Publications
529 results found
Santos RD, Gidding SS, Hegele RA, et al., 2016, Defining severe familial hypercholesterolaemia and the implications for clinical management: a consensus statement from the International Atherosclerosis Society Severe Familial Hypercholesterolemia Panel, The Lancet Diabetes & Endocrinology, Vol: 4, Pages: 850-861, ISSN: 2213-8587
Familial hypercholesterolaemia is common in individuals who had a myocardial infarction at a young age. As many as one in 200 people could have heterozygous familial hypercholesterolaemia, and up to one in 300 000 individuals could be homozygous. The phenotypes of heterozygous and homozygous familial hypercholesterolaemia overlap considerably; the response to treatment is also heterogeneous. In this Review, we aim to define a phenotype for severe familial hypercholesterolaemia and identify people at highest risk for cardiovascular disease, based on the concentration of LDL cholesterol in blood and individuals' responsiveness to conventional lipid-lowering treatment. We assess the importance of molecular characterisation and define the role of other cardiovascular risk factors and advanced subclinical coronary atherosclerosis in risk stratification. Individuals with severe familial hypercholesterolaemia might benefit in particular from early and more aggressive cholesterol-lowering treatment (eg, with PCSK9 inhibitors). In addition to better tailored therapy, more precise characterisation of individuals with severe familial hypercholesterolaemia could improve resource use.
Brownrigg JRW, Hughes CO, Burleigh D, et al., 2016, Microvascular disease and risk of cardiovascular events among individuals with type 2 diabetes: a population-level cohort study, The Lancet Diabetes & Endocrinology, Vol: 4, Pages: 588-597, ISSN: 2213-8587
BackgroundDiabetes confers a two times excess risk of cardiovascular disease, yet predicting individual risk remains challenging. The effect of total microvascular disease burden on cardiovascular disease risk among individuals with diabetes is unknown.MethodsA population-based cohort of patients with type 2 diabetes from the UK Clinical Practice Research Datalink was studied (n=49 027). We used multivariable Cox models to estimate hazard ratios (HRs) for the primary outcome (the time to first major cardiovascular event, which was a composite of cardiovascular death, non-fatal myocardial infarction, or non-fatal ischaemic stroke) associated with cumulative burden of retinopathy, nephropathy, and peripheral neuropathy among individuals with no history of cardiovascular disease at baseline.FindingsDuring a median follow-up of 5·5 years, 2822 (5·8%) individuals experienced a primary outcome. After adjustment for established risk factors, significant associations were observed for the primary outcome individually for retinopathy (HR 1·39, 95% CI 1·09–1·76), peripheral neuropathy (1·40, 1·19–1·66), and nephropathy (1·35, 1·15–1·58). For individuals with one, two, or three microvascular disease states versus none, the multivariable-adjusted HRs for the primary outcome were 1·32 (95% CI 1·16–1·50), 1·62 (1·42–1·85), and 1·99 (1·70–2·34), respectively. For the primary outcome, measures of risk discrimination showed significant improvement when microvascular disease burden was added to models. In the overall cohort, the net reclassification index for USA and UK guideline risk strata were 0·036 (95% CI 0·017–0·055, p<0·0001) and 0·038 (0·013–0·060, p<0·0001), respectively.InterpretationThe cumulative burden of microvascular diseas
Robinson JG, Ray K, 2016, Moving toward the next paradigm for cardiovascular prevention, Circulation, Vol: 133, Pages: 1533-1536, ISSN: 0009-7322
Ray KK, Hovingh GK, 2016, Familial hypercholesterolaemia: a common disease., European Heart Journal, Vol: 37, Pages: 1395-1397, ISSN: 1522-9645
This editorial refers to ‘Mutations causative of familialhypercholesterolaemia: screening of 98 098 individualsfrom the Copenhagen General Population Study estimateda prevalence of 1 in 217’, by M. Benn et al. doi:10.1093/eurheartj/ehw028
Robinson JG, Ray K, 2016, Counterpoint: Low-Density Lipoprotein Cholesterol Targets Are Not Needed in Lipid Treatment Guidelines, Arteriosclerosis, Thrombosis, and Vascular Biology, Vol: 36, Pages: 586-590, ISSN: 1079-5642
On the basis of accumulating evidence, low-density lipoprotein cholesterol (LDL-C) treat-to-goal approaches no longer seem to be the best way to optimize lipid-modifying therapy to prevent atherosclerotic cardiovascular disease (ASCVD). The potential for a net ASCVD risk reduction benefit is a more individualized approach to clinical decision making and may better inform patient preferences. However, risk estimation tools will need to be developed to facilitate more personalized CVD risk estimation in statin-treated patients. In the meantime, LDL-C thresholds rather than targets may aid in determining which patients might benefit from additional LDL-C–lowering therapy beyond statins.
