European Society of Cardiology: the 2023 Atlas of Cardiovascular Disease Statistics.

This report from the European Society of Cardiology (ESC) Atlas Project updates and expands upon the 2021 report in presenting cardiovascular disease (CVD) statistics for the ESC member countries. This paper examines inequalities in cardiovascular healthcare and outcomes in ESC member countries utilizing mortality and risk factor data from the World Health Organization and the Global Burden of Disease study with additional economic data from the World Bank. Cardiovascular healthcare data were collected by questionnaire circulated to the national cardiac societies of ESC member countries. Statistics pertaining to 2022, or latest available year, are presented. New material in this report includes contemporary estimates of the economic burden of CVD and mortality statistics for a range of CVD phenotypes. CVD accounts for 11% of the EU's total healthcare expenditure. It remains the most common cause of death in ESC member countries with over 3 million deaths per year. Proportionately more deaths from CVD occur in middle-income compared with high-income countries in both females (53% vs. 34%) and males (46% vs. 30%). Between 1990 and 2021, median age-standardized mortality rates (ASMRs) for CVD decreased by median >50% in high-income ESC member countries but in middle-income countries the median decrease was <12%. These inequalities between middle- and high-income ESC member countries likely reflect heterogeneous exposures to a range of environmental, socioeconomic, and clinical risk factors. The 2023 survey suggests that treatment factors may also contribute with middle-income countries reporting lower rates per million of percutaneous coronary intervention (1355 vs. 2330), transcatheter aortic valve implantation (4.0 vs. 153.4) and pacemaker implantation (147.0 vs. 831.9) compared with high-income countries. The ESC Atlas 2023 report shows continuing inequalities in the epidemiology and management of CVD between middle-income and high-income ESC member countries. These inequalities are exemplified by the changes in CVD ASMRs during the last 30 years. In the high-income ESC member countries, ASMRs have been in steep decline during this period but in the middle-income countries declines have been very small. There is now an important need for targeted action to reduce the burden of CVD, particularly in those countries where the burden is greatest.

Artificial intelligence in detecting left atrial appendage thrombus by transthoracic echocardiography and clinical features: the Left Atrial Thrombus on Transoesophageal Echocardiography (LATTEE) registry.

AIMS: Transoesophageal echocardiography (TOE) is often performed before catheter ablation or cardioversion to rule out the presence of left atrial appendage thrombus (LAT) in patients on chronic oral anticoagulation (OAC), despite associated discomfort. A machine learning model [LAT-artificial intelligence (AI)] was developed to predict the presence of LAT based on clinical and transthoracic echocardiography (TTE) features. METHODS AND RESULTS: Data from a 13-site prospective registry of patients who underwent TOE before cardioversion or catheter ablation were used. LAT-AI was trained to predict LAT using data from 12 sites (n = 2827) and tested externally in patients on chronic OAC from two sites (n = 1284). Areas under the receiver operating characteristic curve (AUC) of LAT-AI were compared with that of left ventricular ejection fraction (LVEF) and CHA2DS2-VASc score. A decision threshold allowing for a 99% negative predictive value was defined in the development cohort. A protocol where TOE in patients on chronic OAC is performed depending on the LAT-AI score was validated in the external cohort. In the external testing cohort, LAT was found in 5.5% of patients. LAT-AI achieved an AUC of 0.85 [95% confidence interval (CI): 0.82-0.89], outperforming LVEF (0.81, 95% CI 0.76-0.86, P < .0001) and CHA2DS2-VASc score (0.69, 95% CI: 0.63-0.7, P < .0001) in the entire external cohort. Based on the proposed protocol, 40% of patients on chronic OAC from the external cohort would safely avoid TOE. CONCLUSION: LAT-AI allows accurate prediction of LAT. A LAT-AI-based protocol could be used to guide the decision to perform TOE despite chronic OAC.

Resistin is Associated with Inflammation and Renal Function, but not with Insulin Resistance in Type 2 Diabetes.

