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Patient specific geometrical data on human coronary arteries can be reliably obtained multislice computer tomography (MSCT) imaging. MSCT cannot provide hemodynamic variables, and the outflow through the side branches must be estimated. The impact of two different models to determine flow through the side branches on the wall shear stress (WSS) distribution in patient specific geometries is evaluated. Murray's law predicts that the flow ratio through the side branches scales with the ratio of the diameter of the side branches to the third power. The empirical model is based on flow measurements performed by Doriot et al. (2000) in angiographically normal coronary arteries. The fit based on these measurements showed that the flow ratio through the side branches can best be described with a power of 2.27. The experimental data imply that Murray's law underestimates the flow through the side branches. We applied the two models to study the WSS distribution in 6 coronary artery trees. Under steady flow conditions, the average WSS between the side branches differed significantly for the two models: the average WSS was 8% higher for Murray's law and the relative difference ranged from −5% to +27%. These differences scale with the difference in flow rate. Near the bifurcations, the differences in WSS were more pronounced: the size of the low WSS regions was significantly larger when applying the empirical model (13%), ranging from −12% to +68%. Predicting outflow based on Murray's law underestimates the flow through the side branches. Especially near side branches, the regions where atherosclerotic plaques preferentially develop, the differences are significant and application of Murray's law underestimates the size of the low WSS region.

Endurance training decreases resting and submaximal heart rate, while maximum heart rate may decrease slightly or remain unchanged after training. The effect of endurance training on various indices of heart rate variability remains inconclusive. This may be due to the use of inconsistent analysis methodologies and different training programmes that make it difficult to compare the results of various studies and thus reach a consensus on the specific training effects on heart rate variability. Heart rate recovery after exercise involves a coordinated interaction of parasympathetic re-activation and sympathetic withdrawal. It has been shown that a delayed heart rate recovery is a strong predictor of mortality. Conversely, endurance-trained athletes have an accelerated heart rate recovery after exercise. Since the autonomic nervous system is interlinked with many other physiological systems, the responsiveness of the autonomic nervous system in maintaining homeostasis may provide useful information about the functional adaptations of the body. This review investigates the potential of using heart rate recovery as a measure of training-induced disturbances in autonomic control, which may provide useful information for training prescription.

Populations with low vitamin D status, such as blacks living in the US or UK, have increased blood pressure (BP) compared with whites. We analyzed the association between serum 25-hydroxyvitamin D (25OHD) and BP to determine whether low 25OHD explains any of the increased BP in blacks. The Third US National Health and Nutrition Examination Survey (NHANES III) is a cross-sectional survey representative of the US civilian population during 1988 to 1994. Analyses were restricted to 12,644 people aged ≥20 years with measurements of BP and 25OHD, after excluding those on hypertensive medication. Adjusted mean serum 25OHD was lowest in non-Hispanic blacks (49 nmol/L), intermediate in Mexican Americans (68 nmol/L), and highest in non-Hispanic whites (79 nmol/L). When participants were divided into 25OHD quintiles, mean (standard error) systolic BP was 3.0 (0.7) mm Hg lower ( P = .0004) and diastolic BP was 1.6 (0.6) mm Hg lower ( P = .011) for participants in the highest quintile (25OHD ≥85.7 nmol/L) compared with the lowest (25OHD ≤40.4 nmol/L), adjusting for age, sex, ethnicity, and physical activity. Further adjustment for body mass index (BMI) weakened the inverse association between 25OHD and BP, which remained significant for systolic BP ( P < .05). The inverse association between 25OHD and systolic BP was stronger in participants aged ≥50 years than younger ( P = .021). Ethnic differences in 25OHD explained about half of the increased hypertension prevalence in non-Hispanic blacks compared with whites. Vitamin D status, which is amenable to intervention by safely increasing sun exposure or vitamin D supplementation, was associated inversely with BP in a large sample representative of the US population.