Sahebkar A, Serban C, Ursoniu S, et al., 2016, The impact of statin therapy on plasma levels of von Willebrand factor antigen Systematic review and meta-analysis of randomised placebo-controlled trials, THROMBOSIS AND HAEMOSTASIS, Vol: 115, Pages: 520-532, ISSN: 0340-6245
Serban M-C, Sahebkar A, Mikhailidis DP, et al., 2016, Impact of L-carnitine on plasma lipoprotein(a) concentrations: A systematic review and meta-analysis of randomized controlled trials, Scientific Reports, Vol: 6, ISSN: 2045-2322
We aimed to assess the impact of L-carnitine on plasma Lp(a) concentrations through systematic review and meta-analysis of available RCTs. The literature search included selected databases up to 31st January 2015. Meta-analysis was performed using fixed-effects or random-effect model according to I2 statistic. Effect sizes were expressed as weighted mean difference (WMD) and 95% confidence interval (CI). The meta-analysis showed a significant reduction of Lp(a) levels following L-carnitine supplementation (WMD: −8.82 mg/dL, 95% CI: −10.09, −7.55, p < 0.001). When the studies were categorized according to the route of administration, a significant reduction in plasma Lp(a) concentration was observed with oral (WMD: −9.00 mg/dL, 95% CI: −10.29, −7.72, p < 0.001) but not intravenous L-carnitine (WMD: −2.91 mg/dL, 95% CI: −10.22, 4.41, p = 0.436). The results of the meta-regression analysis showed that the pooled estimate is independent of L-carnitine dose (slope: −0.30; 95% CI: −4.19, 3.59; p = 0.878) and duration of therapy (slope: 0.18; 95% CI: −0.22, 0.59; p = 0.374). In conclusion, the meta-analysis suggests a significant Lp(a) lowering by oral L-carnitine supplementation. Taking into account the limited number of available Lp(a)-targeted drugs, L-carnitine might be an effective alternative to effectively reduce Lp(a). Prospective outcome trials will be required to fully elucidate the clinical value and safety of oral L-carnitine supplementation.
Vallejo-Vaz AJ, Ray KK, 2016, Promoting high-density lipoprotein function via intravenous infusion: the rebirth of apoA-I Milano?, European Heart Journal- Cardiovascular Pharmacotherapy, Vol: 2, Pages: 30-31, ISSN: 2055-6845
Abbas AS, Dehbi H-M, Ray KK, 2015, Cardiovascular and non-cardiovascular safety of dipeptidyl peptidase-4 inhibition: a meta-analysis of randomized controlled cardiovascular outcome trials, Diabetes Obesity & Metabolism, Vol: 18, Pages: 295-299, ISSN: 1463-1326
The full licensing of dipeptidyl peptidase-4 (DPP-4) inhibitors in the USA and Europe requires demonstration of cardiovascular (CV) safety with an upper boundary of harm of <30%. We report a total of 3334 CV events during 86 716 person-years of follow-up in 36 543 patients, when combining data from three trials with formal and prospectively assessed endpoints. Fixed-effect meta-analysis showed that, compared with placebo, DPP-4 inhibition did not increase the upper boundary of risk for the composite endpoint, nor for any individual component by >30%. Relative risks (RRs) were: 0.99 [confidence interval (CI) 0.93–1.06] for composite CV-specific death, non-fatal myocardial infarction (MI) and non-fatal stroke; 1.01 (CI 0.91–1.12) for CV-specific death; 0.98 (CI 0.89–1.09) for non-fatal MI; and 1.00 (CI 0.86–1.16) for non-fatal stroke. The risk of acute pancreatitis was increased (RR 1.79; CI 1.13–2.81), equating to 5.5 extra cases/10 000 patients/year (weighted mean) and a number needed to harm of 1940/year. These data provide reassurance about the safety of DPP-4 inhibitors with regard to individual atherothrombotic events and a safety signal for pancreatitis.
