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Bilovol et al.                                                                                                                                     Relationship between atrial fibrillation, BMI and adipokines

           disease (CVD), including an increased risk of incidence   and CVD. Adiponectin is reduced in obesity, CHD, HF,
           of sudden cardiac death, atrium fibrillation and other   AF  and  T2DM,  and  increased  following  weight  loss.
           form of arrhythmias .                              Adiponectin levels were independently associated
                             [1]
                                                              with  the  incident  of  AF [16,17] .  However,  it  remains
           In contrast, a large review from Flegal et al.  analyzed   unclear whether these are markers of failed regulatory
                                                 [3]
           97 studies of 2.9 million individuals, including >   pathways that lead to AF or are directly involved in AF
           270,000 deaths, and demonstrated that optimal      pathogenesis.
           survival occurred in “overweight” patients [body mass
           index (BMI): 25 to 30 kg/m ], who had a significant 6%   Our study aimed to elucidate the causal relationship
                                   2
           lower mortality than the “normal-weight” BMI cohort   between AF and BMI or adipokine levels, specifically
           (BMI: 18.5 to 25 kg/m ) .                          serum leptin and high-molecular-weight  adiponectin
                              2 [3]
                                                              (HMWAN), among the general population.
           Patients with elevated BMI, but normal insulin sensitivity,
           lipid profiles and blood pressure (BP), are considered   METHODS
           to be metabolically healthy obesity (MHO) .  Some
                                                   [4]
           epidemiological data suggest that MHO carries a
           lower risk of CVD, lower risk of AF development and   This study comprised 398 patients randomly selected
           less all-cause mortality than being normal weight yet   while visiting the out-patient unit due to any reason,
           metabolically unhealthy .  The precise mechanism   except acute heart pathology, provided they had not
                                 [5]
           that induces AF in obesity is still unknown. Metabolic   had heart rate disorders in their past medical history.
           comorbidities are common in obese people and could
           be  the  main  reason  for  increased  AF  risk  and  total   Among  allotted  patients  there  were  142  with  arterial
           cardiovascular risk, apart from obesity itself. There are   hypertension (AH) (35.7%), 118 suffering from ischemic
           several proposed mechanisms that connect obesity   heart disease (29.6%), 73 with diabetes mellitus II type
           and AF [6-10] .                                    (DM-2) (18.3%), provided DM-2 was compensated.

           Enhanced neurohormonal activation, impaired insulin   Also excluded were those patients who had developed
           tolerance,  dyslipoproteinemia,  hypertension  and  kidney, liver diseases, heart diseases, heart failure
           pathological changes in circulating renin-angiotensin-  (more than 2 functional class according to New York
           aldosterone system accompanies obesity and may     Heart Association), chronic obstructive lung pathology,
           contribute  to  left  atrial  enlargement  and  electrical   malignant neoplasms or alcoholism.
           instability, which may result in AF development [11] .
                                                              Patients’ age ranged from 37 to 56 years old (mean
           Studies on the mechanisms by which obesity induces   age: 41.4 ± 2.3  year). All patients involved  in this
           AF  show  that  obesity  causes  atrial  arrhythmogenic   study were examined according to the same protocol.
           remodeling. Progression of atrial fibrosis is a key event   Anthropometry was assessed with measurements
           in the pathogenesis of AF [12,13] , and can be caused by   of waist circumference and BMI calculated by Kettle
           aging, underlying cardiac diseases, systemic diseases   formula. Additionally, BP was measured along with
           or  inflammatory  processes,  or  AF  itself.  Obese   a panel of laboratory tests: fasting serum glucose
           individuals, even without cardiovascular disease, have   (glucosoxidative  approach);  serum  lipoproteins
           left atrium (LA) enlargement [14]  and different electrical   [serum cholesterol, triglycerides (TG), cholesterol of
           properties, such as slower conduction from the LA   high-density lipoprotein (HDL) by enzyme colorimetric
           entering  the  pulmonary  vein  (PV)  and  a  significantly   approach with kit of “Human” (Germany)]; C-reactive
           shorter effective refractory period in the LA and PV .  protein  (CP)  by  solid  phase  enzyme  immunoassay
                                                        [15]
                                                              (EIA) (NycoCard CRP, Axis-Shield); serum Leptin by
           Adipokines are bioactive proteins produced by the   EIA kit Leptin ELISA [Diaghostics Biochem Canada
           adipose compartment that have wide-ranging effects   Inc (DBC Inc) cat № ABIN362629 CAN-L-4260]; and
           across organs and tissues. Leptin and adiponectin are   serum HMWAN by EIA with use of kit DRG (USA). The
           both  closely  related with  obesity  and have  recently   homeostatic model assessment of insulin resistance
           been implicated with AF. These hormones are secreted   (HOMA-IR) was calculated: НОМА-IR = insulin, mcU/mL
           primarily by adipocytes, while the stromovascular tissue   × glucose, mmol/L ÷ 22.5).
           surrounding fat secretes tumor necrosis factor-alpha
           (TNF-α) and macrophages secrete resistin [16,17] . These   Overweight patients (BWI: 25-29.9 kg/m ) and those
                                                                                                   2
                                                                                      2
           adipokines have been proposed as  links  between   with AO and BMI ≥ 30 kg/m  were classified according
           adiposity and insulin resistance, glucose deregulation,   to Wildman criteria (2008) as “MHO” and “metabolically
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