Outbreak simulation on the neonatal ward using silica nanoparticles with encapsulated DNA - unmasking of key spread areas.

PURPOSE: Nosocomial infections pose a serious threat. In neonatal intensive care units (NICUs) in particular, there are repeated outbreaks caused by microorganisms without the sources or dynamics being conclusively determined. This study aims to use amorphous silica nanoparticles with encapsulated DNA (SPED) to simulate outbreak events and to visualize dissemination patterns in a NICU to gain a better understanding of these dynamics. METHODS: Three types of SPED were strategically placed on the ward to mimic three different dissemination dynamics among real-life conditions and employee activities. SPED DNA, resistant to disinfectants, was sampled at 22 predefined points across the ward for four days and qPCR analysis was conducted. RESULTS: Starting from staff areas, a rapid ward-wide SPED dissemination including numerous patient rooms was demonstrated. In contrast, a primary deployment in a patient room only led to the spread in the staff area, with no distribution in the patient area. CONCLUSION: This study pioneers SPED utilization in simulating outbreak dynamics. By unmasking staff areas as potential key trigger spots for ward-wide dissemination the revealed patterns could contribute to a more comprehensive view of outbreak events leading to rethinking of hygiene measures and training to reduce the rate of nosocomial infections in hospitals.

Clinical use of CRT-D devices with left ventricular sensing: Impact of the desynchronization-detection algorithm.

The use of CRT-D devices with left ventricular (LV) sensing has created controversy about programming various parameters especially the left ventricular T wave protection (LVTP) designed to prevent the delivery of a pacing stimulus into the LV vulnerable period. Such devices are available from two manufacturers. This review focuses only on those provided by Biotronik. As the LVTP controls LV sensing, some investigators have advocated turning off the LVTP to prevent episodic desynchronization known a CRT pacing interrupt. However, LVTP off reduces but does not eliminate this type of desynchronization if triggering of an LV stimulus upon right ventricular sensing (RVs) is programmed on. Deactivation of the LVTP incurs loss of diagnostic data provided by CRT pacing interrupt itself. By choice, the occurrence of CRT pacing interrupt can be totally eliminated by appropriate programming of the LV upper rate interval, LVTP and triggering of an LV pacing event upon RVs. Various programmability options are available according to clinical circumstances. As a rule, clinical judgement must weigh the potential diagnostic benefit of preserving the LVTP capable of recording of episodic CRT pacing interrupt against the loss of diagnostic benefit when LVTP is programmed off (with or without triggering of an LV stimulus upon RVs).

Sensing of concealed ventricular extrasystoles by pacemakers. Fifty years later.

Whether a pacemaker can sense concealed ventricular extrasystoles still remains debatable since its occurrence was first proposed in 1972. It must remain a diagnosis of exclusion if it really exists. Isoelectric complexes and all the causes of oversensing especially discrete false signals generated by a defective pacemaker lead must be excluded before concealed ventricular extrasystoles can be postulated.

Magnetic field-induced interactions between phones containing magnets and cardiovascular implantable electronic devices: Flip it to be safe?

BACKGROUND: Recent case reports and small studies have reported activation of the magnet-sensitive switches in cardiovascular implantable electronic devices (CIEDs) by the new iPhone 12 series, initiating asynchronous pacing in pacemakers and suspension of antitachycardia therapies in implantable cardioverter-defibrillators (ICDs). OBJECTIVE: The purpose of this prospective single-center observational study was to quantify the risk of magnetic field interactions of the iPhone 12 with CIEDs. METHODS: A representative model of each CIED series from all manufacturers was tested ex vivo. Incidence and minimum distance necessary for magnet mode triggering were analyzed in 164 CIED patients with either the front or the back of the phone facing the device. The magnetic field of the iPhone 12 was analyzed using a 3-axis Hall probe. RESULTS: Ex vivo, magnetic interference occurred in 84.6% with the back compared to 46.2% with the front of the iPhone 12 facing the CIED. In vivo, activation of the magnet-sensitive switch occurred in 30 CIED patients (18.3%; 21 pacemaker, 9 ICD) when the iPhone 12 was placed in close proximity over the CIED pocket and the back of the phone was facing the skin. Multiple binary logistic regression analysis identified implantation depth (95% confidence interval 0.02-0.24) as an independent predictor of magnet-sensitive switch activation. CONCLUSION: Magnetic field interactions occur only in close proximity and with precise alignment of the iPhone 12 and CIEDs. It is important to advise CIED patients to not put the iPhone 12 directly on the skin above the CIED. Further recommendations are not necessary.

Low-voltage shock impedance measurements: A false sense of security.