Danese M, Gleeson M, Kutikova L, et al., 2015, COSTS OF CARDIOVASCULAR (CV) EVENTS IN THE UNITED KINGDOM (UK) USING REAL-WORLD DATA, VALUE IN HEALTH, Vol: 18, Pages: A387-A387, ISSN: 1098-3015
- Author Web Link
- Cite
- Citations: 2
Danese M, Gleeson M, Kutikova L, et al., 2015, LIPID MODIFYING THERAPY TREATMENT PATTERNS AND CHOLESTEROL CONTROL AFTER CARDIOVASCULAR EVENTS IN THE UNITED KINGDOM, VALUE IN HEALTH, Vol: 18, Pages: A406-A406, ISSN: 1098-3015
Wong B, Villa G, Kutikova L, et al., 2015, THE MAGNITUDE OF INCREASED CARDIOVASCULAR (CV) RISK ASOCIATED WITH FAMILIAL HYPERCHOLESTEROLEMIA (FH) FOR USE IN ECONOMIC ANALYSES, VALUE IN HEALTH, Vol: 18, Pages: A340-A340, ISSN: 1098-3015
- Author Web Link
- Cite
- Citations: 1
Hartgers ML, Ray KK, Hovingh GK, 2015, New approaches in detection and treatment of familial hypercholesterolemia, Current Cardiology Reports, Vol: 17, ISSN: 1534-3170
Familial hypercholesterolemia (FH) is an autosomal dominant genetic disorder that clinically leads to increased low density lipoprotein-cholesterol (LDL-C) levels. As a consequence, FH patients are at high risk for cardiovascular disease (CVD). Mutations are found in genes coding for the LDLR, apoB, and PCSK9, although FH cannot be ruled out in the absence of a mutation in one of these genes. It is pivotal to diagnose FH at an early age, since lipid lowering results in a decreased risk of cardiovascular complications especially if initiated early, but unfortunately FH is largely underdiagnosed. While a number of clinical criteria are available, identification of a pathogenic mutation in any of the three aforementioned genes is seen by many as a way to establish a definitive diagnosis of FH. It should be remembered that clinical treatment is based on LDL-C levels and not solely on presence or absence of genetic mutations as LDL-C is what drives risk. Traditionally, mutation detection has been done by means of dideoxy sequencing. However, novel molecular testing methods are gradually being introduced. These next generation sequencing-based methods are likely to be applied on broader scale once their efficacy and effect on cost are being established. Statins are the first-line therapy of choice for FH patients as they have been proven to reduce CVD risk across a range of conditions including hypercholesterolemia (though not specifically tested in FH). However, in a significant proportion of FH patients LDL-C goals are not met, despite the use of maximal statin doses and additional lipid-lowering therapies. This underlines the need for additional therapies, and inhibition of PCSK9 and CETP is among the most promising new therapeutic options. In this review, we aim to provide an overview of the latest information about the definition, diagnosis, screening, and current and novel therapies for FH.
Banach M, Serban C, Sahebkar A, et al., 2015, Impact of statin therapy on coronary plaque composition: a systematic review and meta-analysis of virtual histology intravascular ultrasound studies, BMC Medicine, Vol: 13, ISSN: 1741-7015
BackgroundVirtual histology intravascular ultrasound (VH-IVUS) imaging is an innovative tool for the morphological evaluation of coronary atherosclerosis. Evidence for the effects of statin therapy on VH-IVUS parameters have been inconclusive. Consequently, we performed a systematic review and meta-analysis to investigate the impact of statin therapy on plaque volume and its composition using VH-IVUS.MethodsThe search included PubMed, Cochrane Library, Scopus and Embase (through 30 November 2014) to identify prospective studies investigating the effects of statin therapy on plaque volume and its composition using VH-IVUS.ResultsWe identified nine studies with 16 statin treatment arms and 830 participants. There was a significant effect of statin therapy in reducing plaque volume (standardized mean difference (SMD): −0.137, 95 % confidence interval (CI): −0.255, −0.019; P = 0.023), external elastic membrane volume (SMD: −0.097, 95 % CI: −0.183, −0.011; P = 0.027) but not lumen volume (SMD: −0.025, 95 % CI: −0.110, +0.061; P = 0.574). There was a significant reduction in fibrous plaque volume (SMD: −0.129, 95 % CI: −0.255, −0.003; P = 0.045) and an increase of dense calcium volume (SMD: +0.229, 95 % CI: +0.008, +0.450; P = 0.043), while changes in fibro-fatty (SMD: −0.247, 95 % CI: −0.592, +0.098; P = 0.16) and necrotic core (SMD: +0.011, 95 % CI: −0.144, +0.165; P = 0.892) tissue volumes were not statistically significant.ConclusionsThis meta-analysis indicates a significant effect of statin therapy on plaque and external elastic membrane volumes and fibrous and dense calcium volumes. There was no effect on lumen volume, fibro-fatty and necrotic tissue volumes.
