Prospective evaluation of cinefluoroscopy and chest radiography for Riata lead defects: implications for future lead screening.

INTRODUCTION: Lead insulation defects with externalization of the conductors exist in Riata defibrillator leads. Cinefluoroscopy is currently the gold standard to detect such defects. Prospective evaluation of alternative screening options such as chest radiography (CXR), which has been recommended by the FDA, is not well described. METHODS AND RESULTS: Patients with Riata leads underwent cinefluoroscopy, CXR, and device interrogation. Leads were classified as abnormal (clear cable separation), borderline, or normal by independent evaluation of cinefluoroscopy and CXR. CXR evaluation was done in two ways as follows: (1) routine CXR read by daily staff radiologists for lead screening and (2) CXR evaluation by a radiologist educated about the lead defect. One hundred two patients were evaluated at our institution. Cinefluoroscopy showed externalized conductors in 33 patients (32 %). Twenty-five of 33 patients (76 %) who had abnormal cinefluoroscopic findings had abnormal CXR findings on blinded review by the educated radiologist. All 25 patients with abnormal CXR had abnormal findings on cinefluoroscopy. Daily staff radiologists without direct education other than prompts for lead screening detected CXR abnormalities in only 8 out of 102 (8 %) cases. CONCLUSION: Cinefluoroscopy appears to be more sensitive than CXR for the detection of Riata cable extrusion. Interpretation of CXR by a radiologist with education in lead defects correlates highly with cinefluoroscopy with very high specificity. Depending on available resources for screening, CXR may be a reasonable alternative to cinefluoroscopy. Multidisciplinary collaboration across specialties (radiology and electrophysiology) can lead to improved diagnostic capability and thus the potential for enhanced quality of care.

Sudden cardiac death risk stratification in patients with heart failure.

The multiplicity of mechanisms contributing to arrhythmogenesis in patients with heart failure carries obvious implications for risk stratification. If patients having the propensity to develop arrhythmias by these different mechanisms are to be identified, tests must be devised that reveal the substrates or other factors that relate to each mechanism. In the absence of this, efforts to risk stratify patients are likely to be neither cost-effective nor accurate. This article reviews the current knowledge base of risk stratification for sudden death in patients with heart failure, while acknowledging several limitations in the studies examined.

Safety of nerve conduction studies in patients with peripheral intravenous lines.

Nerve conduction studies (NCS) may be deferred because of a perceived risk of cardiac arrhythmia in the presence of same-limb peripheral intravenous lines. Patients with implanted pacemakers or defibrillators provide a model in whom this risk can be assessed. Twenty patients, seven with pacemakers and 13 with defibrillators, had peripheral intravenous lines placed during routine care and underwent NCS in the same limb. NCS were performed with the intravenous line clamped and then with saline open to gravity. The implanted cardiac device was interrogated before and after the study. During NCS the surface electrocardiogram and intracardiac electrograms were monitored continuously. Electrical impulses generated during routine NCS were never detected by the sensing amplifiers of the pacemakers/defibrillators and did not affect the programmed settings or interfere with pacing of the device. Routine NCS are safe in patients with same-limb peripheral intravenous lines, even with saline open to gravity.

Electrophysiological studies of transgenic long QT type 1 and type 2 rabbits reveal genotype-specific differences in ventricular refractoriness and His conduction.

We have generated transgenic rabbits lacking cardiac slow delayed-rectifier K(+) current [I(Ks); long QT syndrome type 1 (LQT1)] or rapidly activating delayed-rectifier K(+) current [I(Kr); long QT syndrome type 2 (LQT2)]. Rabbits with either genotype have prolonged action potential duration and QT intervals; however, only LQT2 rabbits develop atrioventricular (AV) blocks and polymorphic ventricular tachycardia. We therefore sought to characterize the genotype-specific differences in AV conduction and ventricular refractoriness in LQT1 and LQT2 rabbits. We carried out in vivo electrophysiological studies in LQT1, LQT2, and littermate control (LMC) rabbits at baseline, during isoproterenol infusion, and after a bolus of dofetilide and ex vivo optical mapping studies of the AV node/His-region at baseline and during dofetilide perfusion. Under isoflurane anesthesia, LQT2 rabbits developed infra-His blocks, decremental His conduction, and prolongation of the Wenckebach cycle length. In LQT1 rabbits, dofetilide altered the His morphology and slowed His conduction, resulting in intra-His block, and additionally prolonged the ventricular refractoriness, leading to pseudo-AV block. The ventricular effective refractory period (VERP) in right ventricular apex and base was significantly longer in LQT2 than LQT1 (P < 0.05) or LMC (P < 0.01), with a greater VERP dispersion in LQT2 than LQT1 rabbits. Isoproterenol reduced the VERP dispersion in LQT2 rabbits by shortening the VERP in the base more than in the apex but had no effect on VERP in LQT1. EPS and optical mapping experiments demonstrated genotype-specific differences in AV conduction and ventricular refractoriness. The occurrence of infra-His blocks in LQT2 rabbits under isoflurane and intra-His block in LQT1 rabbits after dofetilide suggest differential regional sensitivities of the rabbit His-Purkinje system to drugs blocking I(Kr) and I(Ks).

Left ventricular ejection fraction for sudden death risk stratification and guiding implantable cardioverter-defibrillators implantation.

Current guidelines for use of implantable cardioverter-defibrillators (ICDs) for primary prevention of sudden death in patients with coronary disease and nonischemic dilated cardiomyopathy are based primarily on ejection fraction (EF) <30%-35%. The origin of this is based on EF as the common variable in several randomized clinical trials evaluating the ability of ICDs to reduce mortality. However, although low EF identifies one patient population at relatively increased risk for sudden death, there are a number of limitations to use of EF as the primary indication for ICD. Patients with low EF are not uniform with regard to other prognostic markers, and not all are at high risk for sudden death. Conversely, although patients with EF >35% as a group are at lower risk for sudden death, these patients are not uniform with regard to other prognostic variables. A variety of tests, including measures of reduced repolarization reserve and measures of altered sympathetic/parasympathetic balance, have identified patients with EF >35% at relatively high risk for sudden death. One explanation for this "disconnect" is that there is no evidence of any direct mechanistic link between low EF and mechanisms responsible for ventricular tachyarrhythmias.

Sudden cardiac death in athletes.

Sudden cardiac death in athletes, although relatively uncommon, is a well-recognized condition generally associated with some congenital abnormalities. It, however, continues to be of vast interest to the public as athletes are seen as a distinct group of individuals who are especially able to tolerate more intense physical activities than the general population. Obviously, intense activities predispose susceptible athletes to sudden cardiac death, hence the importance of pre-participation screening tests. As the cost of healthcare continues to be on the rise, there will be increasing difficulty justifying a nation-wide method of screening cost-effectively. This article is intended to describe the possible underlying causes of sudden cardiac death discovered thus far, as well as methods for detection, pre-participation guidelines, and emerging therapy.