What physicians do in case of a failure of the pace-sense part of a defibrillation lead : Survey in Germany, Austria and Switzerland.

BACKGROUND: The possible treatment strategies for defects of the pace-sense (P/S) part of a defibrillation lead are either implantation of a new high-voltage (HV)-P/S lead, with or without extraction of the malfunctioning lead, or implantation of a P/S lead. METHODS: We conducted a Web-based survey across cardiac implantable electronic device (CIED) centers to investigate their procedural practice and decision-making process in cases of failure of the P/S portion of defibrillation leads. In particular, we focused on the question of whether the integrity of the HV circuit is confirmed by a test shock before decision-making. The questionnaire included 14 questions and was sent to 951 German, 341 Austrian, and 120 Swiss centers. RESULTS: The survey was completed by 183 of the 1412 centers surveyed (12.7% response rate). Most centers (90.2%) do not conduct a test shock to confirm the integrity of the HV circuit before decision-making. Procedural practice in lead management varies depending on the presentation of lead failure and whether the center applies a test shock. In centers that do not conduct a test shock, the majority (69.9%) implant a new HV-P/S lead. Most centers (61.7%) that test the integrity of the HV system implant a P/S lead. The majority of centers favor DF-4 connectors (74.1%) over DF-1 connectors (25.9%) at first CIED implantation. CONCLUSION: Either implanting a new HV-P/S lead or placing an additional P/S lead are selected strategies if the implantable cardioverter-defibrillator lead failure is localized to the P/S portion. However, conducting a test shock to confirm the integrity of the HV component is rarely performed.

Extent and magnitude of low-voltage areas assessed by ultra-high-density electroanatomical mapping correlate with left atrial function.

INTRODUCTION: The extent of left atrial (LA) adverse remodeling as a cardiac disease marker has become increasingly important. In patients with atrial fibrillation (AF), atrial remodeling (AR) is accompanied by increased mortality. The relation between LA function and the extent of low-voltage areas (LVAs) has not yet been systematically investigated. METHODS: In patients with AF undergoing catheter-ablation, LA was studied using echocardiography and ultra-high-density mapping (Rhythmia®). Fibrosis (i.e. extent of LVAs) was estimated by quantifying areas with bipolar electrogram amplitudes of ≤0.5, ≤0.4, ≤0.3, ≤0.2 or ≤0.1 mV. RESULTS: A total of 22 patients with a mean LVEF of 53 ±â€¯2% was studied. Mean LA volume index (LAVI) was significantly increased at 39 ±â€¯3 ml/m2 indicating AR. Size of LVAs was 57 ±â€¯7 cm2 representing 47 ±â€¯5% of the total LA area (low-voltage set to ≤0.5 mV). With low-voltage set to ≤0.4, ≤0.3, ≤0.2 and ≤0.1, total area decreased to 34 ±â€¯6, 28 ±â€¯6, 22 ±â€¯5 and 12 ±â€¯3 cm2. LAVI positively correlated with the extent of LVAs at all cut-offs. Mean LA emptying fraction was 42 ±â€¯3% and showed a negative correlation with LVAs with low-voltage set to ≤0.4 mV. Moreover, mean LA strain was 13 ±â€¯2% and correlated with LVAs with low-voltage at all cut-offs further supporting the notion that the extent of LVAs impacts LA function. Notably, with low-voltage set to ≤0.2, ≤0.3 and ≤0.4 mV impaired LA strain was detected with an accuracy of >76% (p < 0.05). CONCLUSION: Structural (i.e. LAVI) and functional (i.e. LA emptying fraction and LA strain) parameters of the LA correlate with the extent of LVAs.

Unmasking of myopotential oversensing by an integrated bipolar defibrillator lead following AV node ablation.

A 73-year-old man with nonischemic cardiomyopathy underwent catheter ablation of ventricular tachycardia that had resulted in frequent shocks from his implanted cardiac resynchronization therapy defibrillator (CRT-D). Coexisting atrial fibrillation required AV node ablation which rendered the patient pacemaker dependent. During follow-up, recurrent episodes of dizziness occurred caused by inhibition of pacing due to oversensing of pectoral muscle myopotentials. Surgical revision was performed and the intraoperative examination revealed an intact integrated bipolar defibrillator lead with appropriate connections to the CRT-D header. The placement of an additional pace/sense lead completely resolved the patient's symptoms and no further myopotential oversensing was recorded.

Cardiac markers (BNP, NT-pro-BNP, Troponin I, Troponin T, in female amateur runners before and up until three days after a marathon.

PURPOSE: Transient cardiac ventricular dysfunction or sudden cardiac deaths have been reported for male athletes participating in marathon racing. Less is known about the myocardial response in females. We examined natriuretic peptides and cardiac troponins in female athletes after a marathon. METHODS: At the 31st real,- Berlin Marathon plasma levels of NT-pro-BNP, BNP, cTnI and cTnT were measured in 15 women (age 35+/-6 years; finishing times between 3:22 h and 5:21 h) at four different time points (before, immediately after, day one and day three). RESULTS: An increase in [NT-pro-BNP] was observed immediately after the marathon (median [NT-pro-BNP] before: 39.6 pg ml(-1), after: 138.6 pg ml(-1), p=0.003) with a further increase on day one. [BNP] did not increase immediately after the marathon but increased on day one (median [BNP] before: 15 pg ml(-1), day one: 27.35 pg ml(-1), p=0.006). On day three, [NT-pro-BNP] and [BNP] returned to initial values. [cTnI] was under the detection limit prior to the marathon in all runners. [cTnT] was under the detection limit before the marathon except in one runner who presented a concentration of 0.03 ng ml(-1). Cardiac troponins (median [cTnl] after: 0.098 ng ml(-1), p=0.028; median [cTnT] after: 0.032 ng ml(-1), p=0.012) increased immediately after the marathon and returned to initial values on day one [cTnT] and three [cTnI]. DISCUSSION: Parameters representing cardiac stress increased in females after a marathon. Different kinetics of natriuretic peptides BNP and NT-pro-BNP post-marathon could be due to their different half-lives and dependence on renal function. The increase of cTnI and cTnT may result from minor myocardial lesions.