Vallejo-Vaz AJ, Seshasai SRK, Della C, et al., 2015, Familial hypercholesterolaemia: a global call to arms, Atherosclerosis, Vol: 243, Pages: 257-259, ISSN: 1879-1484
Sahebkar A, Serban C, Mikhailidis DP, et al., 2015, Association between statin use and plasma D-dimer levels, THROMBOSIS AND HAEMOSTASIS, Vol: 114, Pages: 546-557, ISSN: 0340-6245
- Author Web Link
- Cite
- Citations: 130
Kotani K, Sahebkar A, Serban C, et al., 2015, Tibolone decreases Lipoprotein(a) levels in postmenopausal women: A systematic review and meta-analysis of 12 studies with 1009 patients, ATHEROSCLEROSIS, Vol: 242, Pages: 87-96, ISSN: 0021-9150
- Author Web Link
- Cite
- Citations: 45
Hovingh GK, Ray KK, Boekholdt SM, 2015, Is Cholesteryl Ester Transfer Protein Inhibition an Effective Strategy to Reduce Cardiovascular Risk? <i>CETP as a Target to Lower CVD Risk</i>: <i>Suspension of Disbelief</i>?, CIRCULATION, Vol: 132, Pages: 433-439, ISSN: 0009-7322
- Author Web Link
- Cite
- Citations: 24
Banach M, Serban C, Sahebkar A, et al., 2015, Impact of statin therapy on coronary plaque composition: a systematic review and meta-analysis of virtual histology-intravascular ultrasound studies, Congress of the European-Society-of-Cardiology (ESC), Publisher: OXFORD UNIV PRESS, Pages: 261-261, ISSN: 0195-668X
Ray KK, Vallejo-Vaz AJ, 2015, The evolving role of CETP inhibition: beyond HDL cholesterol, Lancet, Vol: 386, Pages: 412-414, ISSN: 0140-6736
De Backer G, Besseling J, Chapman J, et al., 2015, Prevalence and management of familial hypercholesterolaemia in the EUROASPIRE IV project, Congress of the European-Society-of-Cardiology (ESC), Publisher: OXFORD UNIV PRESS, Pages: 359-359, ISSN: 0195-668X
Sahebkar A, Kotani K, Serban C, et al., 2015, Statin therapy reduces plasma endothelin-1 concentrations: A meta-analysis of 15 randomized controlled trials, ATHEROSCLEROSIS, Vol: 241, Pages: 433-442, ISSN: 0021-9150
- Author Web Link
- Cite
- Citations: 128
Vallejo-Vaz AJ, Seshasai SRK, Kurogi K, et al., 2015, Effect of pitavastatin on glucose, HbA1c and incident diabetes: A meta-analysis of randomized controlled clinical trials in individuals without diabetes, ATHEROSCLEROSIS, Vol: 241, Pages: 409-418, ISSN: 0021-9150
- Author Web Link
- Cite
- Citations: 75
Saraf S, Ray KK, 2015, New worldwide lipid guidelines, CURRENT OPINION IN CARDIOLOGY, Vol: 30, Pages: 447-453, ISSN: 0268-4705
- Author Web Link
- Cite
- Citations: 4
Mark L, Vallejo-Vaz AJ, Reiber I, et al., 2015, Non-HDL cholesterol goal attainment and its relationship with triglyceride concentrations among diabetic subjects with cardiovascular disease: A nationwide survey of 2674 individuals in Hungary, ATHEROSCLEROSIS, Vol: 241, Pages: 62-68, ISSN: 0021-9150
- Author Web Link
- Cite
- Citations: 20
Vallejo-Vaz AJ, Mark L, Reiber I, et al., 2015, RELATIONSHIP OF NON-HDL-CHOLESTEROL LEVELS AND GOAL ATTAINMENT WITH TRIGLYCERIDES AND REMNANT LIPOPROTEINS IN A NATIONWIDE SURVEY OF OVER 2600 DIABETIC SUBJECTS WITH CARDIOVASCULAR DISEASE, 83rd Congress of the European-Atherosclerosis-Society (EAS), Publisher: ELSEVIER IRELAND LTD, Pages: E58-E58, ISSN: 0021-9150
