Performance of an implantable cardioverter-defibrillator lead family

Background: Lead failure is the major limitation in implantable cardioverter‐ defibrillator (ICD) therapy. Long‐term follow‐up data for Biotronik Linox ICD leads are limited. Therefore, we analyzed the performance of all these leads implanted at our institution. Materials and Methods: All Linox and Linox Smart ICD leads implanted between 2006 and 2015 were identified. Lead failure was defined as electrical dysfunction (oversensing, abnormal impedance, exit block). Lead survival was described, according to Kaplan–Meier. Associations between lead failure and specific variables were examined. p < .05 was considered significant. Results: We included 417 ICD leads. The median follow‐up time for Linox (n = 205) was 81 months and for Linox Smart (n = 212) 75 months. During that follow‐up time, 30 Linox (14.6%) and 16 Linox Smart leads (7.6%) showed a malfunction. The 5‐year lead survival probability was 97.4% for Linox and 95.2% for Linox Smart (log‐rank test, p = .19). The 6‐ and 8‐year lead survival probability for Linox was 93.6% and 84.6%, and for Linox Smart 93% and 91.9%. The only factor significantly associated with lead failure was younger patient age at implantation (hazard ratio/year: 0.97, 95% CI: 0.94–0.99, p = .002). Conclusion: This relatively large study with a long follow‐up period highlights a relevant failure rate of Biotronik Linox leads. The performance of Linox versus Linox Smart ICD leads was comparable. Although we show an acceptable 5‐year lead survival probability, we observed a marked drop after just 1 more year of follow‐up. In an era of improving heart failure survival probability, a prolonged follow‐up of ICD leads is increasingly clinically relevant

What is the role of increased heart rate and why is it beneficial to reduce it?

Increased heart rate is an independent risk factor for patients with cardiovascular disease, in particular those with arterial hypertension, myocardial infarction, coronary artery disease, heart failure, and extracardiac comorbidities like microalbuminuria. This relation is supported by a large number of animal studies as well as clinical trials, which are summarized in this article. These studies demonstrate the detrimental effects of increased heart rate on the structure and function of the cardiovascular system. Heart rate can be easily measured during physical examination of the patient, therefore allowing us to make a simple assessment of the prognosis and efficiency of therapy. Thus heart rate, which can selectively be reduced by If channel inhibition, seems to be a therapeutic target in cardiolog

Renal Sympathetic Denervation Suppresses Postapneic Blood Pressure Rises and Atrial Fibrillation in a Model for Sleep Apnea

The aim of this study was to identify the relative impact of adrenergic and cholinergic activity on atrial fibrillation (AF) inducibility and blood pressure (BP) in a model for obstructive sleep apnea. Obstructive sleep apnea is associated with sympathovagal disbalance, AF, and postapneic BP rises. Renal denervation (RDN) reduces renal efferent and possibly also afferent sympathetic activity and BP in resistant hypertension. The effects of RDN compared with beta-blockade by atenolol on atrial electrophysiological changes, AF inducibility, and BP during obstructive events and on shortening of atrial effective refractory period (AERP) induced by high-frequency stimulation of ganglionated plexi were investigated in 20 anesthetized pigs. Tracheal occlusion with applied negative tracheal pressure (NTP; at -80 mbar) induced pronounced AERP shortening and increased AF inducibility in all of the pigs. RDN but not atenolol reduced NTP-induced AF-inducibility (20% versus 100% at baseline; P=0.0001) and attenuated NTP-induced AERP shortening more than atenolol (27 +/- 5 versus 43 +/- 3 ms after atenolol; P=0.0272). Administration of atropine after RDN or atenolol completely inhibited NTP-induced AERP shortening. AERP shortening induced by high-frequency stimulation of ganglionated plexi was not influenced by RDN, suggesting that changes in sensitivity of ganglionated plexi do not play a role in the antiarrhythmic effect of RDN. Postapneic BP rise was inhibited by RDN and not modified by atenolol. We showed that vagally mediated NTP-induced AERP shortening is modulated by RDN or atenolol, which emphasizes the importance of autonomic disbalance in obstructive sleep apnea-associated AF. Renal denervation displays antiarrhythmic effects by reducing NTP-induced AERP shortening and inhibits postapneic BP rises associated with obstructive events. (Hypertension. 2012; 60: 172-178.) circle Online Data Supplemen

Renal Sympathetic Denervation Provides Ventricular Rate Control But Does Not Prevent Atrial Electrical Remodeling During Atrial Fibrillation

Renal denervation (RDN) reduces renal efferent and afferent sympathetic activity thereby lowering blood pressure in resistant hypertension. The effect of modulation of the autonomic nervous system by RDN on atrial electrophysiology and ventricular rate control during atrial fibrillation (AF) is unknown. Here we report a reduction of ventricular heart rate in a patient with permanent AF undergoing RDN. Subsequently, we investigated the effect of RDN on AF-induced shortening of atrial effective refractory period, AF inducibility, and ventricular rate control during AF maintained by rapid atrial pacing in 12 pigs undergoing RDN (n = 7) or sham procedure (n = 5). During sinus rhythm, RDN reduced heart rate (RR-interval, 708 +/- 12 versus 577 +/- 19 ms; P=0.0021) and increased atrioventricular node conduction time (PQ-interval, 112 +/- 12 versus 88 +/- 9 ms; P=0.0001). Atrial tachypacing for 30 minutes increased AF inducibility and decreased AF cycle length. This was not influenced by RDN. RDN reduced ventricular rate during AF episodes by approximate to 24% (119 +/- 9 versus 158 +/- 19 bpm; P=0.0001). AF episodes were shorter after RDN compared with sham (12 +/- 3 versus 34 +/- 4 s; P=0.0091), but atrial effective refractory period was not modified by RDN. RDN reduced heart rate and reduced atrioventricular node conduction time during sinus rhythm and provided rate control during AF. AF- induced atrial electrical remodeling, AF inducibility, and AF cycle length were not modified, but duration of AF episodes was shorter after RDN. Modulation of the autonomic nervous system by RDN might provide rate control and reduce susceptibility to AF. Whether RDN may provide rate control in a larger number of patients with AF deserves further clinical studies. (Hypertension. 2013;61:225-231.