dippers.

OS 13-02 ASSOCIATION BETWEEN URIC ACID, METABOLIC VARIABLES AND ARTERIAL STIFFNESS IN THE EARLY PHASE OF HYPERTENSION.

Objective: High serum uric acid (SUA) is often associated with the metabolic syndrome and is a risk factor for cardiovascular disease. Whether high SUA is associated with arterial stiffness in the early stage of hypertension is not well known. Design and Method: We addressed this issue in 340 non-diabetic subjects from the HARVEST study (73% males) with a mean age of 31 ± 8 years and a mean blood pressure (BP) of 145 ± 11/92 ± 6 mmHg. Patients were divided into SUA tertiles (T1: 1.30–4.47, T2: 4.50–5.50, T3: 5.55–8.60 mg/dl). Arterial stiffness was assessed by pulse wave velocity (PWV), augmentation index (AIx), pulse pressure (PP) amplification and systolic BP (SBP) amplification. Results: Patients in the highest SUA tertile were heavier (BMI, T3: 25.7 ± 0.3 kg/m2, T2: 24.9 ± 0.3 kg/m2, T1: 24.4 ± 0.3 kg/m2; p = 0.031) and had a worse metabolic profile, with higher age-and-sex-adjusted total cholesterol (TC) (T3: 201.5 ± 3.8 mg/dl, T2:188.8 ± 3.6mg/dl, T1:193.2 ± 3.8 mg/dl; p = 0.048), triglycerides (T3: 150.9 ± 7.8 mg/dl, T2: 99.6 ± 7.5 mg/dl, T1: 96.3 ± 7.7 mg/dl; p < 0.0001) and glucose (T3: 93.0 ± 1.1 g/dl, T2: 92.6 ± 1.1 g/dl, T1: 89.5 ± 1.1 mg/dl; p = 0.059), and lower HDL-C (T3: 50.6 ± 1.6 mg/dl, T2: 54.9 ± 1.6 mg/dl, T1: 56.8 ± 1.7 mg/dl; p = 0.033) than subjects in the lower SUA tertiles. No significant difference in peripheral BP and central BP was found according to SUA tertile. Patients in the highest SUA tertile showed lower SBP amplification (p = 0.037 adjusted for age, sex, BMI, and metabolic data). This difference remained significant after inclusion in the model of lifestyle habits (p = 0.021) and of peripheral BPs and heart rate (p = 0.005). Similarly patients in the highest SUA tertile presented a lower PP amplification (p = 0.021 adjusted for all the above mentioned variables). No significant difference in PWV and AIx was found across SUA tertiles. Conclusions: These data show that among young to middle-age stage I hypertensives higher SUA is associated with metabolic abnormalities and initial impairment of arterial elasticity.

OP.5A.01] CENTRAL BLOOD PRESSURE RELATES MORE STRONGLY TO RETINAL ARTERIOLAR NARROWING THAN BRACHIAL BLOOD PRESSURE

Objective: Although central blood pressure (BP) is considered to be more closely associated with large arterial remodeling and cardiovascular outcomes than brachial BP, few studies have investigated these associations with changes in small arteries. As morphological changes in retinal vessels might be associated with cardiovascular outcomes, we conducted a cross-sectional study to investigate the association of central BP with retinal vessel caliber. Design and method: Study subjects consisted of 8,054 apparently healthy middle-aged to elderly citizens (52 ± 13 years old) who were participants of the Nagahama Study. Basic clinical parameters, including plasma markers, were measured at baseline. Central BP was estimated by the radial arterial waveform by calibrating brachial BP. Central retinal arteriolar equivalent (CRAE) was computationally measured using fundus photography. Results: CRAE was decreased with age. Basic factors that were significantly associated with CRAE included age (r = −0.210, p < 0.001), habitual smoking (current smoker 128.7 ± 11.7, non-smoker 125.7 ± 11.9 μm, p < 0.001), and drinking (habitual drinker 125.2 ± 11.9, non-drinker 126.6 ± 11.9, μm, p < 0.001). CRAE was most strongly associated with central systolic BP (SBP) (r = −0.324, p < 0.001), followed by diastolic BP (r = −0.292, p < 0.001), and central pulse pressure (PP) (r = −0.226, p < 0.001). Results of Meng-Rosenthal-Rubin method analysis indicated that the correlation coefficient between BPs and CRAE was significantly larger in central BP than brachial BP (r = −0.300, p < 0.001). After adjustment for possible covariates, brachial SBP (β = −0.221, p < 0.001) and central SBP (β = −0.239, p < 0.001) were independently associated with CRAE. Further, higher brachial SBP (β = −0.226, p < 0.001) and smaller PP amplification (β = 0.092, p < 0.001) were identified as independent determinants of narrowing of CRAE in the same equation, which indicated the superiority of central BP. Central BP-determined hypertensive subjects (HT) had a significantly narrower CRAE independently of brachial BP (central/brachial: HT/HT 121.4 ± 11.5, HT/normotension (NT) 120.9 ± 11.2, NT/HT 125.1 ± 11.9, NT/NT 128.1 ± 11.5 μ). Conclusions: Central BP was more closely associated with the narrowing of CRAE than brachial BP. Slight increases in central BP might be involved in the morphological changes in small retinal arteries, even in subjects with optimal brachial BP.