Andrea Magnani

Cardiac Dyssynchrony Quantitated by Time-to-Peak or Temporal Uniformity of Strain at Longitudinal, Circumferential, and Radial Level: Implications for Resynchronization Therapy

BACKGROUND The standard deviation of time to peak strain (TPS-SD) has been proposed as an index of left ventricular (LV) dyssynchrony in patients to be resynchronized. However, TPS-SD is sensitive to noise, and the influence of outliers on TPS-SD is also relevant. Alternatively, dyssynchrony can be indexed by temporal uniformity of strain (TUS), whereby a time plot of regional strains, arranged for LV location, is subjected to Fourier analysis. If segments shorten simultaneously (synchronously), the plot appears as a straight line, with power only in the zero-order Fourier term, whereas regionally clustered dyssynchrony generates an undulating plot with higher power in the first-order term. TUS index reflects zero-order relative to first-order plus zero-order power. METHODS In this study, TUS and TPS-SD were computed in 68 patients (QRS duration >/= 120 ms; ejection fraction </= 0.35) in whom longitudinal, circumferential, and radial strains were measured using speckle-tracking two-dimensional echocardiography before and 3 to 6 months after cardiac resynchronization therapy (CRT), together with LV volumes. RESULTS Following CRT, LV volume decreased (diastolic, -10 +/- 20%) and ejection fraction improved from 0.23 +/- 0.07% to 0.30 +/- 0.10% (P < .001 for both). Circumferential strain was ameliorated as well (P = .054). Two-way analysis of variance revealed TUS improvement after CRT (P = .043), with a trend for CRT to contrast asynchrony at the circumferential (+0.06 +/- 0.25) and longitudinal (+0.05 +/- 0.18) levels compared with the radial level (-0.002 +/- 0.18) (interaction P = .06). This was not true for TPS-SD. Multivariate analysis revealed that only TUS, assessed before CRT circumferentially, predicted ejection fraction improvement after CRT. Other asynchrony variables failed in the model. CONCLUSION Dyssynchrony indexed by circumferential TUS yields greater CRT benefits than that indexed by TPS-SD, supporting the idea of targeting TUS-measured dyssynchrony as a more informative quantitative measurement in CRT patients.

Respiratory‐Dependent Atrial Pacing, Management of Sinus Node Disease

The effectiveness of respiratory‐dependent atrial pacing (AAI‐RD) was assessed in 23 patients (11 male, 12 female; 68 ± 10 years) with symptomatic isolated sinus node disease (SND). Follow‐up was performed at 3 month intervals and included history taking, physical examination, ECG recording and 24‐hour Holter monitoring. An incremental treadmill exercise test was performed in 21/23 patients before pacemaker implantation, in 23/23 patients after implantation (at least two tests with different programmed settings of respiratory rate/paced rate ratio); 21/23 patients underwent treadmill tests during both fixed rate 70 bpm and AAI‐RD pacing. Physiological sensitivity of AAI‐RD pacing was found excellent in 34 tests (85%) and fair in six (15%). Spontaneous heart rate was significantly higher after pacemaker implantation fbpm 115 ± 20 vs 98 ± 24, P < 0.001). In 10/21 patients paced rate was significantly higher during AAI‐RD vs AAI pacing (131 ±9 vs 106 ± 16, P < 0.001) with better total work time (min 9.9 ± 4 AAI‐RD vs 6.8 ± 2.6 AAI, P < 0.002), higher oxygen consumption at anaerobic threshold (ml/min 1137 ± 406 AAI‐RD vs 882 ± 268 AAI‐RD vs 5.5 ± 2.6 AAI, P ‐ 0.001). No significant difference was found in 7/21 patients (overlap between spontaneous and paced rate during both AAI‐RD and AAI programming); 4/21 patients did not reach anaerobic threshold owing to osteomuscular limitations. AV block was detected in 1/23 patients, Biorate circuital failure in 1/23, sporadic undersensing in 5/23, short and symptom‐free myopotential inhibitions in 10/23. We concluded that AAI‐RD pacing is a reliable, safe and useful modality in pacemaker management of isolated SNA, especially in patients with abnormal rate response to exercise.

