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Wendy S. Post, MD, MS

Ciccarone Center Research

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Wendy S. Post, MD, MS

Wendy S. Post, MD, MS
Post, Wendy S., MD, MS

Wendy S. Post, MD, MS is a Professor of Medicine at the Johns Hopkins University, School of Medicine. She is also a Professor of Epidemiology at Johns Hopkins Bloomberg School of Public Health. Additionally she is part of the associate faculty at the Welch Center for Prevention and Clinical Research and Epidemiology divisions of Johns Hopkins University.

View my Johns Hopkins Medicine profile for more information and to request an appointment.

 

Landmark Articles

Impact of ancestry and common genetic variants on QT interval in African Americans.

By: Smith JG, Avery CL, Evans DS, Nalls MA, Meng YA, Smith EN, Palmer C, Tanaka T, Mehra R, Butler AM, Young T, Buxbaum SG, Kerr KF, Berenson GS, Schnabel RB, Li G, Ellinor PT, Magnani JW, Chen W, Bis JC, Curb JD, Hsueh WC, Rotter JI, Liu Y, Newman AB, Limacher MC, North KE, Reiner AP, Quibrera PM, Schork NJ, Singleton AB, Psaty BM, Soliman EZ, Solomon AJ, Srinivasan SR, Alonso A, Wallace R, Redline S, Zhang ZM, Post WS, Zonderman AB, Taylor HA, Murray SS, Ferrucci L, Arking DE, Newton-Cheh C, et al.; CARe and COGENT consortia.
This study tested the hypotheses that African ancestry and common genetic variants are associated with prolonged duration of cardiac repolarization, a central pathophysiological determinant of arrhythmia. However, no difference in duration of cardiac repolarization with global genetic indices of African-American ancestry was noted.
Read on Pubmed

Gene-centric meta-analysis of lipid traits in African, East Asian and Hispanic populations.

By: Elbers CC, Guo Y, Tragante V, van Iperen EP, Lanktree MB, Castillo BA, Chen F, Yanek LR, Wojczynski MK, Li YR, Ferwerda B, Ballantyne CM, Buxbaum SG, Chen YD, Chen WM, Cupples LA, Cushman M, Duan Y, Duggan D, Evans MK, Fernandes JK, Fornage M, Garcia M, Garvey WT, Glazer N, Gomez F, Harris TB, Halder I, Howard VJ, Keller MF, Kamboh MI, Kooperberg C, Kritchevsky SB, LaCroix A, Liu K, Liu Y, Musunuru K, Newman AB, Onland-Moret NC, Ordovas J, Peter I, Post W, Redline S, Reis SE, Saxena R, Schreiner PJ, Volcik KA, Wang X, Yusuf S, Zonderland AB, Anand SS, Becker DM, Psaty B, Rader DJ, Reiner AP, Rich SS, Rotter JI, Wilson JG, Keating BJ, et al.
Meta-analyses of European populations has successfully identified genetic variants in over 100 loci associated with lipid levels. This study seeks to expand our knowledge in other ethnicities, which remains limited.

Large-scale gene-centric meta-analysis across 32 studies identifies multiple lipid loci.

By: Asselbergs FW, Guo Y, van Iperen EP, Sivapalaratnam S, Tragante V, Lanktree MB, Lange LA, Almoguera B, Appelman YE, Barnard J, Baumert J, Beitelshees AL, Bhangale TR, Chen YD, Gaunt TR, Gong Y, Hopewell JC, Johnson T, Kleber ME, Langaee TY, Li M, Li YR, Liu K, McDonough CW, Meijs MF, Middelberg RP, Musunuru K, Post WS, et al.
This large meta-analysis of lipid phenotypes with the use of a dense gene-centric approach identified multiple single nucleotide polymorphisms not previously described in established lipid genes and several previously unknown loci, suggesting that a focused genotyping approach can further increase the understanding of heritability of plasma lipids.

Association of SRB1 variants with subclinical atherosclerosis and incident cardiovascular disease: The Multi-Ethnic Study of Atherosclerosis.

By: Manichaikul A, Naj AC, Herrington D, Post W, Rich SS, Rodriguez A.

We previously reported a statistically significant association of SCARB1 intronic single nucleotide polymorphism (SNP) rs10846744 with common carotid intimal-medial artery thickness in each of the 4 Multi-Ethnic Study of Atherosclerosis racial/ethnic groups (white, Chinese, black, and Hispanic). The SCARB1 SNP, rs10846744, exerts a major effect on subclinical atherosclerosis and incident cardiovascular disease in humans.

Herpes simplex virus type 2 (HSV-2) as a coronary atherosclerosis risk factor in HIV-infected men: Multicenter AIDS Cohort Study.

By: Hechter RC, Budoff M, Hodis HN, Rinaldo CR, Jenkins FJ, Jacobson LP, Kingsley LA, Taiwo B, Post WS, Margolick JB, Detels R.

