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The need for the introduction of economical and quicker retrofitting techniques is increasing due to the ever-aging infrastructure and damages produced by major catastrophic events around the world. The application of Carbon Fiber Reinforced Polymers (CFRP) for strengthening and retrofitting of reinforced concrete structures is gaining popularity due to its higher strength, lightweight, durability, corrosion resistance, and aesthetic value. This study presents the results of two strengthened and two retrofitted beams in comparison to control specimens. Two specimens were strengthened and two were retrofitted by attaching CFRP (Sika Carbo-Dur S812 or Sika-Wrap 230C) to the tension side of the beams using high strength epoxy. The results show that one CFRP strip/wrap simply attached at the tension side can help the damaged beam regain/pass the original strength. All specimens fail due to debonding of CFRP from the concrete surface emphasizing the need for efficient anchorage systems. Among the four patterns adopted, CFRP strips along with u-shaped anchorages at the ends provided the highest strength enhancement of 17.36%.

This study is focused on influence of dielectric barrier discharge (DBD) plasma on surface functionality and coating properties of cotton fabric ultrasonically coated with zinc oxide nanoparticles. Zinc ions were reduced to zinc oxide with Aloe vera leaf extraction and simultaneously coated over plasma-functionalized fabric in an ultrasonic bath. The pad dry method was used for multiple coating cycles. The electron temperature in DBD zone was measured about 1.34 eV. The emission spectrum of DBD revealed the formation of OH−, N2, O, O3, NO, $${\text{N}}_{2}^{ + }$$ , $${\text{O}}_{2}^{ + }$$ and O+ radicals in the discharge zone. The coated fabric was tested for its resistance to the growth of E. coli bacteria, which determines its applications in medical products. The electrical conductivity of fabrics after 2, 4 and 6 pad dry cycles was 2.56 $$\times$$ 10–2, 2.61 $$\times$$ 10–2, and 2.69 $$\times$$ 10–2 Siemens/cm, respectively. The increased conductivity of fabric on coating suggests the growth of a UV protective layer of ZnO nanoparticles on the surface of the fabric. The transmittance of UV-A radiations from blank and ZnO-coated fabrics was measured about 18.42% and 0.89%, respectively. Similarly, UV-B transmittance from blank and ZnO-coated fabrics was measured about 8.41% and 0.29%, respectively. The low UV transmittance and high UV protection factor reveal high practical value of ZnO-coated fabrics.

Introduction Some studies report that assessing regional 123I-cardiac MIBG uptake can aid in the diagnosis of Lewy body disease, but others report heterogeneity in healthy controls. We aimed to evaluate regional cardiac MIBG uptake patterns in healthy older adults and patients with dementia. Methods 31 older adults with normal cognition, 15 Alzheimer’s disease (AD), and 17 Dementia with Lewy bodies (DLB) patients were recruited. 5 individuals had previous myocardial infarction. Participants with sufficient cardiac uptake for regional SPECT analysis (29/31 controls, 15/15 AD, 5/17 DLB) had relative uptake pattern recorded. Controls were assessed for risk of future cardiovascular events using QRISK2, a validated online tool. Results In controls uptake was reduced in the inferior wall (85%), apex (23%), septum (15%), and lateral wall (8%). AD and DLB showed similar patterns to controls. Lung or liver interference was present in 61% of cases. Myocardial infarction cases showed regional reductions in uptake, but normal/borderline planar uptake. In controls, there was no relationship between cardiovascular risk score and uptake pattern. Conclusions Significant variability of regional cardiac 123I-MIBG uptake is common in cases with normal planar cardiac uptake. Heterogeneity of regional uptake appears non-specific and unlikely to aid in the diagnosis of Lewy body disease.

