Background—: Transesophageal echocardiography (TEE) is the gold standard for the exclusion of thrombi in the left atrial appendage (LAA) before ablation for atrial fibrillation. Intracardiac echocardiography (ICE) is used to assist atrial fibrillation ablation; however, it can also be used for LAA imaging. The aim of our study was to determine whether ICE could replace TEE and to identify the optimal ICE placement for LAA visualization. Methods and Results—: Seventy-six consecutive patients (56 men; mean age, 55±9.6 years) scheduled for atrial fibrillation ablation underwent TEE before the procedure and LAA assessment by ICE. An 8F AcuNav probe was introduced into right atrium, pulmonary artery, and coronary sinus. LAA structure was analyzed by the echocardiographer and electrophysiologist who were blinded to the results of TEE. ICE probe was positioned in the right atrium in all patients, in the pulmonary artery in 64 of 74 (86%) patients, and in the coronary sinus in 49 of 74 (66%) patients. The LAA was properly visualized in 56 of 64 (87.5%) patients from the pulmonary artery versus 13 of 49 (26%) patients from the coronary sinus ( P <0.001). From the right atrium, the whole LAA cavity could not be seen in any patient. In those patients in whom LAA was visualized properly by ICE, a perfect agreement between ICE and TEE was obtained (both techniques detected LAA thrombus in 2 patients and excluded LAA thrombus in the remaining patients). Conclusions—: ICE can be used safely and effectively for the evaluation of LAA in patients undergoing atrial fibrillation ablation. ICE imaging from pulmonary artery is accurate for LAA visualization. Clinical Trial Registration—: URL: http://www.clinicaltrials.gov . Unique identifier: NCT01371279.

Atrial fibrillation (AF) increases the risk of thromboembolic events by promoting clot formation in the left atrial appendage (LAA). Transesophageal echocardiography (TEE) is routinely used to exclude the presence of an LAA thrombus before AF ablation. So far, it has not been established what is the optimal combination of noninvasive parameters for thromboembolic risk stratification in this setting and whether patients at very low risk require TEE. The aim of the study was to assess predisposing factors for an LAA thrombus in patients scheduled for AF ablation and to identify those patients in whom preprocedural TEE is not necessary. In consecutive 151 patients (107 men; mean age, 57 ±10 years) the type of AF and renal function were assessed in addition to the CHA2DS2VASc score to improve thromboembolic risk stratification. An LAA thrombus or dense echo contrast with a strong suspicion of a probable thrombus was detected in 15 patients (10%). Diabetes, age of 65 years or older, persistent AF, and estimated glomerular filtration rate (eGFR) of less than 60 ml/min/1.73 m2 were predictors of the LAA thrombus. A multivariate logistic regression analysis showed that only persistent AF and an eGFR of less than 60 ml/min/1.73 m2 were independent predictors of the LAA thrombus. The receiver operating characteristic curves showed that the greatest area under the curve (0.845) was achieved for the CHA2DS2VASc-AFR (CHA2DS2VASc plus the type of AF and renal function); the difference was not significant. A CHA2DS2VASc-AFR score of 2 or greater or a CHA2DS2VASc score of 1 or greater identified patients with the LAA thrombus with a sensitivity of 100% (and specificity of 54% and 36%, respectively). In patients scheduled for AF ablation, an LAA thrombus or dense echo contrast is a relatively common finding despite routine anticoagulant treatment. The addition of AF type and renal function to the CHA2DS2VASc score slightly improves thromboembolic risk stratification and may help identify patients who do not need preprocedural TEE.

Obesity is strongly associated with an increased risk of heart failure. Recent studies indicate that epicardial adipose tissue plays a critical role in the development of obesity-related cardiomyopathy. This distinct visceral fat depot, located between the myocardium and the visceral pericardium, is involved in direct cross-talk with the adjacent myocardium, influencing both its structural integrity and electrophysiological function. This review aims to provide an up-to-date overview of the morphological, metabolic, immunological, and functional alterations of this adipose compartment in the context of obesity, and to explore its contribution to the pathogenesis of heart failure. Moreover, the article synthesizes current evidence on the potential cardioprotective effects of emerging anti-obesity pharmacotherapies—particularly GLP-1 and dual GLP-1/GIP receptor agonists—on metabolic pathways associated with epicardial fat that are implicated in obesity-induced cardiomyopathy. Further clinical trials are required to clarify the impact of these therapies on the course and prognosis of heart failure, as well as on the epidemiology and societal burden of the disease.

Background: Chronotropic incompetence in patients taking beta-blockers is associated with poor prognosis; however, its impact on exercise capacity (EC) remains unclear. Methods: We analyzed data from consecutive patients taking beta-blockers referred for cardiopulmonary exercise testing to assess EC. Chronotropic incompetence was defined as chronotropic index (CI) ≤ 62%. Results: Among 140 patients all taking beta-blockers (age 61 ± 9.7 years; 73% males), 64% with heart failure, chronotropic incompetence was present in 80.7%. EC assessed as peak oxygen uptake was lower in the group with chronotropic incompetence, 18.3 ± 5.7 vs. 24.0 ± 5.3 mL/kg/min, p < 0.001. EC correlated positively with CI (β = 0.14, p < 0.001) and male gender (β = 5.12, p < 0.001), and negatively with age (β = −0.17, p < 0.001) and presence of heart failure (β = −3.35, p < 0.001). Beta-blocker dose was not associated with EC. Partial correlation attributable to CI accounted for more than one-third of the variance in EC explained by the model (adjusted R² = 59.8%). Conclusions: In patients taking beta-blockers, presence of chronotropic incompetence was associated with lower EC, regardless of the beta-blocker dose. CI accounted for more than one-third of EC variance explained by our model.