To investigate the effects of both non-Newtonian behavior and the pulsation of blood flow on the distributions of luminal surface LDL concentration and oxygen flux along the wall of the human aorta, we numerically compared a non-Newtonian model with the Newtonian one under both steady flow and in vivo pulsatile flow conditions using a human aorta model constructed from MRI images. The results showed that under steady flow conditions, although the shear thinning non-Newtonian nature of blood could elevate wall shear stress (WSS) in most regions of the aorta, especially areas with low WSS, it had little effect on luminal surface LDL concentration (cw) in most regions of the aorta. Nevertheless, it could significantly enhance cw in areas with high luminal surface LDL concentration through the shear dependent diffusivity of LDLs. For oxygen transport, the shear thinning non-Newtonian nature of blood could slightly reduce oxygen flux in most regions of the aorta, but this effect became much more apparent in areas with already low oxygen flux. The pulsation of blood flow could significantly reduce cw and enhance oxygen flux in these disturbed places. In most other regions of the aorta, the oxygen flux was also significantly higher than that for the steady flow simulation. In conclusion, the shear shining non-Newtonian nature of blood has little effect on LDL and oxygen transport in most regions of the aorta, but in the atherogenic-prone areas where luminal surface LDL concentration is high and oxygen flux is low, its effect is apparent. Similar is for the effect of pulsatile flow on the transport of LDLs. But, the pulsation of blood flow can apparently affect oxygen flux in the aorta, especially in areas with low oxygen flux.

The determination of arterial wave speed and the separation of the forward and backward waves have been established using simultaneous measurements of pressure ( P) and velocity ( U). In this work, we present a novel algorithm for the determination of local wave speed and the separation of waves using the simultaneous measurements of diameter ( D) and U. The theoretical basis of this work is the solution of the 1 D equations of flow in elastic tubes. A relationship between D and U is derived, from which, local wave speed can be determined; C=±0.5( dU ±/ d ln D ±). When only unidirectional waves are present, this relationship describes a linear relationship between ln D and U. Therefore, constructing a ln DU-loop should result in a straight line in the early part of the cycle when it is most probable that waves are running in the forward direction. Using this knowledge of wave speed, it is also possible to derive a set of equations to separate the forward and backward waves from the measured D and U waveforms. Once the forward and backward waveforms of D and U are established, we can calculate the energy carried by the forward and backward waves, in a similar way to that of wave intensity analysis. In this paper, we test the new algorithm in vitro and present results from data measured in the carotid artery of human and the ascending aorta of canine. We conclude that the new technique can be reproduced in vitro, and in different vessels of different species, in vivo. The new algorithm is easy to use to determine wave speed and separate D and U waveforms into their forward and backward directions. Using this technique has the merits of utilising noninvasive measurements, which would be useful in the clinical setting.

The branching angle and diameter ratio in epicardial coronary artery bifurcations are two important determinants of atherogenesis. Murray's cubed diameter law and bifurcation angle have been assumed to yield optimal flows through a bifurcation. In contrast, we have recently shown a 7/3 diameter law (HK diameter model), based on minimum energy hypothesis in an entire tree structure. Here, we derive a bifurcation angle rule corresponding to the HK diameter model and critically evaluate the streamline flow through HK and Murray-type bifurcations. The bifurcations from coronary casts were found to obey the HK diameter model and angle rule much more than Murray's model. A finite element model was used to investigate flow patterns for coronary artery bifurcations of various types. The inlet velocity and pressure boundary conditions were measured by ComboWire. Y-bifurcation of Murray type decreased wall shear stress-WSS (10%–40%) and created an increased oscillatory shear index-OSI in atherosclerosis-prone regions as compared with HK-type bifurcations. The HK-type bifurcations were found to have more optimal flow patterns (i.e., higher WSS and lower OSI) than Murray-type bifurcations which have been traditionally believed to be optimized. This study has implications for changes in bifurcation angles and diameters in percutaneous coronary intervention.