Objectives The aim of the study was to evaluate the role of plasma Kaposi sarcoma herpesvirus (KSHV) as a diagnostic and prognostic biomarker in people living with HIV (PLWH) and diagnosed with KSHV-associated diseases. Methods Using quantitative nested polymerase chain reaction (PCR) targeting the open reading frame-26 gene of KSHV, plasma levels of KSHV were measured in consecutive PLWH with KSHV-associated diseases or as part of the investigation of lymphadenopathy. Results Plasma KSHV assays were performed on samples from 684 PLWH and 20 HIV-seronegative people with KSHV-associated malignancies. In PLWH, plasma KSHV was detected in 39% of those with KS, 99% of those with multicentric Castleman disease (MCD), 9% of those with non-Hodgkin lymphoma (NHL), 2% of those with non-AIDS-defining malignancies and 0% of those with nonmalignant lymphadenopathy. There was no significant difference in plasma KSHV viral load among those with KS, MCD and KSHV-associated NHL. The 5-year overall survival rate from KS diagnosis of 335 PLWH was 95.2% (95% confidence interval 92.6–97.8%). Plasma KSHV viraemia did not predict overall survival in those with KS (P = 0.73), nor when those with T0 stage KS (P = 0.52) or T1 stage KS (P = 0.62) were analysed separately. Conclusions Measuring the plasma levels of KSHV as a biomarker in KSHV-associated disease has a very limited value in either diagnosis or prognostication. The only potential role of clinical value is the suggestion that an undetectable plasma KSHV excludes a diagnosis of MCD in PLWH.

Dubas bug, Ommatissus lybicus, is a major pest of date palm in Panjgur Balochistan. Both the nymphs and adults suck the sap from fruit stalk, leaves and may cause about 50 % of economic losses. Chlorophyll contents and leaf thickness was measured by using SPAD-502 chlorophyll meter and vernier caliper respectively. Eggs distribution density was highly significant in different frond rows and within frond during spring (1st) and summer (2nd) generations. In both generations number of eggs per leaflet decreased towards the apex fronds rows and within frond number of eggs decreased towards the terminal leaflets. Eggs distribution had negative correlation with leaf thickness; chlorophyll contents (SPAD value) and frond row (bottom to top). Apparently shade affect the eggs laying behaviour of dubas bug.

The aim of the study was to evaluate the role of plasma Kaposi sarcoma herpesvirus (KSHV) as a diagnostic and prognostic biomarker in people living with HIV (PLWH) and diagnosed with KSHV-associated diseases.Using quantitative nested polymerase chain reaction (PCR) targeting the open reading frame-26 gene of KSHV, plasma levels of KSHV were measured in consecutive PLWH with KSHV-associated diseases or as part of the investigation of lymphadenopathy.Plasma KSHV assays were performed on samples from 684 PLWH and 20 HIV-seronegative people with KSHV-associated malignancies. In PLWH, plasma KSHV was detected in 39% of those with KS, 99% of those with multicentric Castleman disease (MCD), 9% of those with non-Hodgkin lymphoma (NHL), 2% of those with non-AIDS-defining malignancies and 0% of those with nonmalignant lymphadenopathy. There was no significant difference in plasma KSHV viral load among those with KS, MCD and KSHV-associated NHL. The 5-year overall survival rate from KS diagnosis of 335 PLWH was 95.2% (95% confidence interval 92.6-97.8%). Plasma KSHV viraemia did not predict overall survival in those with KS (P = 0.73), nor when those with T0 stage KS (P = 0.52) or T1 stage KS (P = 0.62) were analysed separately.Measuring the plasma levels of KSHV as a biomarker in KSHV-associated disease has a very limited value in either diagnosis or prognostication. The only potential role of clinical value is the suggestion that an undetectable plasma KSHV excludes a diagnosis of MCD in PLWH.

OBJECTIVE—To determine the proportion of the population, firstly, with cholesterol ⩾ 5.0 mmol/l and, secondly, with any cholesterol concentration, who might benefit from statin treatment for the following: secondary prevention of coronary heart disease (CHD); primary prevention at CHD risk 30%, 20%, 15%, and 6% over 10 years; and primary prevention at projected CHD risk 20% over 10 years (CHD risk at age 60 years if actual age

