“…In healthy humans 25,26 or rodents, 27 owing to the mechanical properties of the vasculature along the arterial tree, SBP is higher at peripheral sites, the brachial or tail artery compared with a central site such as the thoracic aorta. Direct SBP measurements in cats were performed in the distal abdominal aorta, whereas HDO measurements were performed at the level of the coccygeal artery.…”
This study compared indirect blood pressure measurements using a non-invasive method, high-definition oscillometry (HDO), with direct measurements using a radio-telemetry device in awake cats. Paired measurements partitioned to five sub-ranges were collected in six cats using both methods. The results were analysed for assessment of correlation and agreement between the two methods, taking into account all pressure ranges, and with data separated in three sub-groups, low, normal and high ranges of systolic (SBP) and diastolic (DBP) blood pressure. SBP data displayed a mean correlation coefficient of 0.92 ± 0.02 that was reduced for low SBP. The agreement level evaluated from the whole data set was high and slightly reduced for low SBP values. The mean correlation coefficient of DBP was lower than for SBP (ie, 0.81 ± 0.02). The bias for DBP between the two methods was 22.3 ± 1.6 mmHg, suggesting that HDO produced lower values than telemetry. These results suggest that HDO met the validation criteria defined by the American College of Veterinary Internal Medicine consensus panel and provided a faithful measurement of SBP in conscious cats. For DBP, results suggest that HDO tended to underestimate DBP. This finding is clearly inconsistent with the good agreement reported in dogs, but is similar to outcomes achieved in marmosets and cynomolgus monkeys, suggesting that this is not related to HDO but is species related. The data support that the HDO is the first and only validated non-invasive blood pressure device and, as such, it is the only non-invasive reference technique that should be used in future validation studies.
“…In healthy humans 25,26 or rodents, 27 owing to the mechanical properties of the vasculature along the arterial tree, SBP is higher at peripheral sites, the brachial or tail artery compared with a central site such as the thoracic aorta. Direct SBP measurements in cats were performed in the distal abdominal aorta, whereas HDO measurements were performed at the level of the coccygeal artery.…”
This study compared indirect blood pressure measurements using a non-invasive method, high-definition oscillometry (HDO), with direct measurements using a radio-telemetry device in awake cats. Paired measurements partitioned to five sub-ranges were collected in six cats using both methods. The results were analysed for assessment of correlation and agreement between the two methods, taking into account all pressure ranges, and with data separated in three sub-groups, low, normal and high ranges of systolic (SBP) and diastolic (DBP) blood pressure. SBP data displayed a mean correlation coefficient of 0.92 ± 0.02 that was reduced for low SBP. The agreement level evaluated from the whole data set was high and slightly reduced for low SBP values. The mean correlation coefficient of DBP was lower than for SBP (ie, 0.81 ± 0.02). The bias for DBP between the two methods was 22.3 ± 1.6 mmHg, suggesting that HDO produced lower values than telemetry. These results suggest that HDO met the validation criteria defined by the American College of Veterinary Internal Medicine consensus panel and provided a faithful measurement of SBP in conscious cats. For DBP, results suggest that HDO tended to underestimate DBP. This finding is clearly inconsistent with the good agreement reported in dogs, but is similar to outcomes achieved in marmosets and cynomolgus monkeys, suggesting that this is not related to HDO but is species related. The data support that the HDO is the first and only validated non-invasive blood pressure device and, as such, it is the only non-invasive reference technique that should be used in future validation studies.
“…Selective and nonselective aldosterone blockers attenuate cfPWV and AIx (185;186) in select patient groups by increasing nitric oxide (NO) bioactivity and improving endothelial vasodilator dysfunction (187). Vasodilating drugs, such as hydralazine and dipyridamole, primarily increase arteriolar caliber and therefore decrease peripheral resistance and mean arterial pressure via their action on arteriolar smooth-muscle cells with little effect on aortic wave reflections (188). Nitrates primarily relax smooth muscle cells in large conduit muscular arteries and therefore decrease arterial stiffness, aortic wave reflection amplitude and duration and reduce central systolic and PP with little change in brachial cuff systolic and PP (189–191).…”
Section: Section 4: Arterial Stiffness Wave Reflections and LV Aftermentioning
“…27 In genetically hypertensive rats that have equal central and peripheral pressures, giving ACE inhibitors or calcium-channel blockers restores the pulse pressure gradient but hydralazine does not. 18 However, there is evidence that ACE inhibitors, by causing an equal decrease in brachial and aortic PP may not actually increase PP amplification, despite reducing wave reflection in patients with essential hypertension 14 although some studies have shown a restoration of pulse pressure gradient in patients with end-stage renal disease. 13 In the present study, we have observed that valsartan when added to an ACE inhibitor, preferentially decreased central pulse pressure, favourably modifying pulse pressure amplification, restoring it to normal values.…”
Section: Pulse Pressure Amplificationmentioning
confidence: 99%
“…[10][11][12][13][14][15] Attention is being directed at drugs that reduce early AWR and arterial stiffness, as not all antihypertensives have a beneficial effect on arterial stiffness and AWR despite the same level of blood pressure reduction. 16,17 Angiotensin-converting enzyme (ACE) inhibitors, in particular, have been shown to delay AWR and increase the pulse pressure gradient between the central and peripheral circulation in both animal 18 and human studies. 13 We hypothesised that combined angiotensin II (ATII) antagonism, by adding an AT 1 receptor antagonist to an ACE inhibitor, might provide a more complete block of the renin-angiotensin system.…”
Objective: Angiotensin-converting enzyme (ACE) inhibitors have beneficial effects on arterial compliance and distensibility and favourably modify the arterial pressure waveform in hypertensive patients. The objective of our study was to explore the possible effects of adding an ATII AT 1 receptor antagonist to an ACE inhibitor on augmentation pressure, a measure of arterial stiffness, and pulse pressure amplification in patients with poorly controlled essential hypertension. Design and methods: We studied a group of 18 patients with poorly controlled hypertension, despite at least three antihypertensive drugs including an ACE inhibitor, before, at 2 h and 2 weeks following the administration of 80 mg of valsartan, an ATII AT 1 receptor antagonist. Haemodynamic responses were measured by cuff sphygmomanometry, arterial pulse-wave analysis and the pulse pressure gradient was calculated as the difference between the brachial pulse pressure (cuff sphygmomanometry) and derived aortic pulse pressure (arterial pulse wave analysis). Results: Blood pressure decreased significantly (P Ͻ 0.001) and the effect was more pronounced on central
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