Wall shear stress as measured in vivo: consequences for the design of the arterial system

Based upon theory, wall shear stress (WSS), an important determinant of endothelial function and gene expression, has been assumed to be constant along the arterial tree and the same in a particular artery across species. In vivo measurements of WSS, however, have shown that these assumptions are far from valid. In this survey we will discuss the assessment of WSS in the arterial system in vivo and present the results obtained in large arteries and arterioles. In vivo WSS can be estimated from wall shear rate, as derived from non-invasively recorded velocity profiles, and whole blood viscosity in large arteries and plasma viscosity in arterioles, avoiding theoretical assumptions. In large arteries velocity profiles can be recorded by means of a specially designed ultrasound system and in arterioles via optical techniques using fluorescent flow velocity tracers. It is shown that in humans mean WSS is substantially higher in the carotid artery (1.1–1.3 Pa) than in the brachial (0.4–0.5 Pa) and femoral (0.3–0.5 Pa) arteries. Also in animals mean WSS varies substantially along the arterial tree. Mean WSS in arterioles varies between about 1.0 and 5.0 Pa in the various studies and is dependent on the site of measurement in these vessels. Across species mean WSS in a particular artery decreases linearly with body mass, e.g., in the infra-renal aorta from 8.8 Pa in mice to 0.5 Pa in humans. The observation that mean WSS is far from constant along the arterial tree implies that Murray’s cube law on flow-diameter relations cannot be applied to the whole arterial system. Because blood flow velocity is not constant along the arterial tree either, a square law also does not hold. The exponent in the power law likely varies along the arterial system, probably from 2 in large arteries near the heart to 3 in arterioles. The in vivo findings also imply that in in vitro studies no average shear stress value can be taken to study effects on endothelial cells derived from different vascular areas or from the same artery in different species. The cells have to be studied under the shear stress conditions they are exposed to in real life

Coronary-aortic interaction during ventricular isovolumic contraction

In earlier work, we suggested that the start of the isovolumic contraction period could be detected in arterial pressure waveforms as the start of a temporary pre-systolic pressure perturbation (AIC(start), start of the Arterially detected Isovolumic Contraction), and proposed the retrograde coronary blood volume flow in combination with a backwards traveling pressure wave as its most likely origin. In this study, we tested this hypothesis by means of a coronary artery occlusion protocol. In six Yorkshire x Landrace swine, we simultaneously occluded the left anterior descending (LAD) and left circumflex (LCx) artery for 5 s followed by a 20-s reperfusion period and repeated this sequence at least two more times. A similar procedure was used to occlude only the right coronary artery (RCA) and finally all three main coronary arteries simultaneously. None of the occlusion protocols caused a decrease in the arterial pressure perturbation in the aorta during occlusion (P > 0.20) nor an increase during reactive hyperemia (P > 0.22), despite a higher deceleration of coronary blood volume flow (P = 0.03) or increased coronary conductance (P = 0.04) during hyperemia. These results show that the pre-systolic aortic pressure perturbation does not originate from the coronary arteries

Initiation of ventricular contraction as reflected in the aortic pressure waveform

Prior to aortic valve opening, aortic pressure is perturbed by ventricular contraction. The onset of this pressure perturbation coincides with the onset of the left ventricular (LV) isovolumic contraction, and hence will be referred to as the start of the arterially detected isovolumic contraction (AIC(start)). In the present study we test the hypothesis that the pressure perturbation indeed has a cardiac origin. In ten Yorkshire-Landrace swine, waveform intensity analysis demonstrated that AIC(start) was followed by a positive intensity wave (0.3 x 10(5) +/- 0.3 x 10(5) W (m(2) s(2))(-1)). Timing analysis of LV and aortic pressure waveform showed that AIC(start) was preceded by a LV pressure perturbation (3.8 +/- 1.8 ms, p < 0.001). These novel cardiac timing and aortic wave intensity findings reveal the cardiac origin of the pressure perturbation. In 15 Yorkshire-Landrace swine, myocardial motion analysis showed a significantly higher rate of segment shortening during the first part of the LV pressure perturbation. Therefore, both the LV and aortic pressure perturbation are most likely caused by the early phase of myocardial contraction, which also causes mitral valve closure. Consequently, AIC(start) is useful in the determination of the isovolumic contraction period, a well-known marker to quantify cardiac dysfunction