Objective To examine the relationship between coronary (CHD) and cardiovascular (CVD) risk in patients with uncomplicated mild hypertension and to determine the accuracy of using CHD risk > or = 15% over 10 years to identify for antihypertensive treatment those patients with CVD risk > or = 20% over 10 years as advised in recent British guidelines. Design Comparison of decisions made using CHD risk > or = 15% over 10 years calculated by the Framingham risk function and estimated using a simple table with CVD risk > or = 20% over 10 years. Setting British population. Subjects People aged 35-64 years with uncomplicated mild systolic hypertension (SBP 140-159 mmHg, n = 624) from the 1995 Scottish Health Survey. Main outcome measures Relationship between CHD and CVD risk. Sensitivity, specificity, positive and negative predictive values (PPV and NPV). Results CHD risk 15% over 10 years was equivalent to CVD risk 21% over 10 years. Exact CHD risk > or = 15% over 10 years had sensitivity 79%, specificity 98%, PPV 94% and NPV 93% in detecting CVD risk > or = 20% over 10 years. Use of the table to estimate CHD risk > or = 15% over 10 years gave sensitivity 88%, specificity 90%, PPV 76% and NPV 95%. Conclusion CHD risk appears acceptably accurate for targeting treatment in mild hypertension. The risk assessment table, which slightly overestimates CHD risk, was more sensitive in identifying patients with CVD risk > or = 20% over 10 years and may be preferable to using exact CHD risk. European guidelines which suggest targeting treatment for mild hypertension at CHD risk > or = 20% over 10 years are over-conservative compared with British guidelines.

To examine the accuracy of a new version of the Sheffield table designed to aid decisions on lipids screening and detect thresholds for risk of coronary heart disease needed to implement current guidelines for primary prevention of cardiovascular disease.Comparison of decisions made on the basis of the table with absolute risk of coronary heart disease or cardiovascular disease calculated by the Framingham risk function. The decisions related to statin treatment when coronary risk is/=30% over 10 years; aspirin treatment when the risk is/=15% over 10 years; and the treatment of mild hypertension when the cardiovascular risk is/=20% over 10 years.The table is designed for use in general practice.Random sample of 1000 people aged 35-64 years from the 1995 Scottish health survey.Sensitivity, specificity, and positive and negative predictive values of the table.13% of people had a coronary risk of/=15%, and 2. 2% a risk of/=30%, over 10 years. 22% had mild hypertension (systolic blood pressure 140-159 mm Hg). The table indicated lipids screening for everyone with a coronary risk of/=15% over 10 years, for 95% of people with a ratio of total cholesterol to high density lipoprotein cholesterol of/=8.0, but for50% with a coronary risk of5% over 10 years. Sensitivity and specificity were 97% and 95% respectively for a coronary risk of/=15% over 10 years; 82% and 99% for a coronary risk of/=30% over 10 years; and 88% and 90% for a cardiovascular risk of/=20% over 10 years in mild hypertension.The table identifies all high risk people for lipids screening, reduces screening of low risk people by more than half, and ensures that treatments are prescribed appropriately to those at high risk, while avoiding inappropriate treatment of people at low risk.

Dietary advice for the reduction of coronary heart disease events emphasizes the importance of a low-fat diet and advice on the consumption of oily fish may also be given. This report reviews the evidence linking fish consumption with coronary risk. On the basis of available evidence, a target of two to three portions of oily fish per week (200–400 g, 7–14 oz) is considered reasonable, particularly for secondary prevention. For those who cannot achieve the suggested dietary intake of oily fish, the partial or complete substitution of fish oil supplements may be appropriate. A range of suitable types of fish oil supplements is given, but an awareness of the potential adverse effects of fish oil supplementation is considered important. Further studies are needed to define the role of fish intake in coronary heart disease.

After myocardial infarction, beta-blockers, aspirin and (in selected patients) ACE inhibitors all reduce substantially the risk of further myocardial infarction or coronary death. With regard to life-style changes, giving up cigarette smoking reduces coronary risk by about 50%. Weight reduction and regular exercise are advised, although the effect of these measures on prognosis is uncertain. Recently, two major trials, the Scandinavian Simvastatin and West of Scotland Pravastatin studies, have radically changed ordinary medical practice. In these trials HMG CoA reductase inhibitor (statin) treatment reduced coronary events by 30–40%, reduced all-cause mortality, and proved safe and well-tolerated. The accepted policy now is to treat all patients with coronary heart disease, who have a cholesterol concentration 5.5 mmol/l or higher, with a statin. Where does this leave cholesterol-lowering dietary advice in secondary prevention? The benefits of statin treatment were attained by reducing serum cholesterol by an average of 25%. Diet change rarely attains such a fall in cholesterol and should therefore be used only as an adjunct to drug therapy. When recommending a lipid-lowering diet there is a danger that patients may be denied highly-effective drug treatment because of the «threshold» effect. A decision on the need for cholesterol reduction should be made before diet change is advised. Once the decision is made the target is a 25% cholesterol reduction, which will require drug therapy in addition to diet changes.

