Despite its importance in everyday clinical practice, the ability of physicians to interpret electrocardiograms (ECGs) is highly variable. ECG patterns are often misdiagnosed, and electrocardiographic emergencies are frequently missed, leading to adverse patient outcomes. Currently, many medical education programs lack an organized curriculum and competency assessment to ensure trainees master this essential skill. ECG patterns that were previously mentioned in literature were organized into groups from A to D based on their clinical importance and distributed among levels of training. Incremental versions of this organization were circulated among members of the International Society of Electrocardiology and the International Society of Holter and Noninvasive Electrocardiology until complete consensus was reached. We present reasonably attainable ECG interpretation competencies for undergraduate and postgraduate trainees. Previous literature suggests that methods of teaching ECG interpretation are less important and can be selected based on the available resources of each education program and student preference. The evidence clearly favors summative trainee evaluation methods, which would facilitate learning and ensure that appropriate competencies are acquired. Resources should be allocated to ensure that every trainee reaches their training milestones and should ensure that no electrocardiographic emergency (class A condition) is ever missed. We hope that these guidelines will inform medical education programs and encourage them to allocate sufficient resources and develop organized curricula. Assessments must be in place to ensure trainees acquire the level-appropriate ECG interpretation skills that are required for safe clinical practice.

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Aims Genetic testing is recommended in specific inherited heart diseases but its role remains unclear and it is not currently recommended in unexplained cardiac arrest (UCA). We sought to assess the yield and clinical utility of genetic testing in UCA using whole-exome sequencing (WES). Methods and results Survivors of UCA requiring external defibrillation were included from the Cardiac Arrest Survivor with Preserved Ejection fraction Registry. Whole-exome sequencing was performed, followed by assessment of rare variants in previously reported cardiovascular disease genes. A total of 228 UCA survivors (mean age at arrest 39 ± 13 years) were included. The majority were males (66%) and of European ancestry (81%). Following advanced clinical testing at baseline, the likely aetiology of cardiac arrest was determined in 21/228 (9%) cases. Whole-exome sequencing identified a pathogenic or likely pathogenic (P/LP) variant in 23/228 (10%) of UCA survivors overall, increasing the proportion of ‘explained’ cases from 9% only following phenotyping to 18% when combining phenotyping with WES. Notably, 13 (57%) of the 23 P/LP variants identified were located in genes associated with cardiomyopathy, in the absence of a diagnosis of cardiomyopathy at the time of arrest. Conclusions Genetic testing identifies a disease-causing variant in 10% of apparent UCA survivors. The majority of disease-causing variants was located in cardiomyopathy-associated genes, highlighting the arrhythmogenic potential of such variants in the absence of an overt cardiomyopathy diagnosis. The present study supports the use of genetic testing including assessment of arrhythmia and cardiomyopathy genes in survivors of UCA.

As an essential constituent of the outer membrane of Gram-negative bacteria, lipopolysaccharide contributes significantly to virulence and antibiotic resistance. The lipopolysaccharide biosynthetic pathway therefore serves as a promising therapeutic target for antivirulence drugs and antibiotic adjuvants. Here we report the structural–functional studies of d-glycero-β-d-manno-heptose 7-phosphate kinase (HldA), an absolutely conserved enzyme in this pathway, from Burkholderia cenocepacia. HldA is structurally similar to members of the PfkB carbohydrate kinase family and appears to catalyze heptose phosphorylation via an in-line mechanism mediated mainly by a conserved aspartate, Asp270. Moreover, we report the structures of HldA in complex with two potent inhibitors in which both inhibitors adopt a folded conformation and occupy the nucleotide-binding sites. Together, these results provide important insight into the mechanism of HldA-catalyzed heptose phosphorylation and necessary information for further development of HldA inhibitors.