Altered dependence of aortic pulse wave velocity on transmural pressure in hypertension revealing structural change in the aortic wall.

Aortic pulse wave velocity (aPWV), a major prognostic indicator of cardiovascular events, may be augmented in hypertension as a result of the aorta being stretched by a higher distending blood pressure or by a structural change. We used a novel technique to modulate intrathoracic pressure and thus aortic transmural pressure (TMP) to examine the variation of intrathoracic aPWV with TMP in hypertensive (n=20; mean±SD age, 52.1±15.3 years; blood pressure, 159.6±21.2/92.0±15.9 mm Hg) and normotensive (n=20; age, 55.5±11.1 years; blood pressure, 124.5±11.9/72.6±9.1 mm Hg) subjects. aPWV was measured using dual Doppler probes to insonate the right brachiocephalic artery and aorta at the level of the diaphragm. Resting aPWV was greater in hypertensive compared with normotensive subjects (897±50 cm/s versus 784±43 cm/s; P<0.05). aPWV was equal in hypertensive and normotensive subjects when measured at a TMP of 96 mm Hg. However, dependence of aPWV on TMP in normotensive subjects was greater than that in hypertensive subjects (9.6±1.6 versus 3.8±0.7 cm/s per mm Hg increase in TMP, respectively, means±SEM; P<0.01). This experimental behavior was best explained by a theoretical model incorporating strain-induced recruitment of stiffer fibers in normotensive subjects and fully recruited stiffer fibers in hypertensive subjects. These results explain previous contradictory findings with respect to isobaric aPWV in hypertensive compared with normotensive subjects. They suggest that hypertension is associated with a profound change in aortic wall mechanical properties possibly because of destruction of elastin leading to less strain-induced stiffening and predisposition to aortic dissection.

Catheter-induced errors in pressure measurements in vessels: an in-vitro and numerical study.

Accurate measurement of blood pressure is important because it is a biomarker for cardiovascular disease. Diagnostic catheterization is routinely used for pressure acquisition in vessels despite being subject to significant measurement errors. To investigate these errors, this study compares pressure measurement using two different techniques in vitro and numerical simulations. Pressure was acquired in a pulsatile flow phantom using a 6F fluid-filled catheter and a 0.014'' pressure wire, which is considered the current gold standard. Numerical simulations of the experimental set-up with and without a catheter were also performed. Despite the low catheter-to-vessel radius ratio, the catheter traces showed a 24% peak systolic pressure overestimation compared to the wire. The numerical models replicated this difference and indicated the cause for overestimation was the increased flow resistance due to the presence of the catheter. Further, the higher frequency pressure oscillations observed in the wire and numerical data were absent in the catheter, resulting in an overestimation of the pulse wave velocity with the latter modality. These results show that catheter geometry produces significant measurement bias in both the peak pressure and the waveform shape even with radius ratios considered acceptable in clinical practice. The wire allows for more accurate pressure quantification, in agreement with the numerical model without a catheter.

Beat-to-beat variation in pulse wave velocity during breathing maneuvers.

PURPOSE: Thoracic pulse wave velocity (PWV) variation due to modulated trans-mural pressure (TMP) may indicate mechanical properties of the aorta. Our aim was to measure beat-to-beat thoracic PWV and TMP to observe its normal variation during respiratory maneuvers. METHODS: We validated PWV measurements from a real-time velocity projection MRI scan in a pulsatile phantom. A volunteer study showed inter-scan repeatability of steady-state PWV, and observed PWV variation when performing Mueller and Valsalva maneuvers. Synchronized to the real-time projection velocity data, TMP was measured using a mouth piece and pressure sensor arrangement monitoring the intra-thoracic pressure and a single arterial pressure measurement. RESULTS: In the phantom, beat-to-beat PWV derived from real-time projection (5.33 ± 0.32 m s(-1) ) agreed well with experimentally derived PWV using ultrasound probes (5.72 ± 0.50 m s(-1) ). The within-subject PWV variation between scans was 0.28 m s(-1) . Volunteers' PWVs increased during Mueller maneuver (TMP increase of 14.67 ± 10.69 mmHg) by 32% (P < 0.001), and during Valsalva maneuver (TMP decrease of TMP = 17.01 ± 12.91 mmHg), PWV response were inconsistent with an average increase of 14% (P < 0.05). CONCLUSION: Gating TMP to beat-to-beat PWV allows insight into how aortic stiffness varies with strain. However, quantifying nonlinear arterial stiffness requires real-time arterial pressure measurement.

Starling-like flow control of a left ventricular assist device: in vitro validation.

The application of rotary left ventricular (LV) assist devices (LVADs) is expanding from bridge to transplant, to destination and bridge to recovery therapy. Conventional constant speed LVAD controllers do not regulate flow according to preload, and can cause over/underpumping, leading to harmful ventricular suction or pulmonary edema, respectively. We implemented a novel adaptive controller which maintains a linear relationship between mean flow and flow pulsatility to imitate native Starling-like flow regulation which requires only the measurement of VAD flow. In vitro controller evaluation was conducted and the flow sensitivity was compared during simulations of postural change, pulmonary hypertension, and the transition from sleep to wake. The Starling-like controller's flow sensitivity to preload was measured as 0.39 L/min/mm Hg, 10 times greater than constant speed control (0.04 L/min/mm Hg). Constant speed control induced LV suction after sudden simulated pulmonary hypertension, whereas Starling-like control reduced mean flow from 4.14 to 3.58 L/min, maintaining safe support. From simulated sleep to wake, Starling-like control increased flow 2.93 to 4.11 L/min as a response to the increased residual LV pulsatility. The proposed controller has the potential to better match device outflow to patient demand in comparison with conventional constant speed control.