Non-invasive assessment of arterial stiffness using oscillometric blood pressure measurement

<p>Abstract</p> <p>Background</p> <p>Arterial stiffness is a major contributor to cardiovascular diseases. Because current methods of measuring arterial stiffness are technically demanding, the purpose of this study was to develop a simple method of evaluating arterial stiffness using oscillometric blood pressure measurement.</p> <p>Methods</p> <p>Blood pressure was conventionally measured in the left upper arm of 173 individuals using an inflatable cuff. Using the time series of occlusive cuff pressure and the amplitudes of pulse oscillations, we calculated local slopes of the curve between the decreasing cuff pressure and corresponding arterial volume. Whole pressure-volume curve was derived from numerical integration of the local slopes. The curve was fitted using an equation and we identified a numerical coefficient of the equation as an index of arterial stiffness (Arterial Pressure-volume Index, API). We also measured brachial-ankle (baPWV) PWV and carotid-femoral (cfPWV) PWV using a vascular testing device and compared the values with API. Furthermore, we assessed carotid arterial compliance using ultrasound images to compare with API.</p> <p>Results</p> <p>The slope of the calculated pressure-volume curve was steeper for compliant (low baPWV or cfPWV) than stiff (high baPWV or cfPWV) arteries. API was related to baPWV (<it>r </it>= -0.53, <it>P </it>< 0.05), cfPWV (<it>r </it>= -0.49, <it>P </it>< 0.05), and carotid arterial compliance (<it>r </it>= 0.32, <it>P </it>< 0.05). A stepwise multiple regression analysis demonstrated that baPWV and carotid arterial compliance were the independent determinants of API, and that API was the independent determinant of baPWV and carotid arterial compliance.</p> <p>Conclusions</p> <p>These results suggest that our method can simply and simultaneously evaluate arterial stiffness and blood pressure based on oscillometric measurements of blood pressure.</p

Integral Effects of Systemic Nitric Oxide Synthase Inhibition on Carotid Arterial Compliance

Decreased arterial compliance (increased arterial stiffness) is associated with cardiovascular events. Nitric oxide regulates vascular tone, which can influence arterial compliance. We previously investigated the effects of systemic nitric oxide synthase (NOS) inhibition on arterial compliance under the systemic α-adrenergic receptor blocking. In the present study, we investigated the effect of systemic NOS inhibition alone on central arterial compliance (via carotid arterial ultrasound imaging and applanation tonometry). Eighteen apparently healthy young adults (26±1 years) underwent intravenous infusions of NG-monomethyl-L-arginine (L-NMMA) or placebo (saline) on separate days. In the placebo control condition, no significant changes were observed in mean arterial pressure, cross-sectional compliance, and β-stiffness index. Mean arterial pressure increased significantly (84±2 vs. 96±3 mmHg) after the administration of L-NMMA, whereas there were no significant changes in cross-sectional compliance (0.11±0.01 vs. 0.12±0.01 mm2/mmHg), β-stiffness index (6.44±0.37 vs. 5.51±0.41 unit), or isobaric arterial compliance. Theses results in young healthy adults are not consistent with the idea that carotid arterial compliance is modulated by nitric oxide. Grant Support: This work was supported by Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology of Japan (18300215, 18650186), JSPS Postdoctoral Fellowships for Research Abroad, and NIH grant AG20966

Differential relationship between decreased muscle oxygenation and blood pressure recovery during supraventricular and ventricular tachycardia

Abstract Vasoconstriction during tachyarrhythmia contributes to maintenance of arterial pressure (AP) by decreasing peripheral blood flow. This cross-sectional observational study aimed to ascertain whether the relationship between peripheral blood flow and AP recovery occurs during both paroxysmal supraventricular (PSVT, n = 19) and ventricular tachycardias (VT, n = 17). Peripheral blood flow was evaluated using forearm tissue oxygen index (TOI), and mean AP (MAP) was measured using a catheter inserted in the brachial or femoral artery during an electrophysiological study. PSVT and VT rapidly decreased MAP with a comparable heart rate (P = 0.194). MAP recovered to the baseline level at 40 s from PSVT onset, but not VT. The forearm TOI decreased during both tachyarrhythmias (P ≤ 0.029). The TOI response was correlated with MAPrecovery (i.e., MAP recovery from the initial rapid decrease) at 20–60 s from PSVT onset (r = -– 0.652 to – 0.814, P ≤ 0.0298); however, this association was not observed during VT. These findings persisted even after excluding patients who had taken vasoactive drugs. Thus, restricting peripheral blood flow was associated with MAP recovery during PSVT, but not VT. This indicates that AP recovery depends on the type of tachyarrhythmia: different cardiac output and/or vasoconstriction ability during tachyarrhythmia

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