The aim of the study was to investigate the association of adipokines (resistin, leptin and adiponectin) with obesity, insulin resistance (IR) and inflammation in type 2 diabetes mellitus (T2DM). A total of 284 patients with T2DM were included. Concentrations of resistin, leptin, adiponectin, and inflammatory markers [high sensitivity C-reactive protein (hsCRP), tumor necrosis factor α (TNF-α), and interleukin 6 (IL-6)] were measured and homeostatic model assessment for IR (HOMA-IR) index was calculated. Resistin correlated negatively with estimated glomerular filtration rate (eGFR) and positively with hsCRP, TNF-α, IL-6, and white blood cell count (WBC). Leptin correlated positively with HOMA-IR, whereas adiponectin correlated negatively. Leptin also correlated positively with body mass index (BMI), waist circumference, IL-6, WBC and negatively with eGFR. Adiponectin correlated negatively with waist circumference, WBC, and eGFR. Multivariate logistic regression indicated lower eGFR and higher WBC and IL-6 as independent predictive factors of resistin concentration above the upper quartile (CAQ3), whereas female sex and higher BMI and HOMA-IR of leptin CAQ3, and lower HOMA-IR and older age of adiponectin CAQ3. In conclusion, in contrast to leptin and adiponectin, in T2DM patients, resistin is not associated with BMI and IR, but with inflammation and worse kidney function.

Vascular disease in patients with atrial fibrillation. A report from Polish participants in the EORP-AF General Long-Term Registry.

AIMS: This study aimed to (1) define the prevalence of vascular disease (VD; coronary (CAD) and/or peripheral artery disease (PAD)) and associated risk factors in patients with atrial fibrillation (AF); (2) establish the relationship of VD and associated treatment patterns on adverse events in AF. METHODS: Data from 701 Polish AF patients enrolled in the EORP-AF General Long-Term Registry in the years 2013-2016 were included in this analysis. During the one-year follow-up, the occurrence of major adverse events (MAE; all-cause death, thromboembolic event, myocardial infraction) and its components was evaluated. RESULTS: VD was recorded in 293 (44%) patients and based on multivariate logistic analysis was associated with age >75, diabetes, hypercholesterolemia, heart failure (HF). There was no significant difference in rates of MAE between patients with and without VD based on Fisher's exact test (8.8% vs 5.7%, P = .16), as well as between patients with concomitant CAD and PAD, PAD and CAD alone based on the Chi-square test (21% vs 7.5% vs 6.7%; P = .09). A higher risk of MAE was associated with HF, chronic kidney disease (in all study group), age >75, HF, diabetes (VD group),chronic obstructive pulmonary disease (non-VD group) based on the multivariate logistic analysis. Relative to patients with VD on vitamin K antagonists (VKA), those treated with non-VKA-oral anticoagulants (NOAC) had lower absolute rate of MAE according to Fisher's exact test (1.4% vs 10%, P = .02) but similar risks for thromboembolic and hemorrhagic events. The concomitant use of triple therapy was associated with increased risk of MAE as compared with those on OAC alone or dual therapy based on the Chi-square test (20% vs 4.8%, 3.2%, P = .02). CONCLUSION: VD was prevalent in almost two-fifths of AF patients. The incidence of MAE was higher in patients with VD on VKA (vs NOAC) and on triple therapy (vs dual therapy, OAC alone) within one-year follow-up.

Thrombus in the left atrial appendage in patients with atrial fibrillation treated with non-vitamin K antagonist oral anticoagulants in clinical practice-A multicenter registry.

BACKGROUND: The prevalence and predictors of left atrial appendage thrombus (LAAT) in patients with non-valvular atrial fibrillation (AF) who have been treated with non-vitamin K antagonist oral anticoagulants (NOACs) are not well defined. We aimed to assess the occurrence and predictors of LAAT on transesophageal echocardiography (TOE) in patients with non-valvular AF treated with NOACs for at least 3 weeks. METHODS: Consecutive patients with non-valvular AF who underwent TOE before catheter ablation or electrical cardioversion in three high-reference centers between 2014 and 2018 were included. Patients on apixaban were excluded from the study due to low numbers in this category. All patients received NOACs for at least 3 weeks before TOE. RESULTS: A total of 1148 patients (female, 38.1%; mean age, 62.1 years) referred to our centers for catheter ablation of AF (52.1%) or electrical cardioversion (47.9%) were included. Patients were on rivaroxaban (51.9%) or dabigatran (48.1%). Preprocedural TOE revealed LAAT in 4.4% of all patients. Multivariable logistic regression analysis showed the CHA2DS2-VASc score ≥2 points (OR = 2.11; 95% CI, 1.15-3.88; P = .0161), non-paroxysmal AF (OR = 6.30; 95% CI, 2.22-17.91; P = .0005), and GFR <60 mL/min/1.73 m2 (OR = 2.05; 95% CI, 1.14-3.67; P = .0160) were independent predictors of LAAT in patients treated with NOACs. CONCLUSIONS: In non-valvular AF patients treated with NOACs, the prevalence of LAAT was 4.4% before electrical cardioversion or ablation. In addition to the CHA2DS2-VASc score, the type of AF and renal function should be considered in the stratification of thromboembolism risk in AF patients and qualification for a preprocedural TOE.