Summary When used for the secondary prevention of coronary heart disease, treatment with an inhibitor of hydroxymethylglutaryl-coenzyme-A reductase results in worthwhile benefit that clearly exceeds any risk in patients whose risk of coronary death is 1·5% or more per year. This evidence can be extrapolated logically to primary prevention of coronary disease provided that treatment is targeted at those with similar or higher risk. We present a table that refines previously proposed methods of risk prediction. The table identifies subjects who have the specified degree of coronary risk; shows the serum cholesterol concentration that confers that degree of risk in the individual; and identifies subjects who will not have this degree of risk, irrespective of their cholesterol concentration. It is simple enough for use in ordinary practice. The table highlights the predominant effect of age on coronary risk; a person who is free of vascular disease and younger than 52 years is unlikely to have the specified degree of risk. Even in older people (60-70 years) several risk factors are generally required to attain this degree of risk. Some people are candidates for lipid-lowering drug treatment with serum cholesterol as low as 5·5 mmol/L, whereas others with cholesterol as high as 9·0 mmol/L are not. Although cholesterol lowering is a powerful method for preventing coronary events in people at high risk, cholesterol measurement by itself is not a good way to identify those with high coronary risk. The method can be adapted readily to target a different level of coronary risk as new evidence on the benefit and risk of treatment becomes available.

1. The 4-hydroxylation of propranolol by rat and human liver microsomes is associated with formation of a chemically reactive species which binds irreversibly to cytochrome P4502D6 (CYP2D6) destroying its catalytic function. Therefore, the effect of propranolol treatment (80 mg twice daily) on debrisoquine phenotype was examined, to see if it resulted in phenocopying in vivo. The role of 4-hydroxypropranolol (4OHP) in the inhibition of CYP2D6 activity was also studied using microsomes from yeast expressing CYP2D6 and from human livers; metoprolol was used as the CYP2D6 substrate. 2. Although a significant effect on apparent oxidation phenotype was demonstrated, the absolute change in the urinary debrisoquine/4-hydroxydebrisoquine ratio (D/4HD) was small, such that no extensive metaboliser who received propranolol treatment was reclassified as a poor metaboliser. The in vitro studies indicated that 4OHP is a potent inhibitor of metoprolol metabolism (Ki approximately 1 microM). This inhibitory effect was enhanced when 4OHP was pre-incubated in the presence of a NADPH generating system and human liver microsomes. The effect was decreased significantly when reduced glutathione was added to the pre-incubation mixture. Metabolism of 4OHP occurred when incubated with human liver microsomes in the presence of a NADPH generating system and irrespective of CYP2D6 phenotype; yeast expressing CYP2D6 did not metabolise 4OHP. 3. We conclude that, although treatment with propranolol 80 mg twice daily significantly decreases the catalytic function of CYP2D6, the inhibition is insufficient to result in phenocopying. The reactive intermediate produced by further metabolism of 4OHP is probably scavenged effectively in vivo by glutathione and other nucleophiles.

The aim of this study was to evaluate the effects of unilateral and bilateral ventralis intermedius (Vim) deep brain stimulation (DBS) on mood and motor function.Thirty-one consecutive medication refractory patients with essential tremor who underwent unilateral or bilateral Vim DBS at University of Florida and returned for at least 6 -month follow-up completed the Visual Analog Mood (VAMS), the Beck Depression Inventory (BDI), and the Tremor Rating Scale (TRS) before and after surgery. We excluded all patients who were implanted at other institutions.The tense subscale of the VAMS improved significantly in both the unilateral and bilateral DBS groups (P0.001). On the VAMS afraid subscale, only the bilateral group trended toward improvement (P = 0.075). There were no significant changes for either group for the happy, confused, sad, angry, energetic or tired VAMS scores. TRS subscale scores all improved after unilateral and bilateral Vim DBS surgery (P0.001).Feelings of tenseness, tremor severity and ADLs improved following unilateral or bilateral Vim DBS for ET.

