Assessment of Esophageal Shifts during Catheter Ablation of Atrial Fibrillation Using Intracardiac Ultrasound Integrated with 3-Dimensional Electroanatomical Mapping System.

Purpose: Atrioesophageal fistula is one of the most feared complications of radiofrequency catheter ablation (RFCA) of atrial fibrillation (AF) as it is associated with high mortality. Determining the esophagus location during RFCA might reduce the risk of esophageal injury. The present study aims to evaluate the feasibility of using intracardiac echocardiography integrated into a 3-dimensional electroanatomical mapping system (ICE/3D EAM) for the assessment of esophageal position and shifts in response to ablation. Methods: We prospectively enrolled 20 patients that underwent RFCA of AF under conscious analgosedation. The virtual anatomy of the left atrium, the pulmonary vein (PV) ostia, and the esophagus was created with ICE/3D EAM. The esophageal positions were obtained at the beginning of the procedure and then after left and right PV isolation (PVI). Esophageal shifts were measured offline after the procedure using the tools available in the 3D EAM system. Results: Most esophagi moved away from the ablated PV ostia. After the left PVI, the median of the shifts was 2.8 mm (IQR 1.0-6.3). In 25% of patients, the esophagus shifted by >5.0 mm (max. 13.4 mm). After right PVI, the median of shifts was 2.0 mm (IQR 0.7-4.9). In 10% of patients, the esophageal shift was >5.0 mm (max. 7.8 mm). Conclusions: ICE/3D EAM enables the intraprocedural visualization of baseline esophageal position and its shifts after PVI. The shifts are variable, but they tend to be small and directed away from the ablation site. Repeated intraprocedural visualization of the esophagus may be needed to reduce the risk of esophageal injury.

Lipoprotein(a) in atherosclerosis: from pathophysiology to clinical relevance and treatment options.

Lipoprotein(a) (Lp(a)) was discovered more than 50 years ago, and a decade later, it was recognized as a risk factor for coronary artery disease. However, it has gained importance only in the past 10 years, with emergence of drugs that can effectively decrease its levels. Lp(a) is a low-density lipoprotein (LDL) with an added apolipoprotein(a) attached to the apolipoprotein B component via a disulphide bond. Circulating levels of Lp(a) are mainly genetically determined. Lp(a) has many functions, which include proatherosclerotic, prothrombotic and pro-inflammatory roles. Here, we review recent data on the role of Lp(a) in the atherosclerotic process, and treatment options for patients with cardiovascular diseases. Currently 'Proprotein convertase subtilisin/kexin type 9' (PCSK9) inhibitors that act through non-specific reduction of Lp(a) are the only drugs that have shown effectiveness in clinical trials, to provide reductions in cardiovascular morbidity and mortality. The effects of PCSK9 inhibitors are not purely through Lp(a) reduction, but also through LDL cholesterol reduction. Finally, we discuss new drugs on the horizon, and gene-based therapies that affect transcription and translation of apolipoprotein(a) mRNA. Clinical trials in patients with high Lp(a) and low LDL cholesterol might tell us whether Lp(a) lowering per se decreases cardiovascular morbidity and mortality.KEY MESSAGESLipoprotein(a) is an important risk factor in patients with cardiovascular diseases.Lipoprotein(a) has many functions, which include proatherosclerotic, prothrombotic and pro-inflammatory roles.Treatment options to lower lipoprotein(a) levels are currently scarce, but new drugs are on the horizon.