Do Patients With Acute Heart Failure and Preserved Ejection Fraction Have Heart Failure at Follow-Up: Implications of the Framingham Criteria.

BACKGROUND: Heart failure (HF) with preserved ejection fraction (HFpEF) may be misdiagnosed. We assessed prevalence and consistency of Framingham criteria signs and symptoms in acute vs subsequent stable HFpEF. METHODS: Three hundred ninety-nine patients with acute HFpEF according to Framingham criteria were re-assessed in stable condition. Four definitions of HFpEF at follow-up: (1) Framingham criteria alone, (2) Framingham criteria and natriuretic peptides (NPs), (3) Framingham criteria, NPs, and European Society of Cardiology HF guidelines echocardiographic criteria, (4) Framingham criteria, NPs, and the Efficacy and Safety of LCZ696 Compared to Valsartan, on Morbidity and Mortality in Heart Failure Patients With Preserved Ejection Fraction (PARAGON) trial echocardiographic criteria. RESULTS: At follow-up, HFpEF was still present in 27%, 22%, 21%, and 22%, respectively. Most prevalent in acute HFpEF were dyspnea at exertion (90%), pulmonary rales (71%), persisting at follow-up in 70% and 13%, respectively. Characteristics at acute HF with greater or lesser odds of stable HFpEF; (1) jugular venous distention (odds ratio [OR] 1.80, 95% confidence interval [CI] 1.13-2.87; P = .013) and pleural effusion (OR 0.45, 95% CI 0.24-0.85; P = .014) and (4), older age (1.04, 95% CI 1.01-1.08; P = .014) and tachycardia (>100 bpm) 0.52, 95% CI 0.27-1.00; P = .048). CONCLUSIONS: In patients with acute HFpEF, one-quarter met the HF definition according to Framingham criteria at ambulatory follow-up. The proportion of patients with postdischarge HFpEF was largely unaffected by additional echocardiographic or NP criteria Older age and jugular venous distention at acute presentation predicted persistent HFpEF at follow-up, whereas pleural effusion and tachycardia may yield false HFpEF diagnoses. This finding has implications for HFpEF trial design.

Randomized controlled trial protocol to investigate the antiplatelet therapy effect on extracellular vesicles (AFFECT EV) in acute myocardial infarction.

Activated platelets contribute to thrombosis and inflammation by the release of extracellular vesicles (EVs) exposing P-selectin, phosphatidylserine (PS) and fibrinogen. P2Y12 receptor antagonists are routinely administered to inhibit platelet activation in patients after acute myocardial infarction (AMI), being a combined antithrombotic and anti-inflammatory therapy. The more potent P2Y12 antagonist ticagrelor improves cardiovascular outcome in patients after AMI compared to the less potent clopidogrel, suggesting that greater inhibition of platelet aggregation is associated with better prognosis. The effect of ticagrelor and clopidogrel on the release of EVs from platelets and other P2Y12-exposing cells is unknown. This study compares the effects of ticagrelor and clopidogrel on (1) the concentrations of EVs from activated platelets (primary end point), (2) the concentrations of EVs exposing fibrinogen, exposing PS, from leukocytes and from endothelial cells (secondary end points) and (3) the procoagulant activity of plasma EVs (tertiary end points) in 60 consecutive AMI patients. After the percutaneous coronary intervention, patients will be randomized to antiplatelet therapy with ticagrelor (study group) or clopidogrel (control group). Blood will be collected from patients at randomization, 48 hours after randomization and 6 months following the index hospitalization. In addition, 30 age- and gender-matched healthy volunteers will be enrolled in the study to investigate the physiological concentrations and procoagulant activity of EVs using recently standardized protocols and EV-dedicated flow cytometry. Concentrations of EVs will be determined by flow cytometry. Procoagulant activity of EVs will be determined by fibrin generation test. The compliance and response to antiplatelet therapy will be assessed by impedance aggregometry. We expect that plasma from patients treated with ticagrelor (1) contains lower concentrations of EVs from activated platelets, exposing fibrinogen, exposing PS, from leukocytes and from endothelial cells and (2) has lower procoagulant activity, when compared to patients treated with clopidogrel. Antiplatelet therapy effect on EVs may identify a new mechanism of action of ticagrelor, as well as create a basis for future studies to investigate whether lower EV concentrations are associated with improved clinical outcomes in patients treated with P2Y12 antagonists.