Increasingly HMG CoA reductase inhibitors (statins) are being used for primary prevention of vascular disease in patients with a raised cholesterol but at low absolute risk of coronary heart disease (CHD). This study uses clinical trial results to explore the limits of absolute safety for statin use in such patients.The major placebo controlled statin outcome trials were identified by automated and manual literature searches. Principal results including all cause mortality in placebo and intervention groups and baseline values of standard coronary risk factors were abstracted for each trial. For the trials identified the reduction in overall mortality with statin treatment for each study was regressed against the underlying CHD risk of the population recruited into that trial using a statistically robust method.The regression line describing the relationship between mortality benefit and risk suggests that statin use could be associated with an increase in mortality of 1% in 10 years. This would be sufficiently large to negate statin's beneficial effect on CHD mortality in patients with a CHD event risk less than 13% over 10 years.Absolute safety of statins has not been demonstrated for patients at low risk of CHD. Patients absolute risk of CHD should be calculated before starting statin treatment for primary prevention. Extensions of such treatment to low risk patients should await further evidence of safety.

We report an intramedullary primary solitary fibrous tumour of the cervical spinal cord in a 33-year-old man. The tumour predominantly consisted of monomorphic spindle cells with a storiform pattern. MRI demonstrated an inhomogeneously enhancing cervical intramedullary tumour. The patient was well without recurrence 18 months after surgery.

Most recent guidelines advise targeting of lipid lowering for primary prevention at those at high absolute coronary (CHD) risk. We compared the accuracy of five CHD risk assessment methods in identifying such patients: one based on total cholesterolor = 6.5 mmol/l plus two risk factors, and four based on the Framingham risk function (the European Task Force chart and Sheffield table, both using total cholesterol and the New Zealand chart and modified Sheffield table, both using total: HDL cholesterol ratio) for predicting CHD event riskor = 2% per year, calculated by an independent risk function, PROCAM, in 126 treated hypertensive men. Cholesterol threshold plus two risk factors had sensitivity 59% and specificity 63%, did not identify some very high-risk patients, and identified very low-risk patients. Framingham-based methods using total cholesterol alone had sensitivity 90-98% and specificity 37-43%, and identified high-risk patients well, but identified some patients at very low risk. Methods based on total: HDL cholesterol ratio had sensitivity 90-98% and specificity 60-63%, and did not identify incorrectly patients at very low CHD risk. Methods based on cholesterol threshold and counting of risk factors are too inaccurate for targeting drug therapy for primary prevention of CHD. Framingham-based methods should incorporate HDL-cholesterol as the total: HDL cholesterol ratio.

Background There is broad agreement that statin treatment should be targeted at absolute coronary heart disease (CHD) risk but no consensus on the level of risk to target. We have examined the implications of adopting three different treatment policies for the management of hypertensive patients in the UK using data from treated hypertensives aged 35-69 years included in the Health Survey for England (1993). Methods We calculated the proportion of hypertensive patients with existing atherosclerotic cardiovascular disease requiring statin treatment for secondary prevention of CHD. For those without atherosclerotic cardiovascular disease (primary prevention), we estimated CHD risk from the Framingham equation and examined the proportion with CHD risk exceeding thresholds of 4.5, 3 and 1.5% per year. Results Twenty-one percent of treated hypertensives would require statin treatment for secondary prevention of CHD. When the CHD event threshold for statin treatment was set at > or =4.5% per year [equivalent to a number needed to treat (NNT) in 5 years of 13] a further 0.6% of hypertensive patients were identified for treatment; at a threshold of 3.0% per year (NNT = 20) 5.5% of patients were identified for primary prevention; and at a threshold of 1.5% per year (NNT = 40) 28.5% of patients were identified for primary prevention. Conclusions Those needing secondary prevention are first priority for statins and 21% of hypertensive patients will require treatment Formulation of guidelines for primary prevention should take into account the NNT; the proportion of patients targeted for treatment; the cost-effectiveness and the total cost of treatment. Current British guidance will entail treating an additional 5.5% of hypertensive patients for primary prevention and therefore 27% of hypertensive patients.