Lack of Influence of Atrioventricular Delay on Stroke Volume at Rest in Patients with Complete Atrioventricular Block and Dual Chamber Pacing

Dual chamber pacing (DDD) maintains atrioventricular (AV) sequence; AV delay program mobility modifies the relationship between atrial and ventricular contraction. To evaluate the hemodynamic effects of such a modification, ten patients with a DDD unit for complete AV block were studied by time‐motion (M‐mode) and Doppler echocardiography during inhibited ventricular pacing (VVI), atrial‐triggered ventricular pacing (VDDJ and atrioventricular sequential pacing (DVI) at different AV delay (90, 140, 390, 240 msec). A significant improvement in stroke volume (SV) (15%–20%, P < 0.05) was seen during DDD versus VVI pacing; no changes, however, were observed in the same patient with different AV delay or during DVI versus VDD pacing. These data suggest that programming of AV delay does not affect systolic performance at rest; longer diastolic filling times recorded during DDD pacing with “short” AV delay (90–340 msec) do not seem to be a hemodynamically relevant epiphenomenon of PM programming.

Effects of closed-loop stimulation vs. DDD pacing on haemodynamic variations and occurrence of syncope induced by head-up tilt test in older patients with refractory cardioinhibitory vasovagal syncope: the Tilt test-Induced REsponse in Closed-loop Stimulation multicentre, prospective, single blind, randomized study

Aims Closed-loop stimulation (CLS) seemed promising in preventing the recurrence of vasovagal syncope (VVS) in patients with a cardioinhibitory response to head-up tilt test (HUTT) compared with conventional pacing. We hypothesized that the better results of this algorithm are due to its quick reaction in high-rate pacing delivered in the early phase of vasovagal reflex, which increase the cardiac output and the blood pressure preventing loss of consciousness. Methods and results This prospective, randomized, single-blind, multicentre study was designed as an intra-patient comparison and enrolled 30 patients (age 62.2 ± 13.5 years, males 60.0%) with cardioinhibitory VVS, carrying a dual-chamber pacemaker incorporating CLS algorithm. Two HUTTs were performed one week apart: one during DDD-CLS 60-130/min pacing and the other during DDD 60/min pacing; patients were randomly and blindly assigned to two groups: in one the first HUTT was performed in DDD-CLS (n = 15), in the other in DDD (n = 15). Occurrence of syncope and haemodynamic variations induced by HUTT was recorded during the tests. Compared with DDD, DDD-CLS significantly reduced the occurrence of syncope induced by HUTT (30.0% vs. 76.7%; P < 0.001). In the patients who had syncope in both DDD and DDD-CLS mode, DDD-CLS significantly delayed the onset of syncope during HUTT (from 20.8 ± 3.9 to 24.8 ± 0.9 min; P = 0.032). The maximum fall in systolic blood pressure recorded during HUTT was significantly lower in DDD-CLS compared with DDD (43.2 ± 30.3 vs. 65.1 ± 25.8 mmHg; P = 0.004). Conclusion In patients with cardioinhibitory VVS, CLS reduces the occurrence of syncope induced by HUTT, compared with DDD pacing. When CLS is not able to abort the vasovagal reflex, it seems to delay the onset of syncope.

Physiological Sensitivity of Respiratory‐Dependent Cardiac Pacing: Four‐Year Follow‐Up

Clinical and physiological data on long‐term follow‐up of 143 patients with respiratory‐dependent pacemakers (RDP3) are reported; 121 patients received ventricular (VVI‐RD) and 22 patients atrial (AAI‐RD) respiratory‐dependent stimulation. Functional evaluation was based on the exercise testing (130 pts) with oxygen uptake V̇O2, ventilation, ECG and arterial pressure monitoring and the dynamic Holter electrocardiogram (95 pts). In each patient, the stimulation rate curve selected was that which produced the best work tolerance and moved the anaerobic threshold to the right. Respiratory levels were assessed by telemetry verifying proper sensing of tidal volume variations and absence of interference and artefacts. In patients with VVIR or AAIR stimulation, exercise tolerance, oxygen uptake and anaerobic threshold increased significantly in comparison with VVI or AAI pacing respectively. The physiological sensitivity of the stimulation system (i.e., a linear relationship of the pacing rate with metabolic requirements) was excellent (up to exhaustion) in 70%, very good (up to anaerobic threshold) in 20% and erratic (no relationship between pacing rate and VE/V̇O2) in 10% of patients. In dynamic electrocardiographic monitoring, the automatic pacing rate was always predominant during the night and during rest periods; the pacing rate increased properly with daily activity; myopotential inhibition (none longer than 3,500 ms) was observed in 38 patients, but without subjective complaints. The incidence of the RDP3 malfunction was less than 8%; it may have stemmed from the pacing system itself, or from other clinical conditions. Oversensing of impedance system pulses has not been recorded in the last 3 years. Partial respiration undersensing results from incorrect accessory lead position, pulmonary emphysema, marked obesity or other causes. Respiratory sensing becomes erratic at the anaerobic threshold point in such patients, but functions well at submaximum exercise levels. In patients with left ventricular failure, exercise tolerance was improved by setting a lower ratio between the pacing rate and respiration, which prevented the occurrence of excessive pacing rates.