BACKGROUND: Implantable cardioverter defibrillators use low-voltage shock impedance measurements to monitor the lead integrity. However, previous case reports suggest that low-voltage shock impedance measurements may fail to detect insulation breaches that can cause life-threatening electrical short circuits. METHODS AND RESULTS: We report six cases of insulation breaches in transvenous defibrillation leads that were not obvious during standard interrogations and testing of the lead beforehand. In two cases, an electrical short circuit during commanded shock delivery for internal electrical cardioversion resulted in a total damage of the ICD generator. In one of these cases, commanded shock delivery induced ventricular fibrillation, which required external defibrillation. In two cases, a shock due to ventricular tachycardia was aborted as the shock impedance was less than 20 Ω. However, in both cases the tiny residual shock energy terminated the ventricular tachycardia. In contrast, in one case the residual energy of the aborted shock did not end ventricular fibrillation induced at defibrillator threshold testing. In one case, the ICD indicated an error code for a short circuit condition detected during an adequate shock delivery. CONCLUSIONS: This case series illustrates that low-voltage shock impedance measurements can fail to detect insulation breaches. These data suggest that in patients without a contraindication, traditional defibrillator threshold testing or high voltage synchronized shock at the time of device replacement should be considered.

Diagnosis of slow ventricular tachycardia by cardiac resynchronization devices utilizing a desynchronization detection algorithm.

Some cardiac resynchronization therapy (CRT) devices equipped with left ventricular (LV) sensing can develop a specific desynchronization rhythm. Contemporary BIOTRONIK devices are designed with an algorithm called "CRT pacing interrupt" exclusively designed to record the occurrence of the specific form of desynchronization. We report six patients in whom the CRT pacing interrupt function permitted the diagnosis of slow ventricular tachycardia (VT). Slow VT was defined as slower than the programmed VT intervention rates. Although the CRT pacing interrupt function is not designed to detect slow VT, certain episodes of the CRT pacing interrupt function were falsely interpreted by the device as a desynchronization arrhythmia, and the recordings then provided data consistent with the presence of slow VT. The CRT pacing interrupt algorithm permitted a diagnosis of slow VT irrespective of the relationship of LV upper rate interval and cycle length of slow VT.

Triple atrial sensing during cardiac resynchronization.

This report describes a patient who underwent cardiac resynchronization complicated by a Twiddler syndrome. This caused triple atrial sensing and an inappropriate shock.

Apparent dual exit pathways during ventricular tachycardia recorded by an ICD.

Ventricular tachycardia (VT) with dual exit pathways has been demonstrated in many ways. In this respect we found suggestive evidence of dual exit behavior during VT in a patient with an implanted cardioverter-defibrillator. The evaluation was done with continuous recordings of the right ventricular (RV) and left ventricular (LV) electrograms. The recordings documented the varying duration of the LV to RV delay and no change in the RV rate during increases in the LV-RV delay. The unchanged rate ruled out RV participation in the VT circuit. This ruled out the presence of VT with dual exit pathways and provided proof of an unusual RV bystander that did not participate in the VT circuit.

Left ventricular inhibition during cardiac resynchronization caused by sensed left-sided ventricular premature complexes.

A recently published case documented left ventricular (LV) inhibition of a Boston Scientific device by a premature complex (VPC) that was undetected by the right ventricular channel. We have observed a similar response in two patients with a BIOTRONIK cardiac resynchronization device also designed with LV sensing. A spurious response simulating that of the two true cases was also observed in a third patient with a defective LV lead which created isolated false signals. The responses of the BIOTRONIK devices were identical to that of the previously reported findings with the Boston Scientific device. The observations provide insight into the timing function of cardiac resynchronization devices designed with LV sensing.

Termination of desynchronization rhythm and restoration of cardiac resynchronization by left-sided ventricular premature complexes.

Cardiac resynchronization devices that sense left ventricular (LV) activity and can detect interruptions of resynchronization therapy are able to record all forms of desynchronization rhythms, which are triggered by misalignment of LV timing cycles. We report five cases of this desynchronization rhythm that were terminated by isolated left-sided ventricular premature complexes (LVPC) undetected by the right ventricular (RV) channel and unaccompanied by changes in the duration of the RV pacing cycles. In three cases, the devices did not even sense the LVPCs responsible for desynchronization termination. The restoration of resynchronization in our cases is in contrast to the traditional termination mode that is invariably associated with changes in the duration of the RV cycles.

Interruption of cardiac resynchronization therapy triggered by the automatic right-ventricular pacing threshold test.

We report on three patients with heart failure and left bundle branch block who received a BIOTRONIK implantable defibrillator with resynchronization therapy which manifested loss of resynchronization only at a specific time of the night. Desynchronization was sudden and repeatedly initiated by the daily automatic right ventricular pacing threshold test. Loss of resynchronization occurred after switching back from the temporary test mode to the permanent biventricular pacing mode due to the reactivation of the left ventricular (LV) control of the timing cycles. LV sensed events prevented the emission of an LV paced event by virtue of a realigned LV upper rate interval, thus inhibiting LV pacing.