OBJECTIVES—To estimate the cost effectiveness of statin treatment in preventing coronary heart disease (CHD) and to examine the effect of the CHD risk level targeted and the cost of statins on the cost effectiveness of treatment. DESIGN—Cohort life table method using data from outcome trials. MAIN OUTCOME MEASURES—The cost per life year gained for lifelong statin treatment at annual CHD event risks of 4.5% (secondary prevention) and 3.0%, 2.0%, and 1.5% (all primary prevention), with the cost of statins varied from £100 to £800 per year. RESULTS—The costs per life year gained according to annual CHD event risk were: for 4.5%, £5100; 3.0%, £8200; 2.0%, £10 700; and 1.5%, £12 500. Reducing the cost of statins increases cost effectiveness, and narrows the difference in cost effectiveness across the range of CHD event risks. CONCLUSIONS—At current prices statin treatment for secondary prevention, and for primary prevention at a CHD event risk 3.0% per year, is as cost effective as many treatments in wide use. Primary prevention at lower CHD event risks (

Weight reduction, moderate salt restriction and alcohol reduction are effective in lowering blood pressure (BP), and are feasible interventions for long-term management of hypertension. When used in combination these non-pharmacological measures are significantly inferior to drug therapy in anti-hypertensive effect. When they are implemented as a first step in the treatment of mild hypertension, resorting to drug therapy only if non-pharmacological measures fail, anti-hypertensive drugs can be avoided in about 40% of patients. However, BP control is again significantly inferior with this strategy compared with drug therapy without non-pharmacological advice. Those given advice on non-pharmacological measures may therefore have suboptimal protection against cardiovascular complications. This is particularly so when the threshold for drug treatment is set at a DBP ofor = 100 mmHg, as many patients will be left untreated with DBPs between 90 and 99 mm Hg as a result of non-pharmacological measures. Non-pharmacological treatment may thus stand between patients and anti-hypertensive drug therapy, which nowadays is simple, well-tolerated, safe and proven effective in preventing cardiovascular disease. The role of non-pharmacological therapy needs to be reconsidered.

Guidelines for the management of hypertension, and those for hyperlipidaemia, advocate measurement of cholesterol in all hypertensive subjects. It is suggested that knowledge of serum cholesterol should influence the choice of anti-hypertensive agent because thiazides and beta-blockers may influence lipids adversely. However, the changes in lipids associated with low-dose thiazides and beta-blockers are small, not sustained and do not appear to affect prognosis adversely. Some believe that knowledge of serum cholesterol may help target the treatment of mild hypertension more accurately by predicting an increased risk of vascular complications of hypertension. However, serum cholesterol does not predict the risk of cardiovascular complications in hypertensive women. It does predict coronary heart disease (but not stroke) in men, but coronary risk can be estimated satisfactorily without knowledge of serum cholesterol. Suggestions that cholesterol should be lowered in hypercholesterolaemic hypertensive patients to reduce the incidence of coronary heart disease are understandable. However, the diet recommended for this has no useful effect on serum cholesterol, and the benefit of lipid-lowering drugs for cholesterol reduction only exceeds the risk in patients at very high risk of coronary mortality, for example those who have had a myocardial infarction. Hypertension alone will not place individuals at high enough risk to warrant drug therapy for cholesterol reduction. We conclude that the current guidelines are incorrect, and that routine measurement of cholesterol in all hypertensive patients is not justified.

