This study confirms that the HCM Risk-SCD model provides accurate prognostic information that can be used to target implantable cardioverter defibrillator therapy in patients at the highest risk of SCD.

Our study emphasises the importance of access to CMR for heart attack centres. If myocarditis is suspected, CMR scanning should be performed within 14 days. Myocarditis should not be regarded as benign, even when EF is preserved.

Simultaneous PET/MR is an accurate method for diagnosing CS. FDG-PET and CMR combined offers complementary information on disease pathophysiology. The presence of LGE and FDG uptake on PET/MR identifies patients at higher risk of adverse events. PET and CMR should therefore be considered in the assessment of disease presence, stage, and prognosis in CS.

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Background Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) is a heritable heart muscle disease that causes sudden cardiac death in the young. Inflammatory myocardial infiltrates have been described at autopsy and on biopsy, but there are few data on the presence of myocarditis in living patients with ARVC using non-invasive imaging techniques. FDG-PET is a validated technique for detecting myocardial inflammation in clinically suspected myocarditis. We aimed to determine the prevalence of myocardial inflammation in patients with ARVC using 18 Ffluorodeoxyglucose positron emission tomography (FDG-PET). Methods and Results We performed a retrospective analysis of a single centre cohort of patients with ARVC referred for FDG-PET scans between 2012 and 2017 for investigation of symptoms or suspected device infection. Sixteen patients (12 male; age 42±13 years) with a definite diagnosis of ARVC were identified. Seven had positive FDG-PET scans, two of whom had cardiac sarcoidosis on endomyocardial biopsy. Of the remaining five, two carried pathogenic desmoplakin mutations. FDG uptake was found in the left ventricular myocardium in all cases. One patient also had right ventricular uptake. Conclusion In this exploratory study, we show that some patients with ARVC have evidence for myocardial inflammation on FDG-PET, suggesting that myocarditis plays a role in disease pathogenesis.

The diagnostic utility of Holter monitoring in patients being investigated for palpitations and altered consciousness is very limited, particularly in young patients for whom alternative diagnostic methods should be considered.

Objectives: To compare serum potassium concentrations in diabetic and non-diabetic patients in the early phase of acute coronary syndromes. Background: Acute phase hypokalaemia occurs in response to adrenergic activation, which stimulates membrane bound sodium-potassium-ATPase and drives potassium into the cells. It is not known whether the hypokalaemia is attenuated in patients with diabetes because of the high prevalence of sympathetic nerve dysfunction. Methods: Prospective cohort study of 2428 patients presenting with acute coronary syndromes. Patients were stratified by duration of chest pain, diabetic status, and pretreatment with β blockers. Results: The mean (SD) serum potassium concentration was significantly higher in diabetic than in non-diabetic patients (4.3 (0.5) v 4.1 (0.5) mmol/l, p < 0.0001). Multivariate analysis identified diabetes as an independent predictor of a serum potassium concentration in the upper half of the distribution (odds ratio 1.66, 95% confidence interval 1.38 to 2.00). In patients presenting within 6 hours of symptom onset, there was a progressive increase in plasma potassium concentrations from 4.08 (0.46) mmol/l in patients presenting within 2 hours, to 4.20 (0.47) mmol/l in patients presenting between 2-4 hours, to 4.24 (0.52) mmol/l in patients presenting between 4-6 hours (p = 0.0007). This pattern of increasing serum potassium concentration with duration of chest pain was attenuated in patients with diabetes, particularly those with unstable angina. Similar attenuation occurred in patients pretreated with β blockers. Conclusion: In acute coronary syndromes, patients with diabetes have significantly higher serum potassium concentrations and do not exhibit the early dip seen in non-diabetics. This may reflect sympathetic nerve dysfunction that commonly complicates diabetes. P atients presenting with acute coronary syndromes are commonly hypokalaemic, 1-3 which may increase the risk of lethal ventricular arrhythmias.4-6 Hypokalaemia can be regarded as an acute phase response to adrenergic activation, which stimulates membrane bound sodium-potassiumATPase and drives potassium into the cells. [7][8][9] Experimentally, hypokalaemia can be induced in human volunteers by infusion of physiological concentrations of adrenaline but not isoproterenol.10 11 The hypokalaemia is prevented by specific β 2 antagonists, identifying β 2 receptors in skeletal muscle as the likely target for this adrenergic response. 12Another potential mechanism of hypokalaemia in acute coronary syndromes is reactive hyperinsulinaemia in response to adrenergically driven increases in serum glucose. 13 Thus, pharmacological doses of insulin reduce serum potassium concentrations, an effect ascribed to insulin mediated uptake of potassium by muscle and liver.14 15 In contrast, however, physiological changes in circulating insulin concentrations have very little effect on potassium in diabetic or non-diabetic patients.16 17 This mechanism was discounted by Brown and colleagues 10 because in their study serum p...

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