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Dilated cardiomyopathy (DCM) is a common yet challenging cardiac disease. Great strides have been made in improving DCM prognosis due to heart failure but sudden cardiac death (SCD) due to ventricular arrhythmias remains significant and challenging to predict. High-risk patients can be effectively managed with implantable cardioverter defibrillators (ICDs) but because identification of what is high risk is very limited, many patients unnecessarily experience the morbidity associated with an ICD implant and many others are not identified and have preventable mortality. Current guidelines recommend use of left ventricular ejection fraction and New York Heart Association class as the main markers of risk stratification to identify patients who would be at higher risk of SCD. However, when analysing the data from the trials that these recommendations are based on, the number of patients in whom an ICD delivers appropriate therapy is modest. In order to improve the effectiveness of therapy with an ICD, the patients who are most likely to benefit need to be identified. This review article presents the evidence behind current guideline-directed SCD risk markers and then explores new potential imaging, electrophysiological and genetic risk markers for SCD in DCM. [ABSTRACT FROM AUTHOR]

A 72 year old woman presented with A troponin positive acute coronary syndrome and was transferred to a tertiary centre a week later. Her admission ECG showed minimal ST depression in V2-V6 with a sinus bradycardia of 38 beats/mm. There was resolution of symptoms and ECG changes on optimized medical treatment which included low molecular weight heparin. Coronary angiography showed a giant thrombus in the distal left main stem. Ostial disease was present in the left anterior descending, circumflex, and obtuse marginal vessels. The right coronary artery was a non-dominant vessel with moderate proximal disease.

This article focuses on a study that explores the effect of nitric oxide (NO) on electrical restitution and ventricular fibrillation (VF) in the isolated rabbit heart with mechanism underlying the antifibrillatory effects of vagus nerve activity. Researchers have previously shown that vagus nerve stimulation decreases the susceptibility of the heart to VF, an effect which is reversed by NO synthase inhibitor. SNP flattens the electrical restitution curve and increases VFT, indicating direct effects of NO on ventricular electrophysiology.

This article focuses on a study that shows that ventricular septal pacing reduces incidence of atrial fibrillation in dual chamber paced patients. Right ventricular apical (RVA) pacing can produce detrimental effects on left ventricular function. Pacing from RVS results in less atrial fibrillation than traditional RVA lead placement within 6 months and this effect appears to continue to 12 month follow up. This finding may explain some of the difficulties in demonstrating benefits of DDD over VVIR pacing in recent studies and supports the increasing use of non-RVA pacing sites.