Prof. Dr. J. Wouter Jukema

Professor J. Wouter Jukema is head of the department of cardiology at Leiden University Medical Center (LUMC) in Leiden, the Netherlands and Board Member of the Netherlands Heart Institute, Utrecht, the Netherlands. He is professor of cardiology and medicine since 2005 with a special focus on atherothrombosis and regenerative medicine. He completed his cardiology training at the LUMC and went on to his doctoral thesis at the Netherlands Heart Institute in Utrecht (1996). He completed his training with a fellowship provided by the European Society of Cardiology at the University of Texas Southwestern Medical Center in Dallas, Texas. He is a past established clinical investigator of the Netherlands Heart Foundation and founding director of the Durrer Center for Cardiovascular Research in Amsterdam. He is currently the chairman of vascular medicine at the Leiden University Medical Center as well as co-chairman of the Dutch Atherosclerosis Society. Prof. Jukema has been the principal investigator of several major national and international interventional cardiology and atherothrombosis studies and the holder of multiple major European Union grants. His current research interests, which comprise the majority of topics in his more than 1000 peer-reviewed articles (with many in top journals like New England Journal of Medicine, Lancet, Nature Genetics, Nature Reviews, Science, Circulation, and European Heart Journal), focus on vascular biology, lipids, atherothrombosis, genetics and interventional cardiology in pre-clinical and clinical studies. His Web of Science citation H-index is > 120 with more than 150,000 citations.

