ABSTRACT
BACKGROUND: Cardiac resynchronisation therapy (CRT) is an established treatment option for chronic heart failure patients with left bundle branch block. Although a concomitant functional mitral regurgitation is often reduced by CRT, many patients need additional mitral valve repair. Placing a CARILLON® Mitral Contour System (CMCS) over a transvenous CRT lead is currently not recommended, since both of them are implanted in the coronary sinus (CS). The aim of this study was to investigate the feasibility of sequential implantation of a transvenous LV lead followed by CMCS implantation, and to assess LV lead performance and possibility of extraction. METHODS AND RESULTS: Standard transvenous LV leads were implanted in the CS of five female sheep. After establishing regular anatomical position with stable electrical parameters of the LV lead, a CMCS was additionally implanted in the CS. After an observation period of 100 days, lead performance and positions of lead and CMCS were studied. Sequential implantation of the two components was feasible in sheep. After 100 days, all leads showed regular measurements of impedance, threshold, and sensing. There was no migration of either the LV lead or the CMCS. In all cases, the LV lead could be completely extracted without migration of the CMCS. There were no acute or long-term complications. CONCLUSIONS: In an animal model of healthy adult sheep, implantation of CMCS with a transvenous LV lead already in place was feasible and without major problems with either the CMCS or the LV lead. Electrical performance of the LV leads was excellent. All LV leads could be extracted without migration of the CMCS.
Subject(s)
Cardiac Resynchronization Therapy/methods , Catheterization, Peripheral/methods , Electrodes, Implanted , Heart Failure/therapy , Heart Ventricles/physiopathology , Mitral Valve/diagnostic imaging , Pacemaker, Artificial , Animals , Coronary Angiography , Disease Models, Animal , Female , Heart Failure/physiopathology , Jugular Veins , Sheep , Treatment OutcomeABSTRACT
For the past few years, children affected by an inherited channelopathy have been counseled to avoid (recreational) sports activities and all competitive sports so as to prevent exercise-induced arrhythmia and sudden cardiac death. An increased understanding of the pathophysiological mechanisms, better anti-arrhythmic strategies, and, in particular, more epidemiological data on exercise-induced arrhythmia in active athletes with channelopathies have changed the universal recommendation of "no sports," leading to revised, less strict, and more differentiated guidelines (published by the American Heart Association/American College of Cardiology in 2015). In this review, we outline the disease- and genotype-specific mechanisms of exercise-induced arrhythmia; give an overview of trigger-, symptom-, and genotype-dependent guidance in sports activities for children with long QT syndrome (LQTS), Brugada syndrome (BrS), catecholaminergic polymorphic ventricular tachycardia (CPVT), or short QT syndrome (SQTS); and highlight the novelties in the current guidelines compared with previous versions. While it is still recommended for patients with LQT1 and CPVT (even when asymptomatic) and all symptomatic LQTS patients (independent of genotype) to avoid any competitive and high-intensity sports, other LQTS patients successfully treated with anti-arrhythmic therapies and phenotype-negative genotype-positive patients may be allowed to perform sports at different activity levels - provided they undergo regular, sophisticated evaluations to detect any changes in arrhythmogenic risk.