Failure to detect life-threatening arrhythmias in ICDs using single-chamber detection criteria.

BACKGROUND: There are anecdotal reports of sudden death despite a functional implantable cardioverter defibrillator (ICD). We sought to describe scenarios leading to fatal or near-fatal outcome due to inappropriately inhibited ICD therapy in devices programmed with single-chamber detection criteria. METHODS: Programmed settings, episode lists, and intracardiac electrograms from 24 patients with a life-threatening event (n = 12) or fatal outcome (n = 12) related to failed ventricular arrhythmia detection were used to clarify the underlying scenario. RESULTS: Fifty episodes of failed ventricular arrhythmia detection were identified and categorized into six scenarios: (1) spontaneous ventricular tachycardia (VT) or ventricular fibrillation (VF) with a rate below the detection limits, (2) misclassification of polymorphic VT (PVT) or VF as supraventricular tachycardia (SVT), (3) misclassification of VT/VF as cluster of nonsustained VT episodes, (4) misclassification of monomorphic VT (MVT) as SVT, (5) inappropriate shock abortion, and (6) false termination detection. These scenarios occurred respectively 6, 9, 3, 9, 8, and 15 times. In 9/9 (100%) patients with PVT/VF classified as SVT, rate stability was active for rates ranging from 222 to 250 beats/min. MVT detected as SVT was due to the sudden onset criterion in 7/9 (78%) patients and twice a consequence of the rate stability criterion active for rates ranging from 200 to 250 beats/min. CONCLUSION: We describe six scenarios leading to failure of ventricular arrhythmia detection in a single-chamber detection setting withholding life-saving therapy. These scenarios are more likely to occur with high-rate programming and long detection times, especially if combined with rate stability and sudden onset.

Cardiac Implantable Electronic Device Interrogation at Forensic Autopsy: An Underestimated Resource?

BACKGROUND: Postmortem interrogations of cardiac implantable electronic devices (CIEDs), recommended at autopsy in suspected cases of sudden cardiac death, are rarely performed, and data on systematic postmortem CIED analysis in the forensic pathology are missing. The aim of the study was to determine whether nonselective postmortem CIED interrogations and data analysis are useful to the forensic pathologist to determine the cause, mechanism, and time of death and to detect potential CIED-related safety issues. METHODS: From February 2012 to April 2017, all autopsy subjects in the department of forensic medicine at the University Hospital Charité who had a CIED underwent device removal and interrogation. Over the study period, 5368 autopsies were performed. One hundred fifty subjects had in total 151 CIEDs, including 109 pacemakers, 35 defibrillators, and 7 implantable loop recorders. RESULTS: In 40 cases (26.7%) time of death and in 51 cases (34.0%) cause of death could not be determined by forensic autopsy. Of these, CIED interrogation facilitated the determination of time of death in 70.0% of the cases and clarified the cause of death in 60.8%. Device concerns were identified in 9 cases (6.0%), including 3 hardware, 4 programming, and 2 algorithm issues. One CIED was submitted to the manufacturer for a detailed technical analysis. CONCLUSIONS: Our data demonstrate the necessity of systematic postmortem CIED interrogation in forensic medicine to determine the cause and timing of death more accurately. In addition, CIED analysis is an important tool to detect potential CIED-related safety issues.

Desynchronization in a cardiac resynchronization device induced by a pacemaker-mediated tachycardia algorithm.

This report describes the occurrence of desynchronization in a patient with a cardiac resynchronization device programmed with an active pacemaker-mediated tachycardia algorithm based on AV delay modification. Desynchronization was precipitated by sinus tachycardia and the abrupt return of the prevailing AV delay that followed the periodic prolongation of the AV delay mandated by activity of the algorithm. Prevention of desynchronization in this setting requires programming a right ventricular upper rate interval longer than the sum of the programmed ventriculoatrial interval and the AV delay.

Interruption of cardiac resynchronization therapy by atrial premature complexes.

Biotronik devices used for cardiac resynchronization therapy (CRT) combined with defibrillation function (CRT-D) are capable of left ventricular (LV) sensing. Under certain circumstances, LV sensing may cause loss of CRT. The third generation of the Biotronik i-family CRT-Ds enables the recording of event-triggered tracings of the electrogram particularly those involving "CRT pacing interrupt" episodes. We report three cases of a sudden "CRT pacing interrupt" initiated by an atrial premature complex. This was caused by realignment of the LV timing cycles induced by the APCs whereupon LV pacing was inhibited and a self-perpetuating desynchronization process was initiated. In all cases it is the repeated occurrence of LV sensed events that prevents the emission of LV paced events because it displaces the LV upper rate interval from its normal position. Prevention of desynchronization requires programming an LV upper rate faster than the maximum sensor-driven rate or right ventricular upper rate.