Background The NICE guideline for chest pain of recent onset recommends diagnosis of angina based on clinical assessment and estimated likelihood of coronary artery disease (CAD). Pre-test likelihood (PTL) estimates are provided in a simplified table based on the Pryor risk equation. If the PTL of CAD is 90%, further diagnostic testing is not required. If 10%–29% cardiac CT should be offered, if 30%–60% functional imaging, and if 61%–90% coronary angiography. We compared risk estimation methods to determine how much use of the table in an uncritical manner vs use of the full risk equation led to a different referral pattern. We also investigated whether interpolation for risk factor profiles would improve assessment. Methods Data were collected prospectively for all patients referred to the Rapid Access Chest Pain Clinic, Newcastle upon Tyne, between February 2002 and August 2011. For each patient, PTL of CAD was assessed by three methods: (1) Reference to the NICE table based on chest pain (typical or atypical), age in deciles, sex and risk factors—smoking, hyperlipidaemia and diabetes dichotomised into high and low risk. For high risk, all three risk factors needed to be present; otherwise the patient was assumed low risk. (2) As per method one, but risk estimates were interpolated between low and high risk values in the NICE table according to the number of risk factors. (3) Calculation by the Pryor equation which includes, in addition, age in years, prior MI, ECG Q waves, and ST/T changes. Results Out of an initial 7022 patients, 1820 were excluded as they had non-anginal chest pain. This left 5202 patients, 2889 with atypical angina and 2313 with typical angina. The number (%) of patients in the five different risk groups by the three risk assessment methods is given in Abstract 140 table 1. Use of the risk equation compared to the table led to half as many people in the category 90% (Abstract 140 figure 1). The corresponding figures correctly classifying people in the five risk categories using the adapted table were 92.9%, 86.4%, 65.2%, 71.2% and 85.9% respectively (Abstract 140 figure 2). Conclusion Use of the NICE table uncritically for assessing PTL of CAD misclassifies a significant proportion of people for further investigation. It is important to include ECG data, interpolate risk factor information, and take into account actual age when using the table rather than the Pryor equation, use of which takes these factors into account automatically.

Background The NICE clinical guideline for chest pain of recent onset (NCG 95) published in March 2010 recommends diagnosing angina based on clinical assessment and likelihood of coronary artery disease (CAD). If the estimated likelihood of CAD is 61%–90%, coronary angiography should be offered. If 30%–60%, functional imaging should be offered, and if 10%–29%, CT calcium scoring should be offered. We determined the number and types of different investigations to diagnose coronary artery disease in patients referred with suspected cardiac pain before the publication of NCG 95 and compared this with the predicted investigations after the application of the guidelines. Methods Data was collected prospectively in a bespoke database for patients referred to the Rapid Access Chest Pain Clinic, Newcastle upon Tyne, UK. Patients with chest pain of suspected cardiac origin were referred from primary care between February 2002 and March 2010. Patients with previous MI, PCI or CABG were excluded. The analysis comprised 5598 men and women with no past history of coronary disease. Likelihood of CAD was calculated by the Pryor equation using the variables age, sex, type of chest pain (typical or atypical), ECG Q waves, smoking, hyperlipidaemia, diabetes and ST/T changes on ECG. The main outcome measures were actual and predicted future frequency of exercise tests, CT coronary angiograms, functional imaging tests and invasive coronary angiograms by pretest likelihood of coronary artery disease. Results The proportion of the study population before and after the guidelines undergoing exercise testing was 50.1% vs 0.0%; for calcium score/CT coronary angiography 0.0% vs 14.7%; for functional imaging 25.6% vs 13.4%; and for invasive coronary angiography 15.3% vs 25.8%. The proportion not requiring further testing was unchanged (30.0% vs 31.0%). Conclusions Application of NICE CG95 will change the investigation of patients with chest pain substantially. A significant reallocation of resources will be required. Exercise testing will be replaced by anatomic or functional imaging. CT coronary angiography will play an important role and replace functional imaging in some patients. Invasive angiography will take on a more important role in the diagnosis of coronary artery disease. It will, however, empower us to reassure almost a third of referrals that they do not have angina on clinical assessment alone.