The citric acid cycle is central to the regulation of energy homeostasis and cell metabolism 1 . Mutations in enzymes that catalyse steps in the citric acid cycle result in human diseases with various clinical presentations 2 . The intermediates of the citric acid cycle are present at micromolar concentration in blood and are regulated by respiration, metabolism and renal reabsorption/extrusion. Here we show that GPR91 (ref. 3 ), a previously orphan G-protein-coupled receptor (GPCR), functions as a receptor for the citric acid cycle intermediate succinate. We also report that GPR99 (ref. 4 ), a close relative of GPR91, responds to α-ketoglutarate, another intermediate in the citric acid cycle. Thus by acting as ligands for GPCRs, succinate and α-ketoglutarate are found to have unexpected signalling functions beyond their traditional roles. Furthermore, we show that succinate increases blood pressure in animals. The succinate-induced hypertensive effect involves the renin–angiotensin system and is abolished in GPR91-deficient mice. Our results indicate a possible role for GPR91 in renovascular hypertension, a disease closely linked to atherosclerosis, diabetes and renal failure 5 , 6 .

Guidelines to prevent and treat hypertension advocate the Dietary Approaches to Stop Hypertension (DASH) diet. We studied whether a greater concordance with the DASH diet is associated with reduced incidence of hypertension (self-reported) and mortality from cardiovascular disease in 20,993 women initially aged 55 to 69 years. We created a DASH diet concordance score using food frequency data in 1986 and followed the women for events through 2002. No woman had perfect concordance with the DASH diet. Adjusted for age and energy intake, incidence of hypertension was inversely associated with the degree of concordance with the DASH diet, with hazard ratios across quintiles of 1.0, 0.91, 0.95, 0.99, and 0.87 ( P trend = .02). There also were inverse, but not monotonic, associations between better DASH diet concordance and mortality from coronary heart disease, stroke, and all cardiovascular disease (CVD). However, after adjustment for other risk factors, there was little evidence that any end point was associated with the DASH diet score. Our results suggest that greater concordance with DASH guidelines did not have an independent long-term association with hypertension or cardiovascular mortality in this cohort. This implies that very high concordance, as achieved in the DASH trials, may be necessary to achieve any benefits of the DASH diet.

Although obesity is known to increase the risk of hypertension, few studies have prospectively evaluated body mass index (BMI) across the range of normal weight and overweight as a primary risk factor. In this prospective cohort, we evaluated the association between BMI and risk of incident hypertension. We studied 13,563 initially healthy, nonhypertensive men who participated in the Physicians’ Health Study. We calculated BMI from self-reported weight and height and defined hypertension as self-reported systolic blood pressure (BP) ≥140 mm Hg, diastolic BP ≥90 mm Hg, or new antihypertensive medication use. After a median 14.5 years, 4920 participants developed hypertension. Higher baseline BMI, even within the “normal” range, was consistently associated with increased risk of hypertension. Compared to participants in the lowest BMI quintile (<22.4 kg/m 2), the relative risks (95% confidence interval) of developing hypertension for men with a BMI of 22.4 to 23.6, 23.7 to 24.7, 24.8 to 26.4, and >26.4 kg/m 2 were 1.20 (1.09–1.32), 1.31 (1.19–1.44), 1.56 (1.42–1.72), and 1.85 (1.69–2.03), respectively ( P for trend, <.0001). Further adjustment for diabetes, high cholesterol, and baseline BP did not substantially alter these results. We found similar associations using other BMI categories and after excluding men with smoking history, those who developed hypertension in the first 2 years, and those with diabetes, obesity, or high cholesterol at baseline. In this large cohort, we found a strong gradient between higher BMI and increased risk of hypertension, even among men within the “normal” and mildly “overweight” BMI range. Approaches to reduce the risk of developing hypertension may include prevention of overweight and obesity.