Complementing sparse vascular imaging data by physiological adaptation rules

Mathematical modeling of pressure and flow waveforms in blood vessels using pulse wave propagation (PWP) models has tremendous potential to support clinical decision making. For a personalized model outcome, measurements of all modeled vessel radii and wall thicknesses are required. In clinical practice, however, data sets are often incomplete. To overcome this problem, we hypothesized that the adaptive capacity of vessels in response to mechanical load could be utilized to fill in the gaps of incomplete patient-specific data sets. We implemented homeostatic feedback loops in a validated PWP model to allow adaptation of vessel geometry to maintain physiological values of wall stress and wall shear stress. To evaluate our approach, we gathered vascular MRI and ultrasound data sets of wall thicknesses and radii of central and arm arterial segments of 10 healthy subjects. Reference models (i.e., termed RefModel, n = 10) were simulated using complete data, whereas adapted models (AdaptModel, n = 10) used data of one carotid artery segment only, and the remaining geometries in this model were estimated using adaptation. We evaluated agreement between RefModel and AdaptModel geometries, as well as that between pressure and flow waveforms of both models. Limits of agreement (bias +/- 2 SD of difference) between AdaptModel and RefModel radii and wall thicknesses were 0.2 +/- 2.6 mm and -140 +/- 557 mu m, respectively. Pressure and flow waveform characteristics of the AdaptModel better resembled those of the RefModels as compared with the model in which the vessels were not adapted. Our adaptation-based PWP model enables personalization of vascular geometries even when not all required data are available.NEW & NOTEWORTHY To benefit personalized pulse wave propagation (PWP) modeling, we propose a novel method that, instead of relying on extensive data sets on vascular geometries, incorporates physiological adaptation rules. The developed vascular adaptation model adequately predicted arterial radius and wall thickness compared with ultrasound and MRI estimates, obtained in humans. Our approach could be used as a tool to facilitate personalized modeling, notably in case of missing data, as routinely found in clinical settings

Aerobic exercise training improves not only brachial artery flow-mediated vasodilatation but also carotid artery reactivity:A randomized controlled, cross-over trial in older men

It is well-known that aerobic exercise training beneficially affects endothelial function as measured by brachial artery flow-mediated vasodilation (FMD). This trial with older sedentary overweight and obese men, therefore, examined the effects of aerobic training on other non-invasive markers of the vasculature, which have been studied in less detail. Seventeen men (67 ± 2 years, BMI: 30.3 ± 2.8 kg/m2 ) participated in this controlled cross-over study. Study participants followed in random order a fully supervised, progressive, aerobic exercise training (three 50-min sessions each week at 70% maximal power) and a no-exercise control period for 8 weeks, separated by a 12-week wash-out period. At the end of each period, endothelial function was assessed by the carotid artery reactivity (CAR) response to a cold pressor test and FMD, and local carotid and regional aortic stiffness by the carotid-to-femoral pulse wave velocity (PWVc-f ). The retinal microvasculature, the serum lipid profile, 24-h ambulatory blood pressure, and 96-h continuous glucose concentrations were also determined. Aerobic training increased CAR from 1.78% to 4.01% (Δ2.23 percentage point [pp]; 95% CI: 0.58, 3.89 pp; p = 0.012) and FMD from 3.88% to 6.87% (Δ2.99 pp; 95% CI: 0.58, 5.41 pp; p = 0.019). The stiffness index β0 increased by 1.1 (95% CI: 0.3, 1.9; p = 0.012), while PWVc-f did not change. Retinal arteriolar width increased by 4 μm (95% CI: 0, 7 μm; p = 0.041). Office blood pressure decreased, but ambulatory blood pressure, and serum lipid and continuous glucose concentrations did not change. Aerobic exercise training improved endothelial function and retinal arteriolar width in older sedentary overweight and obese men, which may reduce cardiovascular risk

Early statin therapy restores endothelial function in children with familial hypercholesterolemia

OBJECTIVES This study was designed to determine whether simvastatin improves endothelial function in children with familial hypercholesterolemia (FH). BACKGROUND Endothelial function measured by flow-mediated dilation of the brachial artery (FMD) is used as a surrogate marker of cardiovascular disease (CVD). Adult studies have shown that statins reverse endothelial dysfunction and therefore reduce the risk for future CVD. METHODS The study included 50 children with FH (9 to 18 years) and 19 healthy, non-FH controls. Children with FH were randomized to receive simvastatin or placebo for 28 weeks. The FMD was performed at baseline and at 28 weeks of treatment. RESULTS At baseline, FMD was impaired in children with FH versus non-FH controls (p <0.024). In the simvastatin FH group, FMD improved significantly, whereas the FMD remained unaltered in the placebo FH group throughout the study period (absolute increase 3.9% +/- 4.3% vs. 1.2% +/- 3.9%, p <0.05). In the simvastatin FH group, FMD increased to a level similar to the non-FH controls (15.6% +/- 6.8% vs. 15.5% +/- 5.4%, p = 0.958). Upon treatment, the simvastatin FH group showed significant absolute reductions of total cholesterol (TC) (-2.16 +/- 1.04 mmol/l, 30.1%) and low-density lipoprotein cholesterol (LDL-C) (-2.13 +/- 0.99 mmol/l, 39.8%). The absolute change of FMD after 28 weeks of therapy was inversely correlated to changes of TC (r = -0.31, p <0.05) and LDL-C (r = -0.31, p <0.05). CONCLUSIONS Our data show significant improvement of endothelial dysfunction towards normal levels after short-term simvastatin therapy in children with FH. These results emphasize the relevance of statin therapy in patients with FH at an early stage, when the atherosclerotic process is still reversible. (C) 2002 by the American College of Cardiology Foundatio