Decreased left atrial appendage emptying velocity as a link between atrial fibrillation type, heart failure and older age and the risk of left atrial thrombus in atrial fibrillation.

INTRODUCTION: Decreased left atrial appendage emptying velocity (LAAV) is a known predictor of LAA thrombus in atrial fibrillation (AF). The aim of our study was to identify which of the clinical risk factors for LAA thrombus are associated with decreased LAAV. METHODS: The study included 1476 consecutive AF patients who underwent transesophageal echocardiography (TEE) before AF direct current cardioversion or ablation in two high-reference cardiology departments. Patients were divided into two groups: 71 (4.8%) patients with LAAV < 20 cm/s and 1405 patients (95%) with LAAV ≥ 20 cm/s. RESULTS: Compared with patients with LAAV ≥ 20 cm/s, those with decreased LAAV were older, more often had non-paroxysmal AF, were burdened with more concomitant diseases (including hypertension, diabetes, vascular disease, and heart failure [HF]) with higher median CHA2 DS2 -VASc score (3 [2-4] vs 2 [1-3], P < .0001), and had lower glomerular filtration rate (GFR). Prevalence of LAA thrombus was higher in patients with decreased LAAV compared with those with LAAV ≥ 20cm/s (20% vs 4.6%, P < .0001). In patients with decreased LAAV, there was no difference in the frequency of LAA thrombus between those treated with VKA and those receiving NOAC, while in patients with LAAV ≥ 20 cm/s a trend was observed towards a benefit with NOAC. In multivariate logistic regression, non-paroxysmal AF, HF and age ≥ 65 years predicted both LAAV < 20 cm/s and LAA thrombus, while GFR < 60 mL/min/1.73 m2 predicted only the presence of LAA thrombus. CONCLUSION: One in five AF patients with decreased LAAV had LAA thrombus, regardless of the type of OAC. Non-paroxysmal AF, HF and age ≥ 65 years might increase LAA thrombus risk via reduced LAAV.

Resistin is a prognostic factor for death in type 2 diabetes.

PURPOSE: To investigate the association of leptin, resistin, and tumour necrosis factor α (TNF-α) with prognosis in type 2 diabetes (T2D). METHODS: Analysis included 284 T2D patients. Apart from routine laboratory parameters, baseline leptin, resistin, and TNF-α concentrations were measured. Patients were followed for a median of 5.4 years. The primary endpoint was all-cause death at follow-up. The secondary endpoint was a composite of death, acute coronary syndrome, and stroke or transient ischemic attack. RESULTS: At baseline, median age was 68 years, and 48% of patients were female. Data on the primary endpoint were obtained for all patients: 32 (11%) died during follow-up. Data on the secondary endpoint were available for 230 patients, of whom 45 (20%) reached the secondary endpoint. In univariate analyses, older age, heart failure, lower-glomerular filtration rate, and higher resistin, TNF-α and NT-proBNP concentrations were predictors of the study endpoints. Of these variables, only resistin remained an independent predictor of both study endpoints in multivariate models. In receiver-operating characteristic analysis, area under the curve for resistin was 0.7. Resistin concentration of greater than or equal to 11.4 ng/mL had sensitivity of 41% and specificity of 91% for prediction of death at follow-up (Youden's index). CONCLUSIONS: Higher resistin is associated with reduced survival in T2D, irrespectively of TNF-α. Resistin concentration of above 11 ng/mL indicates T2D patients at an increased risk of unfavourable outcomes. Leptin was not a prognostic factor. These results suggest that in T2D, association of resistin with unfavourable outcomes might, at least in part, result from its pro-inflammatory properties.

Comparative Analysis of Long-Term Outcomes of Torasemide and Furosemide in Heart Failure Patients in Heart Failure Registries of the European Society of Cardiology.