Editor—Unwin et al highlight the fact that several widely available guidelines for the management of hyperlipidaemia give conflicting advice for the primary prevention of cardiovascular disease.1 Some of the issues deserve further scrutiny. The New Zealand guidelines are based entirely on the ratio of total to high density lipoprotein cholesterol concentrations for calculation of the absolute risk of cardiovascular disease over five years.2 The American national cholesterol education program, however, clearly says that it does not recommend use of the ratio of either total or low density lipoprotein cholesterol to high density lipoprotein cholesterol3; instead it recommends use of the absolute high and low density lipoprotein cholesterol concentrations. The rationale behind this is that these concentrations are independent risk factors with different determinants; combining them into a single number conceals information about either or both, which might be important for making clinical decisions. A patient with raised total, high density lipoprotein, and low density lipoprotein cholesterol concentrations (a common clinical problem) falls into either the low risk category or the high risk category depending on whether the ratio or absolute values are used. The New Zealand guidelines,2 guidelines of the European Atherosclerosis Association,4 and Sheffield tables5 are based largely on age and sex, unlike the guidelines of the American programme,3 which are not; the American guidelines mention, however, that the risk is higher in men than in women. Use of these guidelines would therefore be associated with the highest number of patients requiring antilipid treatment. Only the American guidelines give clear guidance on when measurement of high density lipoprotein cholesterol is indicated in patients with hyperlipidaemia. Measurement of this concentration is labour intensive and expensive and therefore has major implications for laboratories. The New Zealand guidelines necessitate measurement of high density lipoprotein cholesterol in all patients, which would increase the cost substantially. Financial implications may be an important factor for NHS trusts deciding on their policy for managing hyperlipidaemia. Patients are often bewildered when different doctors give them conflicting advice about antilipid treatment. Just as too much of anything is undesirable, too many guidelines end up confusing both patients and doctors.

EDITOR—Two letters last December on the use of statins, by Betteridge et al (p 1619) and Reynolds et al (p 1620), criticised the Sheffield table.1 The rate of coronary heart disease events targeted (3% per year) is not “arbitrarily high,” as Reynolds et al say, but was proposed after consideration of the number needed to treat, cost effectiveness, proportion of adults needing treatment, and total cost of treatment at different thresholds of risk of coronary heart disease.2 The European task force's guidelines3 which suggested the 2% per year threshold for coronary heart disease preferred by the letters' authors predated the statin trials. We do not accept that high risk people over age 65 should be denied treatment,1 and treating those below age 65 with a relative risk of coronary heart disease of 41 seems unwise. A 35 year old woman with a total cholesterol concentration of 7.0 mmol/l, systolic blood pressure of 160 mm Hg, and no other risk factors has a relative risk …

Extension literature on upgrading straws in the tropics (e.g. Schiere and Ibrahim, 1989) advocates applying 1 kg of 40 g/kg urea solution per kg air dry straw and storing under plastic for 4 weeks. Surprisingly, there is little published information on responses to urea solution concentration and amounts to be applied in order to improve digestibility of organic matter (OMD) and maintain alkaline pH to enable preservation of treated straw. The present experiment aimed at providing such information as part of a study to assess the potential of animal or human urines for upgrading straw and bearing in mind that urines contain a range of urea concentrations.

SIR—We regret that there was an important error in the Sheffield table (Aug 10, p 387), and a corrected version is presented on p 1252. The error in the original was in the table for men only, and arose because the column headings indicating different combinations of risk factors were accidentally transposed as the final table was prepared. Thus the numbers in the table are correct, but do not always correspond to the risk factor combinations shown above them. We are aware that some colleagues have used the table to evaluate individuals, and will want to know what the practical consequences may be. The inaccurate table still predicts, on average, a coronary heart disease (CHD) event rate of 3·0% per year. For eight of the twelve columns in the table for men the risk targeted was acceptably accurate, ranging from 2·8 to 3·2% CHD events per year. Two of the columns would target treatment at men with a lower CHD risk—1·9% and 2·3% per year, respectively. Statin treatment is readily justifiable at this level of risk and this inaccuracy should therefore cause no harm. However, in two columns men were signalled as not needing treatment when their risk of CHD was in fact substantially higher than 3·0% per year—at 3·8% and 4·2% per year. These men should be reassessed by the corrected Sheffield table reproduced overleaf. They can in fact be identified readily, because they are all men with hypertension and left ventricular hypertrophy (LVH) shown by electrocardiography. We therefore suggest that any man with hypertension plus LVH who was assessed by the Sheffield table and not treated should be reassessed with the corrected table. We apologise to colleagues for any inconvenience caused by our error.

EDITOR,--The OXCHECK study showed significant reductions in total cholesterol concentration (3.1%) and blood pressure (2.5/1.5 mm Hg) with health checks over three years.1 The reductions in cholesterol concentration are in line with responses shown in previous controlled trials.2 The authors seem in some doubt about whether these effects are large enough to justify the cost of the health checks. This may be clearer when the projected …