LAUSR

Methods Patients We studied 445 white pa‐ tients divided into 2 groups. The first group in‐ cluded 220 patients (59 women and 161 men) with angiographically confirmed premature CAD. The second group comprised 225 blood donors (62 women and 163 men) who served as controls with a negative family history of CAD defined as the absence of CAD, myocardial infarction, or stroke in at least one of the parents. Patients with CAD were recruited from the 1st Depart‐ ment of Cardiology at the Upper Silesian Center of Cardiology in Katowice and the 1st Depart‐ ment of Cardiac Surgery at the Upper Silesian Center of Cardiology in Katowice by the same cli‐ nician. Control individuals were selected among blood donors of the regional centers of blood do‐ nation and blood treatment (in Polish, Region‐ alne Centrum Krwiodawstwa i Krwiolecznict‐ wa) in Katowice and Racibórz. The control group included only individuals without hyperten‐ sion with a systolic blood pressure of less than 140 mm Hg and a diastolic blood pressure of less than 90 mm Hg on the day of blood collection. The levels of blood pressure higher than speci‐ fied above were defined as hypertension.7 Other inclusion and exclusion criteria were described in detail previously.8 Patients and controls were recruited between 2001 and 2006. The study was approved by the ethics com‐ mittee of the Medical University of Silesia in Introduction Coronary artery disease (CAD) is a multifactorial condition. The efficacy of treat‐ ment and prevention methods depends on a bet‐ ter understanding of the genetic background of CAD as well as patient awareness about control of cardiovascular risk factors.1 The biosynthetic pathway of bile acids is the main mechanism of cholesterol catabolism in the human body.2 CYP27A1, encoded by the CYP27A1 gene (2q35), is a mitochondrial enzyme that is expressed in numerous tissues.3 In the liv‐ er, CYP27A1 catalyzes the oxidation of choles‐ terol to 27‐hydroxycholesterol (27‐HC), which is an intermediate metabolite of bile acid synthesis. The role of CYP27A1 in the context of car‐ diovascular diseases remains debatable. Some studies have demonstrated that CYP27A1 is involved in the mechanism protecting against the accumulation of cholesterol in macrophages.4 On the other hand, 27‐HC may enhance ath‐ erosclerotic plaque formation.5 There are lim‐ ited data on the participation of the CYP27A1 variants in predisposing to cardiovascular dis‐ eases. So far, it has been demonstrated that the g.218805152 A>T polymorphism of the CYP27A1 gene (rs4674344) was associated with an increased risk of metabolic syndrome and a decreased level of high ‐density lipoprotein (HDL) cholesterol.6 Because the role of the CYP27A1 polymor‐ phism in the context of CAD risk remains unclear, we decided to assess the potential association of the CYP27A1 rs4674344 haplotype ‐tagging Correspondence to: Joanna Iwanicka, PhD, School of Health Sciences in Katowice, Department of Biochemistry and Medical Genetics, Medical University of Silesia, ul. Medyków 18, 40-752 Katowice, Poland, phone: +48 32 208 88 64, e mail: [email protected] Received: October 29, 2019. Revision accepted: November 26, 2019. Published online: November 27, 2019. Kardiol Pol. 2020; 78 (1): 65-67 doi:10.33963/KP.15071 Copyright by the Author(s), 2020 S H O R T C O M M U N I C A T I O N