PURPOSE: Current clinical recommendations do not emphasise superiority of any of diuretics, but available reports are very encouraging and suggest beneficial effects of torasemide. This study aimed to compare the effect of torasemide and furosemide on long-term outcomes and New York Heart Association (NYHA) class change in patients with chronic heart failure (HF). METHODS: Of 2019 patients enrolled in Polish parts of the heart failure registries of the European Society of Cardiology (Pilot and Long-Term), 1440 patients treated with a loop diuretic were included in the analysis. The main analysis was performed on matched cohorts of HF patients treated with furosemide and torasemide using propensity score matching. RESULTS: Torasemide was associated with a similar primary endpoint (all-cause death; 9.8% vs. 14.1%; p = 0.13) occurrence and 23.8% risk reduction of the secondary endpoint (a composite of all-cause death or hospitalisation for worsening HF; 26.4% vs. 34.7%; p = 0.04). Treatment with both torasemide and furosemide was associated with the significantly most frequent occurrence of the primary (23.8%) and secondary (59.2%) endpoints. In the matched cohort after 12 months, NYHA class was higher in the furosemide group (p = 0.04), while furosemide use was associated with a higher risk (20.0% vs. 12.9%; p = 0.03) of worsening ≥ 1 NYHA class. Torasemide use impacted positively upon the primary endpoint occurrence, especially in younger patients (aged < 65 years) and with dilated cardiomyopathy. CONCLUSIONS: Our findings contribute to the body of research on the optimal diuretic choice. Torasemide may have advantageous influence on NYHA class and long-term outcomes of HF patients, especially younger patients or those with dilated cardiomyopathy, but it needs further investigations in prospective randomised trials.

Next-generation re-sequencing of genes involved in increased platelet reactivity in diabetic patients on acetylsalicylic acid.

The objective of this study was to investigate whether rare missense genetic variants in several genes related to platelet functions and acetylsalicylic acid (ASA) response are associated with the platelet reactivity in patients with diabetes type 2 (T2D) on ASA therapy. Fifty eight exons and corresponding introns of eight selected genes, including PTGS1, PTGS2, TXBAS1, PTGIS, ADRA2A, ADRA2B, TXBA2R, and P2RY1 were re-sequenced in 230 DNA samples from T2D patients by using a pooled PCR amplification and next-generation sequencing by Illumina HiSeq2000. The observed non-synonymous variants were confirmed by individual genotyping of 384 DNA samples comprising of the individuals from the original discovery pools and additional verification cohort of 154 ASA-treated T2DM patients. The association between investigated phenotypes (ASA induced changes in platelets reactivity by PFA-100, VerifyNow and serum thromboxane B2 level [sTxB2]), and accumulation of rare missense variants (genetic burden) in investigated genes was tested using statistical collapsing tests. We identified a total of 35 exonic variants, including 3 common missense variants, 15 rare missense variants, and 17 synonymous variants in 8 investigated genes. The rare missense variants exhibited statistically significant difference in the accumulation pattern between a group of patients with increased and normal platelet reactivity based on PFA-100 assay. Our study suggests that genetic burden of the rare functional variants in eight genes may contribute to differences in the platelet reactivity measured with the PFA-100 assay in the T2DM patients treated with ASA.

Serum Brain-Derived Neurotrophic Factor is Related to Platelet Reactivity but not to Genetic Polymorphisms within BDNF Encoding Gene in Patients with Type 2 Diabetes.

BACKGROUND: The aim of this study was to investigate the association between serum concentrations of the brain-derived neurotrophic factor (BDNF), platelet reactivity and inflammatory markers, as well as its association with BDNF encoding gene variants in type 2 diabetic patients (T2DM) during acetylsalicylic acid (ASA) therapy. MATERIAL/METHODS: This retrospective, open-label study enrolled 91 patients. Serum BDNF, genotype variants, hematological, biochemical, and inflammatory markers were measured. Blood samples were taken in the morning 2-3 h after the last ASA dose. The BDNF genotypes for selected variants were analyzed by use of the iPLEX Sequenom assay. RESULTS: In multivariate linear regression analysis, CADP-CT >74 sec (p<0.001) and sP-selectin concentration (p=0.03) were predictive of high serum BDNF. In multivariate logistic regression analysis, CADP-CT >74 sec (p=0.02) and IL-6 concentration (p=0.03) were risk factors for serum BDNF above the median. Non-significant differences were observed between intronic SNP rs925946, missense SNP rs6265, and intronic SNP rs4923463 allelic groups and BDNF concentrations in the investigated cohort. CONCLUSIONS: Chronic inflammatory condition and enhanced immune system are associated with the production of BDNF, which may be why the serum BDNF level in T2DM patients with high platelet reactivity was higher compared to subjects with normal platelet reactivity in this study.

Younger age, higher body mass index and lower adiponectin concentration predict higher serum thromboxane B2 level in aspirin-treated patients with type 2 diabetes: an observational study.