Vallejo-Vaz AJ, Seshasai SRK, Kurogi K, et al., 2015, EFFECTS OF PITAVASTATIN THERAPYON GLUCOSE, HBA1C AND INCIDENCE OF DIABETES MELLITUS: A META-ANALYSIS OF RANDOMIZED CONTROLLED CLINICAL TRIALS IN NON-DIABETIC INDIVIDUALS, 83rd Congress of the European-Atherosclerosis-Society (EAS), Publisher: ELSEVIER IRELAND LTD, Pages: E143-E143, ISSN: 0021-9150
Preiss D, Campbell RT, Murray HM, et al., 2015, The effect of statin therapy on heart failure events: a collaborative meta-analysis of unpublished data from major randomized trials, European Heart Journal, Vol: 36, Pages: 1536-1546, ISSN: 1522-9645
Aims The effect of statins on risk of heart failure (HF) hospitalization and HF death remains uncertain. We aimed to establishwhether statins reduce major HF events.Methodsand resultsWe searched Medline, EMBASE, and the Cochrane Central Register of Controlled Trials for randomized controlled endpointstatin trials from 1994 to 2014. Collaborating trialists provided unpublished data from adverse event reports. We includedprimary- and secondary-prevention statin trials with .1000 participants followed for .1 year. Outcomes consisted of firstnon-fatal HF hospitalization, HF death and a composite of first non-fatal HF hospitalization or HF death. HF events occurring,30 days after within-trial myocardial infarction (MI) were excluded. We calculated risk ratios (RR) with fixed-effects metaanalyses.In up to 17 trials with 132 538 participants conducted over 4.3 [weighted standard deviation (SD) 1.4] years, statintherapy reduced LDL-cholesterol by 0.97 mmol/L (weighted SD 0.38 mmol/L). Statins reduced the numbers of patientsexperiencing non-fatal HF hospitalization (1344/66 238 vs. 1498/66 330; RR 0.90, 95% confidence interval, CI 0.84–0.97) andthe composite HF outcome (1234/57 734 vs. 1344/57 836; RR 0.92, 95% CI 0.85–0.99) but not HF death (213/57 734 vs. 220/57 836;RR 0.97, 95%CI 0.80–1.17).Theeffect of statinson first non-fatalHF hospitalizationwas similarwhether thiswasprecededby MI (RR 0.87, 95% CI 0.68–1.11) or not (RR 0.91, 95% CI 0.84–0.98).Conclusion In primary- and secondary-prevention trials, statinsmodestly reduced the risksof non-fatalHF hospitalization and acompositeof nonfatalHF hospitalization and HF death with no demonstrable difference in risk reduction between those who suffered an MI or not.
Patti G, Bennett R, Seshasai SRK, et al., 2015, Statin pretreatment and risk of in-hospital atrial fibrillation among patients undergoing cardiac surgery: a collaborative meta-analysis of 11 randomized controlled trials, EUROPACE, Vol: 17, Pages: 855-863, ISSN: 1099-5129
- Author Web Link
- Cite
- Citations: 24
Banach M, Rizzo M, Toth PP, et al., 2015, Statin intolerance - an attempt at a unified definition. Position paper from an International Lipid Expert Panel, EXPERT OPINION ON DRUG SAFETY, Vol: 14, Pages: 935-955, ISSN: 1474-0338
- Author Web Link
- Cite
- Citations: 64
This data is extracted from the Web of Science and reproduced under a licence from Thomson Reuters. You may not copy or re-distribute this data in whole or in part without the written consent of the Science business of Thomson Reuters.