URIC ACID SIGNIFICANTLY CORRELATES WITH THE PRESENCE OF LOW-VOLTAGE AREAS AT THE ENDOCARDIAL MAPPING IN PATIENTS WITH NON-VALVULAR ATRIAL FIBRILLATION

Objective: Interest in the role of atrial substrate in maintaining Atrial Fibrillation (AF) is growing. Fibrosis is the culprit in the electrical derangement of the myoc-ites. Many cardiovascular risk factors are known to be linked to atrial scarring; among them Uric Acid (UA) is emerging. The purpose of our study is to evaluate whether UA is associated with atrial fibrosis in AF patients. Design and method: 81 patients who underwent radiofrequency transcatheter ablation for nonvalvular AF at the cardiological department of the Niguarda Hospital were enrolled. UA levels were analysed before the procedure as well as known predictors of atrial fibrosis. High density electroanatomic mapping of the left atrium was performed and patients were divided according to the presence or not of areas of pathological substrate (bipolar voltage < 0.5 mV in sinus rhythm). Results: 19 patients showed a pathological atrial substrate. The population of patients with pathological atrial substrate was older (64.7±1.6 vs 58.2±10.9 years, p=0.032) and had more often a persistent phenotype of AF (84.3 vs 35.8%, p<0.001). UA levels were significantly higher in the pathological group (6.8±1.9 vs 5.3±1.4, p<0.001) as well as the prevalence of hyperuricemia (26.5 vs 6.5%, p=0.021). The association between uric acid and pathological atrial substrate remains significant even after correction for confounding factors (age, left ventricular dysfunction, valvular disease, AF phenotype and furosemide use). Conclusions: In a population of patients who underwent atrial fibrillation's ablation, higher uric acid's levels were significantly associated with pathological left atrium's substrate at electro-anatomical mapping.

Objective: Obstructive sleep apnea (OSA) increases cardiovascular risk in hypertensive patients and decreases the efficacy of treatment.Our study looked at the ABPM data that could be used to diagnose OSA.

Design and method:
We evaluated 117 hypertensive patients who were previously screened for subclinical organ damage for the presence of OSA using the Epworth Sleepiness Scale (ESS), Berlin Questionnaire, and the STOP-BANG questionnaire who underwent home respiratory polygraphy (HRP).For each questionnaire, patients were divided into high-risk and low-risk.The Apnea-Hypopnea index (AHI) was scored according to AASM 2012 criteria.Patients were classified based on the AHI values without OSA (AHI <5), mild OSA (5<= AHI <15), moderate OSA (15<=AHI <30), and severe OSA (AHI =>30).After this, a 24-hour noninvasive ABPM was recorded on a working day.Subjects recorded a journal of the activities performed and the time of retiring to bed, ABPM recordings being divided into 'awake' or 'asleep' periods based on diary entries.

Results:
After HRP, frequencies of without OSA, mild OSA, moderate OSA, and severe OSA were 19 (16.2%), 25 (21.4%),51 (43.5%), and 22 (18.8%),respectively.There is widespread subclinical organ damage in hypertensive patients with moderate to severe OSA (95.7%).We compared the diagnostic accuracy of the three scores in detecting moderate to severe OSA and found that Berlin had the highest sensitivity (87%) and STOP-BANG had the highest specificity (84%), area under the curve (AUC), and PPV.ESS had the lowest sensitivity (63%) and the specificity was intermediate.The hypertensive patients with moderate to severe OSA (OSA positive) compared with those without it (OSA negative) had significantly higher systolic and diastolic BP, significantly increased variability of both systolic and diastolic BP, and a significantly reduced decrease of both nocturnal systolic and diastolic BP.Almost all (94.5%) patients with a riser nocturnal profile had moderate to severe OSA.

Conclusions:
Hypertension and OSA are a common association that is frequently missed.Assessment of patients, based on clinical scores, is essential for the proper management of each case.ABPM results can be an important tool in OSA diagnosis.

Design and method:
We selected 36 patients who received GPA diagnosis (T0) and evaluated them after 1 (T1) and 2 (T2) years follow-up.All patients were treated with high-dose glucocorticoid, one-year tapered, associated with immunosuppressants.Pathological history and a complete list of drugs at different time points were recorded.

Results:
The study reveals noteworthy alterations in lipid profiles, with a substantial increase observed in total cholesterol during both T1 and T2 in comparison to T0.A similar trend was noted in LDLand triglycerides.Conversely, no discernible differences were identified in HDL levels.Additionally, a considerable decrease in high-sensitivity C-reactive protein was observed at T1 and T2 in relation to T0, with no significant variance between T2 and T1.Furthermore, a notable reduction in erythrocyte sedimentation rate was noted at T2 as opposed to both T1 and T0, as well as at T1 compared to T0.Moreover, an interesting observation pertains to hypertensive patients who exhibited a marked escalation in lipid levels, juxtaposed with a gradual reduction in inflammation when compared to normotensive individuals.In particular, notable distinctions emerge between the two groups at both T1 and T2 concerning total cholesterol and LDL (p=0.027),despite comparable baseline values at T0.Then, while triglyceride levels start at similar values at T0, a substantial increase is observed at T1 in hypertensive patients and, conversely, at T2, normotensive individuals experience a significant rise in triglyceride levels, accompanied by a noteworthy reduction in hypertensive subjects.

Conclusions:
The findings indicate that lipid profile alterations, likely influenced by glucocorticoid treatment, may not be directly linked to inflammation.Furthermore, there is a higher relation between hypertension and these alterations.Actual data doesn't reveal increased mortality in hypertensive GPA patients but further research is required to pinpoint specific patterns characterizing cardiovascular risk and progression in this context.

INFLUENCE OF LIVER FIBROSIS ON LIPID METABOLISM IN PATIENTS WITH ARTERIAL HYPERTENSION AND NON-ALCOHOLIC FATTY LIVER DISEASE
Karina Antyukh 1 , Elena Grigorenko 1,2 , Natalya Mitkovskaya 1,2 . 1 Republican Scientific and Practical Center of Cardiology, Minsk, BELARUS, 2 Belarusian State Medical University, Minsk, BELARU Objective: To study the effect of liver fibrosis on lipid metabolism in patients with arterial hypertension (AH) and non-alcoholic fatty liver disease (NAFLD).

Design and method:
A cross-sectional comparative single-center study was conducted, which involved 72 patients of working age (age 25-59 years) with stage I-II AH and NAFLD.The patients were divided into two groups depending on the presence/absence of liver fibrosis: group 1 -patients with hypertension, NAFLD+liver fibrosis (n=34), average age 47.1±8.9 years and group 2 -patients with hypertension, NAFLD without liver fibrosis (n=38), average age 48.6±8.5 years.To analyze lipid metabolism, a detailed lipid profile was performed to determine the content of total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and atherogenic coefficient (AC).All patients underwent abdominal ultrasound and liver elastography to determine the degree of fibrosis according to the METAVIR scale.Statistical analysis of the obtained data was carried out using the statistical program package SPSS 27.0 (IBM, USA).Differences were considered statistically significant at p<0.05.