1094 American Journal of Hypertension 29(9) September 2016 ORIGINAL ARTICLE Ambulatory blood pressure (BP) monitoring provides more information than conventional BP measurements mainly because it records nighttime BP values. In most healthy indi- viduals, nighttime BP dips by 10%–20% compared to day- time BP values. 1 People with a less than 10% BP decline are referred as “nondippers” and individuals with normal diur- nal BP variation are termed “dippers.” A nondipping profle is associated with target organ damage including renal dis- ease and cardiovascular (CV) complications. 2,3 Te mecha- nisms responsible for individual diferences between dipping patterns are still not completely understood. However, data from previous studies suggest that a nondipping profle of diurnal BP variability is associated with coronary heart dis- ease (CHD). 4 One of the possible mechanisms accounting for an impaired diurnal BP pattern is autonomic nervous system imbalance. 5 Impaired autonomic nervous system activity has been observed in patients with CHD. 6 In addi- tion, some studies have revealed that patients with a blunted nocturnal decline in BP display the highest risk because this pattern exposes these individuals to a greater CV load each day. 2,7 Given the importance of a nondipping profle of BP as a risk factor for CV complications, the infuence of genetic variation on the diurnal BP pattern may be pivotal in CV risk assessment in patients with CHD. However, despite the signifcance of BP fall, little is known about its heritability. In previously performed studies, the heritability of nocturnal BP fall was estimated as 38% for systolic dipping and 9% for diastolic dipping. 8 Although some studies have confrmed heredity of blunted nighttime BP dip in the general popula- tion, no study has addressed heredity of nighttime BP dip in patients with confrmed CHD. In the present study that includes patients with CHD, we aim to determine which sin- gle-nucleotide polymorphisms (SNPs) are related to blunted nighttime BP fall. METHODS Subjects Te present study recruited 1,345 CHD individuals con- secutively admitted to Department of Cardiology, Medical University of Gdansk (between August 2003 and August The Relationship Between Gene Polymorphisms and Dipping Profle in Patients With Coronary Heart Disease Marcin Wirtwein, 1 Olle Melander, 2 Marketa Sjőgren, 2 Michal Hofmann, 3 Krzysztof Narkiewicz, 3 Marcin Gruchala, 4 and Wojciech Sobiczewski 4 BACKGROUND The aim of this study is to report the relationship between certain single-nucleotide polymorphisms (SNPs) and blunted nighttime blood pressure (BP) fall in patients with coronary artery disease confrmed by coronary angiography. METHODS According to the percentage decrease in mean systolic BP (SBP) and diastolic BP (DBP) during the nighttime period, subjects were classified as dippers or nondippers (nighttime relative SBP or DBP decline ≥10% and <10%, respectively). Genetic risk score (GRS18) was constructed to evaluate additive effect of 18 SNPs for nondip- ping status. RESULTS In the present study, 1,345 subjects with coronary heart disease (CHD) were included. During follow-up period (median 8.3 years, interquartile range 5.3–9.0 years), there were 245 all-cause deaths (18.2%) includ- ing 114 cardiovascular deaths (8.5%). There were signifcant diferences in the number of revascularizations between nondippers SBP and DBP and dippers SBP and DBP (48.0% vs. 36.4%, P < 0.01). SNPs of the genes, MIA3, MRAS, PCSK9, SMG6, and ZC3HC1, were related to a higher risk of nondipping SBP and DBP status. CONCLUSIONS In the present study, polymorphisms of genes related to CHD (MIA3, MRAS, PCSK9, SMG6, and ZC3HC1) were associated with nondipping SBP and DBP profle, and GRS18 was associated with nondipping status. In addition, this profle was related to a higher risk of revascularization. Keywords: blood pressure; coronary artery disease; dipping; DNA poly- morphisms; hypertension. doi:10.1093/ajh/hpw040 Correspondence: Marcin Wirtwein (marwirt@interia.pl). Initially submitted November 24, 2015; date of frst revision December 12, 2015; accepted for publication February 29, 2016; online publication May 17, 2016. © American Journal of Hypertension, Ltd 2016. All rights reserved. For Permissions, please email: journals.permissions@oup.com 1 Department of Pharmacology, Medical University of Gdansk, Gdansk, Poland; 2 Department of Clinical Sciences, Lund University, Malmö, Sweden; 3 Department of Hypertension and Diabetology, Medical University of Gdansk, Gdansk, Poland; 4 Department of Cardiology, Medical University of Gdansk, Gdansk, Poland. Downloaded from https://academic.oup.com/ajh/article/29/9/1094/2622260 by guest on 15 September 2022