Radiofrequency ablation (RFA) for the treatment of paroxysmal Atrial Fibrillation (pAF) has a class 1 indication in patients who have not tolerated or responded to antiarrhythmic medications. Antiarrhythmic medications (AAM) are, however, limited not only by modest efficacy, but also by significant side effects. Discontinuation rates for AAM range from 11-40% in trials. The RAAFT-2 trial evaluates the use of RFA as a first line treatment for pAF compared to optimal pharmacological management (1).

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Purpose of reviewThis article summarises current understanding of the genetic architecture underpinning left ventricular noncompaction (LVNC) and highlights the difficulty in differentiating LVNC from hypertrabeculation seen in normal, healthy individuals, that caused by physiological adaptation or that seen in association with cardiomyopathy phenotypes. Recent findingsProgress has been made in better defining the LVNC phenotype and those patients who may benefit from genetic testing. Yield of diagnostic genetic testing may be low in the absence of syndromic features, systolic dysfunction and a family history of cardiomyopathy. Sarcomeric gene variants are most commonly identified but a wide-range of genes are implicated, emphasising the high degree of heterogeneity of studied cohorts. SummaryMore accurate phenotyping and genotype-phenotype correlation are required to better characterise the genetic architecture of LVNC.

Complication rates were not significantly different between groups. These findings suggest that VT and PVC ablation can be performed safely in patients with uninterrupted antithrombotic medications.