BACKGROUND: Evidence from the literature suggests diminished acetylsalicylic acid (ASA) treatment efficacy in type 2 diabetes (DM2). High on-aspirin platelet reactivity (HAPR) in DM2 has been linked to poor glycemic and lipid control. However, there are no consistent data on the association between HAPR and insulin resistance or adipose tissue metabolic activity. The aim of this study was to assess the relationship between laboratory response to ASA and metabolic control, insulin resistance and adipokines in DM2. METHODS: A total of 186 DM2 patients treated with oral antidiabetic drugs and receiving 75 mg ASA daily were included in the analysis. Response to ASA was assessed by measuring serum thromboxane B2 (TXB2) concentration and expressed as quartiles of TXB2 level. The achievement of treatment targets in terms of glycemic and lipid control, insulin resistance parameters (including Homeostatic Model Assessment-Insulin Resistance, HOMA-IR, index), and serum concentrations of high-molecular weight (HMW) adiponectin, leptin and resistin, were evaluated in all patients. Univariate and multivariate logistic regression analyses were performed to determine the predictive factors of serum TXB2 concentration above the upper quartile and above the median. RESULTS: Significant trends in age, body mass index (BMI), HOMA-IR, HMW adiponectin concentration, C-reactive protein concentration and the frequency of achieving target triglyceride levels were observed across increasing quartiles of TXB2. In a multivariate analysis, only younger age and higher BMI were independent predictors of TXB2 concentration above the upper quartile, while younger age and lower HMW adiponectin concentration were predictors of TXB2 concentration above the median. CONCLUSIONS: These results suggest that in DM2, the most important predictor of HAPR is younger age. Younger DM2 patients may therefore require total daily ASA doses higher than 75 mg, preferably as a twice-daily regimen, to achieve full therapeutic effect. Higher BMI and lower HMW adiponectin concentration were also associated with less potent ASA effect. This is the first study to demonstrate an association of lower adiponectin concentration with higher serum TXB2 level in patients treated with ASA.

Position paper of the Polish Expert Group on the use of pitavastatin in the treatment of lipid disorders in Poland endorsed by the Polish Lipid Association.

Lipid disorders, primarily hypercholesterolemia, are the most common cardiovascular (CV) risk factor in Poland (this applies even 3/4 of people). The low-density lipoprotein cholesterol (LDL-C) serum level is the basic lipid parameter that should be measured to determine CV risk and determines the aim and target of lipid-lowering treatment (LLT). Lipid-lowering treatment improves cardiovascular prognosis and prolongs life in both primary and secondary cardiovascular prevention. Despite the availability of effective lipid-lowering drugs and solid data on their beneficial effects, the level of LDL-C control is highly insufficient. This is related, among other things, to physician inertia and patients' fear of side effects. The development of lipidology has made drugs available with a good safety profile and enabling personalisation of therapy. Pitavastatin, the third most potent lipid-lowering statin, is characterised by a lower risk of muscle complications and new cases of diabetes due to its being metabolised differently. Thus, pitavastatin is a very good therapeutic option in patients at high risk of diabetes or with existing diabetes, and in patients at cardiovascular risk. This expert opinion paper attempts at recommendation on the place and possibility of using pitavastatin in the treatment of lipid disorders.

Incidence and predictors of device-related thrombus after left atrial appendage closure with Watchman device.

Introduction: Left atrial appendage closure (LAAC) with Watchman device prevents thromboembolism in patients with atrial fibrillation (AF). However, thrombus may develop on the atrial surface of the device. Aim: To investigate the incidence and predictors of device-related thrombus (DRT) in patients with AF who were treated with LAAC. Material and methods: Ninety-one consecutive patients with AF underwent LAAC procedure using first-generation Watchman 2.5 device followed by antiplatelet therapy. In our analysis we have included all patients (n = 78) who had clinical follow-up visits with transesophageal echocardiography (TEE) after the procedure. Results: The median (IQR) CHA2DS2-VASc score was 4 (4.0-6.0) and HAS-BLED score was 3 (3.0-4.0). DRTs were observed in 5 (6.4%) patients. When compared with patients without DRT, those with DRT presented more often with lower median ejection fraction (40% (23.5-45.5) versus 55% (48.0-60.0); p = 0.005), lower emptying velocity of LAA (25 cm/s (17.5-27.0) versus 53 cm/s (26.5-78.0); p = 0.009), and with greater depth of implantation (18 mm (14.0-20.5) versus 8 mm (5.0-11.0); p < 0.001). Furthermore, patients with DRT had greater depth of LAA (35 mm (29.5-41.0) versus 29 mm (25.5-31.0); p = 0.003), greater mean (SD) dimension in 900 (22.4 mm (3.2) versus 19 mm (2.7); p = 0.02). Patients with DRT were also younger than those without DRT (67.4 years (7) versus 75 years (8.3), p = 0.045). Conclusions: The DRT after Watchman device implantation remains a rare complication. Its formation was related to several patient and procedural characteristics, which need to be confirmed in larger studies.

