Morphometric versus densitometric assessment of coronary vasomotor tone-an overview

The main advantage of the morphometric approach is that the spatial orientation of the vessel with respect to the image intensifier is not very important. Its most severe limitations are that reasonable accuracy can only be obtained with circular lumina, and that accuracy decreases rapidly with the vessel diameter. The densitometric approach is much less dependent on the shape of the lumen and on the correct identification of the vessel wall in the image. A further essential advantage is that one measures directly the cross-sectional area of the vessel instead of a ‘diameter' of low haemodynamic relevance. Severe requirements must however be met if the potential accuracy of densitometry is to be fully exploited. The morphometric approach seems thus preferable for absolute or relative diameter measurements on intact vessels, while densitometry is superior in case of irregular or small lumina. Morphometric calibration using the injection catheter can induce non-negligible errors in both approaches. Grid calibration is probably more accurate, but also more tedious. In the densitometric approach, ‘3D-calibration' by help of a cube of known size allows also determination of the spatial orientation of the vessel in space. This solution requires however biplane imagin

Digital videodensitometric measurement of aortic regurgitation

A videodensitometric method for quantification of aortic regurgitation which requires neither measurement of cardiac output nor determination of enddiastolic and endsystolic left ventricular volumes has been developed. The injection of 20 ml of contrast medium into the left ventricle is digitally recorded at 25 images s−1 during 20 s using an equipment for digital subtraction angiography (Digitron 2, Siemens). The Digitron computes 2 ‘time dilution curves' (TDC) from the unsubtracted image sequence, for 2 regions of interest drawn around the angiographic enddiastolic and endsystolic left ventricular silhouettes. Enddiastolic and endsystolic points of the TDC are then entered into a VAX-750 computer, which calculates the ejection fraction (EF), the forward ejection fraction (FEF) and the regurgitant fraction (RGF). This is performed by a complex fitting algorithm based on a physical model of the washout process of contrast medium, which reconstructs the two best enddiastolic and endsystolic baselines in the washout parts of the two TDC. The EF, FEF and RGF obtained in 9 regurgitant and 11 nonregurgitant patients have been compared with the corresponding values EFv, FEFv and RGFv obtained by a conventional technique (Cardiogreen and biplane LV area-length volumetry). Regression analysis yielded: EF = 0.88 × EFv (regression line forced through the origin), r = 0.77, FEF = 0.76 × FEFv + 3, r = 0.96, RGF = 0.94 × RGFv + 5, r = 0.98 (v stands for volumetry

Could increased axial wall stress be responsible for the development of atheroma in the proximal segment of myocardial bridges?

<p>Abstract</p> <p>Background</p> <p>A recent model describing the mechanical interaction between a stenosis and the vessel wall has shown that axial wall stress can considerably increase in the region immediately proximal to the stenosis during the (forward) flow phases, so that abnormal biological processes and wall damages are likely to be induced in that region. Our objective was to examine what this model predicts when applied to myocardial bridges.</p> <p>Method</p> <p>The model was adapted to the hemodynamic particularities of myocardial bridges and used to estimate by means of a numerical example the cyclic increase in axial wall stress in the vessel segment proximal to the bridge. The consistence of the results with reported observations on the presence of atheroma in the proximal, tunneled, and distal vessel segments of bridged coronary arteries was also examined.</p> <p>Results</p> <p>1) Axial wall stress can markedly increase in the entrance region of the bridge during the cardiac cycle. 2) This is consistent with reported observations showing that this region is particularly prone to atherosclerosis.</p> <p>Conclusion</p> <p>The proposed mechanical explanation of atherosclerosis in bridged coronary arteries indicates that angioplasty and other similar interventions will not stop the development of atherosclerosis at the bridge entrance and in the proximal epicardial segment if the decrease of the lumen of the tunneled segment during systole is not considerably reduced.</p

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