Gaisbo« ck syndrome (polycythemia and hypertension) revisited: results from the national inpatient sample database Parasuram Krishnamoorthy a , Akshaya Gopalakrishnan a , Varun Mittal b , Aditi Kalla a , Leandro Slipczuk a , Janani Rangaswami c , Vincent M. Figueredo a , and Franz H. Messerli d Background: Polycythemia is characterized by increased blood viscosity and a chronic inflammatory state possibly giving rise to excessive thromboembolic events and hypertensive cardiovascular disease. We aimed to study the relationship between polycythemia and cardiac risk factors using a large national registry. Methods: Patients more than 18 years with a diagnosis of polycythemia were identified from the National Inpatient Sample 2009–2010 database using International Classification of Diseases; Ninth Edition (ICD-9) code 238.4. Demographics, cardiac risk factors, and cardiovascular events were identified. Results: Polycythemia was present in 0.1% (n ¼ 37 922) of hospital-discharged patients. Patients with polycythemia had a significantly increased prevalence of all cardiac risk factors and events, except for diabetes mellitus and chronic kidney disease. Hypertension was more prevalent in polycythemia compared to controls (61 vs. 46%; P < 0.0001). After adjusting for age, sex, race, diabetes mellitus, hyperlipidemia, tobacco use, obesity, coronary artery disease, heart failure, and chronic kidney disease, polycythemia was still a determinant of hypertension [1.37 (1.28–1.45); P < 0.001]. Conclusion: Polycythemia had high prevalence of all cardiac risk factors and was independently associated with increased prevalence of hypertension even after adjusting. Our findings from the National Inpatient Sample provide an epidemiological correlate of Gaisbo ¨ ck’s original observation of the association of polycythemia and hypertension more than a century ago. Keywords: chronic inflammation, endothelial dysfunction, hypertension, hyperviscosity, polycythemia Abbreviations: CAD, coronary artery disease; CKD, chronic kidney disease; CRP, C-reactive protein; ICD 9-CM, International Classification of Diseases Ninth Edition Clinical Modification; NIS, National Inpatient Sample INTRODUCTION P olycythemia is characterized by increased blood viscosity associated with microcirculatory disturban- ces, including arterial and venous thromboses [1]. These thrombotic events often precede disease recognition. Polycythemia is also described as a chronic inflammatory state [2]. Chronic inflammation plays an important role in vascular remodeling and atherosclerosis. Barbui et al. [2] reported that blood levels of inflammatory biomarkers, such as C-reactive protein (CRP), correlated with thrombo- sis and the JAK2V617F allele burden in myeloproliferative neoplasms such as essential thrombocythemia and polycy- themia vera. Additionally, they also found that levels of pentraxin-3, an anti-inflammatory marker, were inversely associated with thrombotic events, suggesting vascular inflammation plays an important role in polycythemia- related thrombosis. Several mechanisms have been postulated to explain this pro-inflammatory state in polycythemia. Platelet and leu- kocyte cellular activation, measured by overexpression of CD11b antigen and by elevated plasma levels of serine proteases cathepsin G, elastase, and myeloperoxidase [3], result in increased production of cytokines and other pro- inflammatory products. Endothelial dysfunction from vas- cular inflammation has been observed in patients with essential hypertension [4]. More than 25 years ago, Letcher et al. [5] observed a direct relationship between blood pressure and blood viscosity. The same group also showed that whole blood viscosity was about 10% higher in unmed- icated patients with relatively mild uncomplicated essential hypertension than in apparently normal persons of compa- rable age and gender taken from the same population [6]. Cinar et al., noted a 20% increase in blood pressure for a physiologic compensation of 20% increased viscosity and postulated that atherosclerotic vessels with decreased com- pliance might benefit from treatment modalities aimed at decreasing viscosity [7,8]. Journal of Hypertension 2018, 36:000–000 a Division of Cardiology, b Division of Hematology-Oncology, c Department of Medicine, Albert Einstein Medical Center, Philadelphia, Pennsylvania, USA and d Department of Cardiology, Inselspital, University of Bern, Bern, Switzerland Correspondence to: Parasuram Krishnamoorthy, MD, Chief Cardiology Fellow, Einstein Medical Center, 5501 Old York Road, Levy 3232, Philadelphia, PA 19141, USA. Tel: +1 732 501 5100; fax: +1 215 456 3533; e-mail: parasumk@yahoo.com Received 2 November 2017 Revised 28 April 2018 Accepted 29 April 2018 J Hypertens 36:000–000 Copyright ß 2018 Wolters Kluwer Health, Inc. All rights reserved. DOI:10.1097/HJH.0000000000001805 Journal of Hypertension www.jhypertension.com 1 Original Article Copyright © 2018 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.