Most recent publications

Coronary calcifications as assessed on routine non-gated chest CT; a gatekeeper to tailor downstream additional imaging in patients with stable chest pain
Groen RA, van Dijkman PRM, Jukema JW, Bax JJ, Lamb HJ and de Graaf MA
Currently applied methods for risk-assessment in coronary artery disease (CAD) often overestimate patients' risk for obstructive CAD. To enhance risk estimation, assessment of coronary artery calcium (CAC) can be applied. In 10 % of patients presenting with stable chest pain a previous non-gated computed tomography (CT) has been performed, suitable for CAC-assessment. This study is the first to investigate the clinical utility of CAC-assessment on non-gated CT for risk-assessment of obstructive CAD in symptomatic patients.
Genome-wide analysis in over 1 million individuals of European ancestry yields improved polygenic risk scores for blood pressure traits
Keaton JM, Kamali Z, Xie T, Vaez A, Williams A, Goleva SB, Ani A, Evangelou E, Hellwege JN, Yengo L, Young WJ, Traylor M, Giri A, Zheng Z, Zeng J, Chasman DI, Morris AP, Caulfield MJ, Hwang SJ, Kooner JS, Conen D, Attia JR, Morrison AC, Loos RJF, Kristiansson K, Schmidt R, Hicks AA, Pramstaller PP, Nelson CP, Samani NJ, Risch L, Gyllensten U, Melander O, Riese H, Wilson JF, Campbell H, Rich SS, Psaty BM, Lu Y, Rotter JI, Guo X, Rice KM, Vollenweider P, Sundström J, Langenberg C, Tobin MD, Giedraitis V, Luan J, Tuomilehto J, Kutalik Z, Ripatti S, Salomaa V, Girotto G, Trompet S, Jukema JW, van der Harst P, Ridker PM, Giulianini F, Vitart V, Goel A, Watkins H, Harris SE, Deary IJ, van der Most PJ, Oldehinkel AJ, Keavney BD, Hayward C, Campbell A, Boehnke M, Scott LJ, Boutin T, Mamasoula C, Järvelin MR, Peters A, Gieger C, Lakatta EG, Cucca F, Hui J, Knekt P, Enroth S, De Borst MH, Polašek O, Concas MP, Catamo E, Cocca M, Li-Gao R, Hofer E, Schmidt H, Spedicati B, Waldenberger M, Strachan DP, Laan M, Teumer A, Dörr M, Gudnason V, Cook JP, Ruggiero D, Kolcic I, Boerwinkle E, Traglia M, Lehtimäki T, Raitakari OT, Johnson AD, Newton-Cheh C, Brown MJ, Dominiczak AF, Sever PJ, Poulter N, Chambers JC, Elosua R, Siscovick D, Esko T, Metspalu A, Strawbridge RJ, Laakso M, Hamsten A, Hottenga JJ, de Geus E, Morris AD, Palmer CNA, Nolte IM, Milaneschi Y, Marten J, Wright A, Zeggini E, Howson JMM, O'Donnell CJ, Spector T, Nalls MA, Simonsick EM, Liu Y, van Duijn CM, Butterworth AS, Danesh JN, Menni C, Wareham NJ, Khaw KT, Sun YV, Wilson PWF, Cho K, Visscher PM, Denny JC, , , , , Levy D, Edwards TL, Munroe PB, Snieder H and Warren HR
Hypertension affects more than one billion people worldwide. Here we identify 113 novel loci, reporting a total of 2,103 independent genetic signals (P < 5 × 10) from the largest single-stage blood pressure (BP) genome-wide association study to date (n = 1,028,980 European individuals). These associations explain more than 60% of single nucleotide polymorphism-based BP heritability. Comparing top versus bottom deciles of polygenic risk scores (PRSs) reveals clinically meaningful differences in BP (16.9 mmHg systolic BP, 95% CI, 15.5-18.2 mmHg, P = 2.22 × 10) and more than a sevenfold higher odds of hypertension risk (odds ratio, 7.33; 95% CI, 5.54-9.70; P = 4.13 × 10) in an independent dataset. Adding PRS into hypertension-prediction models increased the area under the receiver operating characteristic curve (AUROC) from 0.791 (95% CI, 0.781-0.801) to 0.826 (95% CI, 0.817-0.836, ∆AUROC, 0.035, P = 1.98 × 10). We compare the 2,103 loci results in non-European ancestries and show significant PRS associations in a large African-American sample. Secondary analyses implicate 500 genes previously unreported for BP. Our study highlights the role of increasingly large genomic studies for precision health research.
Genetic variants for head size share genes and pathways with cancer
Knol MJ, Poot RA, Evans TE, Satizabal CL, Mishra A, Sargurupremraj M, van der Auwera S, Duperron MG, Jian X, Hostettler IC, van Dam-Nolen DHK, Lamballais S, Pawlak MA, Lewis CE, Carrion-Castillo A, van Erp TGM, Reinbold CS, Shin J, Scholz M, Håberg AK, Kämpe A, Li GHY, Avinun R, Atkins JR, Hsu FC, Amod AR, Lam M, Tsuchida A, Teunissen MWA, Aygün N, Patel Y, Liang D, Beiser AS, Beyer F, Bis JC, Bos D, Bryan RN, Bülow R, Caspers S, Catheline G, Cecil CAM, Dalvie S, Dartigues JF, DeCarli C, Enlund-Cerullo M, Ford JM, Franke B, Freedman BI, Friedrich N, Green MJ, Haworth S, Helmer C, Hoffmann P, Homuth G, Ikram MK, Jack CR, Jahanshad N, Jockwitz C, Kamatani Y, Knodt AR, Li S, Lim K, Longstreth WT, Macciardi F, , , Mäkitie O, Mazoyer B, Medland SE, Miyamoto S, Moebus S, Mosley TH, Muetzel R, Mühleisen TW, Nagata M, Nakahara S, Palmer ND, Pausova Z, Preda A, Quidé Y, Reay WR, Roshchupkin GV, Schmidt R, Schreiner PJ, Setoh K, Shapland CY, Sidney S, St Pourcain B, Stein JL, Tabara Y, Teumer A, Uhlmann A, van der Lugt A, Vernooij MW, Werring DJ, Windham BG, Witte AV, Wittfeld K, Yang Q, Yoshida K, Brunner HG, Le Grand Q, Sim K, Stein DJ, Bowden DW, Cairns MJ, Hariri AR, Cheung CL, Andersson S, Villringer A, Paus T, Cichon S, Calhoun VD, Crivello F, Launer LJ, White T, Koudstaal PJ, Houlden H, Fornage M, Matsuda F, Grabe HJ, Ikram MA, Debette S, Thompson PM, Seshadri S and Adams HHH
The size of the human head is highly heritable, but genetic drivers of its variation within the general population remain unmapped. We perform a genome-wide association study on head size (N = 80,890) and identify 67 genetic loci, of which 50 are novel. Neuroimaging studies show that 17 variants affect specific brain areas, but most have widespread effects. Gene set enrichment is observed for various cancers and the p53, Wnt, and ErbB signaling pathways. Genes harboring lead variants are enriched for macrocephaly syndrome genes (37-fold) and high-fidelity cancer genes (9-fold), which is not seen for human height variants. Head size variants are also near genes preferentially expressed in intermediate progenitor cells, neural cells linked to evolutionary brain expansion. Our results indicate that genes regulating early brain and cranial growth incline to neoplasia later in life, irrespective of height. This warrants investigation of clinical implications of the link between head size and cancer.
Prediction of individual lifetime cardiovascular risk and potential treatment benefit: development and recalibration of the LIFE-CVD2 model to four European risk regions
The 2021 European Society of Cardiology prevention guidelines recommend the use of (lifetime) risk prediction models to aid decisions regarding initiation of prevention. We aimed to update and systematically recalibrate the LIFEtime-perspective CardioVascular Disease (LIFE-CVD) model to four European risk regions for the estimation of lifetime CVD risk for apparently healthy individuals.
Safety Of The Pcsk9 Inhibitor Alirocumab: insights From 47,296 Patient-Years Of Observation
Goodman SG, Steg PG, Szarek M, Bhatt DL, Bittner VA, Diaz R, Harrington RA, Jukema JW, White HD, Zeiher AM, Manvelian G, Pordy R, Poulouin Y, Stipek W, Garon G and Schwartz GG
The ODYSSEY OUTCOMES trial, comprising over 47 000 patient-years of placebo-controlled observation, demonstrated important reductions in the risk of recurrent ischaemic cardiovascular events with the monoclonal antibody to proprotein convertase subtilisin/kexin type 9 alirocumab, as well as lower all-cause death. These benefits were observed in the context of substantial and persistent lowering of low-density lipoprotein cholesterol with alirocumab compared to that achieved with placebo. The safety profile of alirocumab was indistinguishable from matching placebo except for a ∼1.7% absolute increase in local injection-site reactions. Further, the safety of alirocumab compared to placebo was evident in vulnerable groups identified before randomization, such as the elderly and those with diabetes mellitus, previous ischaemic stroke, or chronic kidney disease. The frequency of adverse events and laboratory-based abnormalities was generally similar to that in placebo-treated patients. Thus, alirocumab appears to be a safe and effective lipid-modifying treatment over a duration of at least 5 years.