Despite the advent of non-fluoroscopic technology, fluoroscopy remains the cornerstone of imaging in most interventional electrophysiological procedures, from diagnostic studies over ablation interventions to device implantation. Moreover, many patients receive additional X-ray imaging, such as cardiac computed tomography and others. More and more complex procedures have the risk to increase the radiation exposure, both for the patients and the operators. The professional lifetime attributable excess cancer risk may be around 1 in 100 for the operators, the same as for a patient undergoing repetitive complex procedures. Moreover, recent reports have also hinted at an excess risk of brain tumours among interventional cardiologists. Apart from evaluating the need for and justifying the use of radiation to assist their procedures, physicians have to continuously explore ways to reduce the radiation exposure. After an introduction on how to quantify the radiation exposure and defining its current magnitude in electrophysiology compared with the other sources of radiation, this position paper wants to offer some very practical advice on how to reduce exposure to patients and staff. The text describes how customization of the X-ray system, workflow adaptations, and shielding measures can be implemented in the cath lab. The potential and the pitfalls of different non-fluoroscopic guiding technologies are discussed. Finally, we suggest further improvements that can be implemented by both the physicians and the industry in the future. We are confident that these suggestions are able to reduce patient and operator exposure by more than an order of magnitude, and therefore think that these recommendations are worth reading and implementing by any electrophysiological operator in the field.

Brugada syndrome is a channelopathy characterized on ECG by coved ST-segment elevation (≥2 mm) in the right precordial leads and is associated with an increased risk of malignant ventricular arrhythmias. The term Brugada phenocopy is proposed to describe conditions that induce Brugada-like ECG manifestations in patients without true Brugada syndrome. An extensive review of the literature identified case reports that were classified according to their suspected etiological mechanism. Future directions to learn more about these intriguing cases is discussed.

Background: Acquired long QT (LQT) interval is thought to be a consequence of drug therapy and electrolyte disturbances. Hypothesis: We characterize the potential effects of polypharmacy in a case series of acquired LQT and torsades de pointes (TdP) in order to determine whether multiple risk factors play a role in the development of LQT. Methods: The case series consisted of 11 patients presenting to 4 tertiary care hospitals with LQT and ≥2 risk factors for developing LQT. Clinical characteristics, medications, electrolyte disturbances, and course in hospital were analyzed. Results: Mean age was 49.1 ± 5.8 years. Eight patients were female. Four had hypertension, 1 had a history of dilated cardiomyopathy, and 1 patient demonstrated complete atrioventricular block. Average QTc interval at presentation was 633.8 ± 29.2 ms. Nine patients developed TdP. In 3, LQT was not initially detected and amiodarone was administered, followed by development of TdP. Patients were taking an average of 2.8 ± 0.3 QT-prolonging medications-an antidepressant in 6 cases and a diuretic in 8 cases. All patients had an electrolyte abnormality; 8 patients presented with severe hypokalemia (<3.0 mmol/L). Average serum potassium and magnesium were 2.82 ± 0.10 mmol/L and 0.75 ± 0.03 mmol/L, respectively. There were no deaths. Conclusions: This case series highlights the risks of polypharmacy in the development of LQT and TdP. It illustrates the importance of early detection of LQT in patients with multiple risk factors in ensuring appropriate treatment.

fQRS predicts arrhythmic events in patients with HOCM and should be considered in a model of risk stratification.