Background Previous research has suggested that patients with peripheral artery disease (PAD) are not offered adequate risk factor modification, despite their high cardiovascular risk. The aim of this study was to assess the cardiovascular profiles of patients with PAD and quantify the survival benefits of target‐based risk factor modification. Methods The Vascular and Endovascular Research Network (VERN) prospectively collected cardiovascular profiles of patients with PAD from ten UK vascular centres (April to June 2018) to assess practice against UK and European goal‐directed best medical therapy guidelines. Risk and benefits of risk factor control were estimated using the SMART‐REACH model, a validated cardiovascular prediction tool for patients with PAD. Results Some 440 patients (mean(s.d.) age 70(11) years, 24·8 per cent women) were included in the study. Mean(s.d.) cholesterol (4·3(1·2) mmol/l) and LDL‐cholesterol (2·7(1·1) mmol/l) levels were above recommended targets; 319 patients (72·5 per cent) were hypertensive and 343 (78·0 per cent) were active smokers. Only 11·1 per cent of patients were prescribed high‐dose statin therapy and 39·1 per cent an antithrombotic agent. The median calculated risk of a major cardiovascular event over 10 years was 53 (i.q.r. 44–62) per cent. Controlling all modifiable cardiovascular risk factors based on UK and European guidance targets (LDL‐cholesterol less than 2 mmol/l, systolic BP under 140 mmHg, smoking cessation, antiplatelet therapy) would lead to an absolute risk reduction of the median 10‐year cardiovascular risk by 29 (20–38) per cent with 6·3 (4·0–9·3) cardiovascular disease‐free years gained. Conclusion The medical management of patients with PAD in this secondary care cohort was suboptimal. Controlling modifiable risk factors to guideline‐based targets would confer significant patient benefit.

The algae Dunaliella bardawil and Dunaliella salina naturally contain large concentrations of all-trans and 9-cis beta-carotene (betaC). The purpose of this study was to compare the relative serum and tissue accumulation of all-trans and 9-cis betaC in ferrets fed different ratios of all-trans/9-cis betaC derived from two commercial sources, D. bardawil or D. salina (Betatene). Male ferrets (7 wk old) were fed carotene-free, pelleted diets for 27 d. Beginning on d 18, groups of ferrets (n = 6 or 7) received daily, one of six oral supplements varying in ratios of 9-cis and all-trans betaC mixed with approximately 1.0mL of Ensure. Four supplements containing 5.2-8.3 micromol total betaC were prepared from a 20% Betatene preparation, D. bardawil, a high-cis Betatene preparation, and Betatene further enriched in 9-cis betaC with all-trans betaC/9-cis betaC ratios of 2.2, 1.5, 0.6 and 0.4, respectively. Two control supplements, high and low betaC, were prepared from commercial betaC beadlets. The high control supplement had an all-trans/9-cis ratio of 19.0, whereas 9-cis betaC was not detected in the low supplement. On d 27, serum and tissues were obtained for HPLC analysis of betaC and its isomers. Analysis of livers showed that all-trans betaC was the primary isomer present, but 9-cis and other isomers were also detected in all groups. The hepatic all-trans/9-cis ratios were 5.9, 4.9, 2.5, 1.4, 52.2 and47.5, respectively, for the groups listed above. Lower amounts of all-trans and 9-cis betaC were found in kidneys compared with the liver, but ratios of all-trans/9-cis were not different among groups. Only trace amounts of 9-cis betaC were found in serum. These results demonstrate that the algae D. bardawil and D. salina provide a bioavailable source of betaC isomers, but, as in humans, absorption of 9-cis betaC is poor and any 9-cis betaC absorbed is apparently cleared by the liver.

Vitamin A (VA) deficiency remains a serious problem in the world today. Current approaches to preventing or treating VA deficiency, including dietary intervention with provitamin A compounds, rely on the body converting ingested beta-carotene (betaC) to VA. However, it is not known whether betaC that is already in the tissues can be used as a source of VA to prevent deficiency. The objectives of these studies were to determine whether tissue betaC stores are converted to VA when the Mongolian gerbils have low VA status and whether previously fed betaC is retained in the tissues for later conversion to VA. In the first study, gerbils were prefed diets with betaC (20.3 +/- 6.2 nmol/g diet) (+betaC) or without betaC (-betaC), and with VA [2.4 +/- 1.5 nmol/g diet (+betaC diet) or 12.0 +/- 4.2 nmol/g diet (-betaC diet)] for 7 d, and then depleted of both betaC and VA for up to 84 d. On d 0 after the prefeeding period, hepatic betaC stores were 13.3 +/- 9.1 nmol. These stores were significantly lower after 28d of consuming the -VA/-betaC diet (2.16 +/- 1.7 nmol), even though the hepatic VA concentrations did not change. In the second study, the gerbils were prefed a -VA/+betaC diet (74.3 +/- 19. 7 nmol betaC/g diet) for 7 d, and then fed a betaC-free diet either with (7.1 +/- 1.4 nmol/g) or without VA for up to 34 d. Hepatic betaC stores after the 7-d prefeeding period were 38.1 +/- 20.6 nmol, and were significantly higher than after 7d of consuming either a +VA/-betaC (12.4 +/- 10.8 mmol) or -VA/-betaC diet (11.4 +/- 8.0 nmol). The results from both studies suggest that a substantial amount of hepatic betaC is rapidly lost when betaC is eliminated from the diet and therefore is not conserved to meet later VA needs. The presence of VA in the diet (Study 2) did not affect the rate of betaC loss from the serum and tissues. Moreover, no evidence was found that the stored betaC was utilized for VA. The data suggest that there may be two pools of hepatic betaC, one that is lost rapidly and another that is lost more slowly over time, but losses are not affected by VA status.