Clinical and echocardiographic characterization of patients hospitalized for severe tricuspid valve regurgitation: a single tertiary-care center experience with 2-year follow-up.

INTRODUCTION: Tricuspid regurgitation (TR) is a common acquired valvular heart disease. Recently, new transcatheter treatment options for severe TR have emerged that could change management of this condition, which warrants better characterization of this specific patient group. OBJECTIVES: The aim of the study was to describe the clinical and echocardiographic characteristics of patients with severe TR and to evaluate their short- and mid­term prognosis. PATIENTS AND METHODS: This retrospective, observational, single­center study enrolled consecutive patients with severe TR hospitalized between January 2016 and September 2021 in the Department of Cardiology, Medical University of Warsaw, Poland. The severity of heart failure (HF) was evaluated using the New York Heart Association classification. Echocardiographic assessment was performed by an experienced sonographer. EuroSCORE II and TRI­SCORE models were computed for each patient, and 12- and 24­month clinical outcomes were reported. RESULTS: The study comprised 172 patients (93 women [54.1%]) at a mean (SD) age of 76.4 (10.5) years. The most common comorbidities included: atrial fibrillation (84.9%), hypertension (68%), chronic kidney disease (54.1%), coronary artery disease (45.3%), and diabetes mellitus (30.9%). The median (interquartile range) EuroSCORE II and TRI­SCORE values were 4.68% (2.88%-8.05%) and 14% (5%-34%), respectively. The median follow­up was 24 (8.5-41) months. The overall mortality was 29.7% at 1 year and 47.3% at 2 years. TR grade, tricuspid annular plane systolic excursion (TAPSE) above 17 mm, TAPSE to systolic pulmonary artery pressure ratio below 0.26, and increased right atrial area were significant factors associated with mortality. CONCLUSIONS: Patients presenting with severe TR are characterized by a large comorbidity burden and poor prognosis, despite intensive HF management.

Oral anticoagulation therapy in atrial fibrillation patients at high risk of bleeding: Clinical characteristics and treatment strategies based on data from the Polish multicenter register of atrial fibrillation (POL-AF).

BACKGROUND: Despite its benefits, oral anticoagulant (OAC) therapy in patients with atrial fibrillation (AF) is associated with hemorrhagic complications. AIMS: We aimed to evaluate clinical characteristics of AF patients at high risk of bleeding and the frequency of OAC use as well as identify factors that predict nonuse of OACs in these patients. METHODS: Consecutive AF patients hospitalized for urgent or planned reasons in cardiac centers were prospectively included in the registry in 2019. Patients with HAS-BLED ≥3 (high HAS-BLED group) were assumed to have a high risk of bleeding. RESULTS: Among 3598 patients enrolled in the study, 29.2% were at high risk of bleeding (44.7% female; median [Q1-Q3] age 72 [65-81], CHA2DS2-VASc score 5 [4-6], HAS-BLED 3 [3-4]). In this group, 14.5% of patients did not receive OACs, 68% received NOACs, and 17.5% VKAs. In multivariable analysis, the independent predictors of nonuse of oral OACs were as follows: creatinine level (odds ratio [OR], 1.441; 95% confidence interval [CI], 1.174-1.768; P <0.001), a history of gastrointestinal bleeding (OR, 2.918; 95% CI, 1.395-6.103; P = 0.004), malignant neoplasm (OR, 3.127; 95% CI, 1.332-7.343; P = 0.009), and a history of strokes or transient ischemic attacks (OR, 0.327; 95% CI, 0.166-0.642; P = 0.001). CONCLUSIONS: OACs were used much less frequently in the group with a high HAS-BLED score than in the group with a low score. Independent predictors of nonuse of OACs were creatinine levels, a history of gastrointestinal bleeding, and malignant neoplasms. A history of stroke or transient ischemic attack increased the chances of receiving therapy.

Can transesophageal echocardiography be safely omitted in patients scheduled for elective ablation of atrial arrhythmias? Data based on the LATTEE registry.