We assessed associations of herpes simplex virus types 1 and 2 (HSV-1 and -2), cytomegalovirus (CMV), and human herpesvirus 8 (HHV-8) infection with subclinical coronary atherosclerosis in 291 HIV-infected men in the Multicenter AIDS Cohort Study. Coronary artery calcium (CAC) was measured by non-contrast coronary CT imaging. Markers for herpesviruses infection were measured in frozen specimens collected 10-12 years prior to case identification. Multivariable logistic regression models and ordinal logistic regression models were performed. HSV-2 seropositivity was associated with coronary atherosclerosis (adjusted odds ratio [AOR]=4.12, 95% confidence interval [CI]=1.58-10.85) after adjustment for age, race/ethnicity, cardiovascular risk factors, and HIV infection related factors. Infection with a greater number of herpesviruses was associated with elevated CAC levels (AOR=1.58, 95% CI=1.06-2.36). Our findings suggest HSV-2 may be a risk factor for subclinical coronary atherosclerosis in HIV-infected men. Infection with multiple herpesviruses may contribute to the increased burden of atherosclerosis.

Low free testosterone in HIV-infected men is not associated with subclinical cardiovascular disease.

By: Monroe AK, Dobs AS, Xu X, Palella FJ, Kingsley LA, Post WS, Witt MD, Brown TT.

Low testosterone (T) is associated with cardiovascular disease (CVD) and increased mortality in the general population; however, the impact of T on subclinical CVD in HIV disease is unknown. This study examined the relationships among free testosterone (FT), subclinical CVD, and HIV disease. Compared with HIV-uninfected men, HIV-infected men had lower FT, as well as more prevalent carotid lesions. In both groups, FT was not associated with CAC presence, log carotid IMT, or carotid lesion presence, suggesting that FT does not influence subclinical CVD in this population of men with and at risk for HIV infection.

A point-by-point response to recent arguments against the use of statins in primary prevention.

By: Joshi PH, Chaudhari S, Blaha MJ, Jones SR, Martin SS, Post WS, Cannon CP, Fonarow GC, Wong ND, Amsterdam E, Hirshfeld JW, Blumenthal RS.
Early in 2012, a debate over the merits of statin therapy in primary prevention was published in the Wall Street Journal. The statin opponent claimed that statins should only be used in secondary prevention and never in any primary-prevention patients at risk for cardiovascular events. In this evidence-based rebuttal to those claims, we review the evidence supporting the efficacy of statin therapy in primary prevention. Cardiovascular risk is a continuum in which those at an elevated risk of events stand to benefit from early initiation of therapy. Statins should not be reserved until after a patient suffers the catastrophic consequences of atherosclerosis. Contrary to the assertions of the statin opponent, this principle has been demonstrated through reductions in heart attacks, strokes, and mortality in numerous randomized controlled primary-prevention statin trials. In selected at-risk individuals, the combination of pharmacotherapy and lifestyle changes is more effective than either alone. Future investigation in prevention should focus on improving our ability to identify these at-risk individuals.

25-Hydroxyvitamin D deficiency is associated with fatal stroke among whites but not blacks: The NHANES-III linked mortality files.

By: Michos ED, Reis JP, Post WS, Lutsey PL, Gottesman RF, Mosley TH, Sharrett AR, Melamed ML.

Deficient 25-hydroxyvitamin D (25[OH]D) levels are associated with cardiovascular disease (CVD) events and mortality. 25(OH)D deficiency and stroke are more prevalent in blacks. We examined whether low 25(OH)D contributes to the excess risk of fatal stroke in blacks compared with whites. Vitamin D deficiency was associated with an increased risk of stroke death in whites but not in blacks. Although blacks had a higher rate of fatal stroke compared with whites, the low 25(OH)D levels in blacks were unrelated to stroke incidence. Therefore 25(OH)D levels did not explain this excess risk.

Common genetic variation in the 3’-BCL11B gene desert is associated with carotid-femoral pulse wave velocity and excess cardiovascular disease risk: the AortaGen Consortium.

By: Mitchell GF, Verwoert GC, Tarasov KV, Isaacs A, Smith AV, Yasmin, Rietzschel ER, Tanaka T, Liu Y, Parsa A, Najjar SS, O’Shaughnessy KM, Sigurdsson S, De Buyzere ML, Larson MG, Sie MP, Andrews JS, Post WS, et al.

Carotid-femoral pulse wave velocity (CFPWV) is a heritable measure of aortic stiffness that is strongly associated with increased risk for major cardiovascular disease events. Common genetic variation in a locus in the BCL11B gene desert that is thought to harbor 1 or more gene enhancers is associated with higher CFPWV and increased risk for cardiovascular disease. Elucidation of the role this novel locus plays in aortic stiffness may facilitate development of therapeutic interventions that limit aortic stiffening and related cardiovascular disease events.

Read on Pubmed

Prevalence of traditional modifiable cardiovascular risk factors in patients with rheumatoid arthritis: comparison with control subjects from the multi-ethnic study of atherosclerosis.

By: Chung CP, Giles JT, Petri M, Szklo M, Post W, Blumenthal RS, Gelber AC, Ouyang P, Jenny NS, Bathon JM.
We tested the hypotheses that major modifiable cardiovascular risk factors were more frequent and rates of treatment, detection, and control were lower in patients with rheumatoid arthritis than in non-rheumatoid arthritis controls. Hypertension is more common in patients with rheumatoid arthritis, while other traditional CV risk factors are highly prevalent, under-diagnosed, and poorly controlled in patients with rheumatoid arthritis, as well as controls.