BACKGROUND: According to the present guidelines, transesophageal echocardiography (TEE) before scheduled catheter ablation (CA) for atrial arrhythmias (atrial fibrillation [AF] or atrial flutter [AFL]) is not deemed obligatory for optimally anticoagulated patients. However, daily clinical practice significantly differs from the recommendations. AIMS: We aimed to identify transthoracic echocardiographic parameters that could be useful in identifying patients without left atrial thrombus (LAT), which makes it possible to avoid unnecessary TEE before scheduled CA. METHODS: This is a sub-analysis of a multicenter, prospective, observational study - the LATTEE registry. A total of 1346 patients referred for TEE before scheduled CA of AF/AFL were included. RESULTS: LAT was present in 44 patients (3.3%) and absent in the remaining 1302, who were younger, more likely to have paroxysmal AF, and displayed sinus rhythm during TEE. Additionally, they exhibited a lower incidence of heart failure, diabetes, systemic connective tissue disease, and chronic obstructive pulmonary disease. Furthermore, they had a lower CHA2DS2-VASc score and a higher prevalence of direct oral anticoagulants. Echocardiographic parameters, including left ventricular ejection fraction (LVEF) >65%, left atrial diameter (LAD) <40 mm, left atrial area (LAA) <20 cm2, left atrial volume (LAV) <113 ml, and left atrial volume index (LAVI) <51 ml/m2, demonstrated 100% sensitivity and 100% negative predictive value for the absence of LAT and were met by 417 patients. Additional echocardiographic indices: LVEF/LAD ≥1.4, LVEF/LAVI ≥1.6, and LVEF/LAA ≥2.7 identified 57 additional patients, bringing the total of predicted LAT-free patients to 474 (35%). CONCLUSIONS: Simple echocardiographic parameters could help identify individuals for whom TEE could be safely omitted before elective CA due to atrial arrhythmias.

New single nucleotide polymorphisms associated with differences in platelets reactivity in patients with type 2 diabetes treated with acetylsalicylic acid: genome-wide association approach and pooled DNA strategy.

The objective of this study was to use genome-wide association approach and pooled DNA strategy to search for new genomic loci associated with inter-individual differences in platelet reactivity in the diabetic patients during acetylsalicylic acid (ASA) treatment. Study cohort consisted of 297 diabetic patients who had been taking ASA (75 mg daily) for at least 3 months. We tested association of single nucleotide polymorphisms (SNPs) genotyped using high density microarray platform with several platelet reactivity assays, followed by individual genotyping of most significant SNPs identified in the microarray genomic scan. The highest statistical significance (p value of 0.0001-0.008 in individual genotyping) was observed for SNP located within the regulatory G-protein signaling (RGS) 7 gene (rs2502448) using recessive genetic model. The diabetic patients on ASA treatment and homozygotes for its minor allele were characterized by increased odds ratio of at 3.45 (confidence interval: 1.82-6.53) for high on ASA platelet reactivity (i.e. impaired ASA response) when compared with homozygotes for wild-type allele. The genome-wide approach might provide an opportunity to identify novel candidate genes and pathways related to platelet activation in diabetic patients.

Effect of common single-nucleotide polymorphisms in acetylsalicylic acid metabolic pathway genes on platelet reactivity in patients with diabetes.

BACKGROUND: Platelet reactivity in patients on acetylsalicylic acid (ASA) therapy can be influenced by physiological or pathological conditions affecting ASA pharmacokinetics or pharmacodynamics. The mechanism of such variability in the therapeutic response to ASA, particularly in diabetic patients, is poorly understood. The rate of elimination of ASA and its metabolite, salicylic acid (SA), is likely a major factor determining drug efficacy. The objective of this study was to investigate the effect of genetic polymorphisms in the selected candidate genes within the ASA metabolic pathway on the platelet reactivity and concentration of ASA and thromboxane A(2) (TxA(2)) metabolites in a population of patients with type 2 diabetes mellitus (T2DM). MATERIAL AND METHODS: The study cohort consisted of 287 Caucasians with T2DM who had been taking ASA tablets at the dose of 75 mg per day for at least 3 months. Platelet reactivity analyses were performed using VerifyNow Aspirin and PFA-100 assays. The measured ASA metabolite included salicylic acid (ASA), and TxA(2) metabolites included serum TxB(2) and urinary 11-dh-TxB(2). Genotyping for the selected 18 single-nucleotide polymorphisms (SNPs) within 5 genes of the ASA metabolic pathway was performed using a Sequenom iPLEX platform. RESULTS: No statistically significant association was observed between the investigated SNPs genotypes, platelet reactivity, and measured metabolites in the investigated cohort of patients. CONCLUSIONS: The results of our study failed to confirm that the selected variants in the genes within the ASA metabolic pathway might contribute to platelet reactivity in a diabetic population treated with ASA.