Inappropriate Asystole Detection in Early Postoperative Phase after Loop Recorder Implantation

The implantable loop recorder is a useful diagnostic tool for patients with unexplained syncope. The capability to automatically detect and store arrhythmic events, implemented in the last generations of these devices, can further improve the diagnostic yield, but this feature can be compromised by inappropriate detection of false arrhythmias. We herein report the case of a patient in which several inappropriate activations of long-lasting asystole occurred in the two days following the implant, probably because of an intermittently loose contact between the device and subcutaneous tissue for a small pocket haematoma.

Hemodynamic Sensors: Their Impact in Clinical Practice

The need to adjust pacing rate to changing metabolic conditions has led to the development of different sensing systems that integrate the detection of atrial and ventricular electrical signals in permanent pacemakers [1]. All sensors currently available in the clinical setting assess the patient’s metabolic demand indirectly. This is the case for activity sensors, which generally detect the intensity of body motion by an accelerometer, as well as for physiological sensors, which are sensitive to cardiac or respiratory parameters physiologically correlated to the cardiac rate. The activity sensors usually show good sensitivity and prompt rate-response, but may lack specificity, since they cannot distinguish between active and passive motion. Respiratory sensors are more specific, but they show a slow response, resulting in little sensitivity towards the rapid, small changes in a patient’s activity which normally occur in daily life [2]. Cardiac sensors have to present the best compromise between sentivity and speciaficity, since the different aspects of cardiac function are regulated at the same time by the same controller, the autonomic nervous system (ANS). In patients with chronotropic incompetence, a pacemaker would restore normal rate control on the basis of relative changes in the inotropic, dromotropic, or bathmotropic regulation of the heart [3].

Can Hemodynamic Sensors Ensure Physiological Rate Control

Hemodynamic sensors are used mainly in clinical pacing to assess the inotropic state of the heart, with the aim of matching the pacing rate to the contractility level. If the patient’s chronotropic competence is depressed, this approach should allow proper cardiac rate regulation based on the physiological correlation between inotropic and chronotropic function [1–4].

A New Approach to the Prevention of Endless Loop Tachycardia in DDD and VVD Pacing

Endless loop tachycardia (ELT) is a possible complication in dual chamber pacing; it is usually prevented by programming the atrial refractory period (PVARP) longer than the retrograde ventriculoatrial (VA) conduction interval; this in some patients limits the upper rate. In 15 patients with a DDD (nine patients) or a single‐pass lead VDD pacemaker (six patients) and retrograde atrial activation, telemetric recording documented a significant difference in amplitude of antegrade, and retrograde atrial potentials (VDD 1.21 ± 0.32 mV vs 0.56 ± 0.23 mV, P = 0.008; DDD 2.7 ± 1 vs 1.8 ± 1 mV, P ‐ 0.038; Students t‐test for paired data). In 3/15 patients ELT stopped after programming of atrial sensitivity to a value. greater than the retrograde P wave amplitude; in 11/15 patients this occurred at a sensing value lower than or equal to retrograde P wave amplitude with a high pass band filter operating. One patient required PVARP lengthening. Holter monitoring showed no more ELTs. In most patients with a DDD or single‐pass lead VDD pacemaker with widely programmable sensing amplitude and Hi/Low bandpass filters. individual programming of atrial channel sensitivity prevents ELT without affecting the PVARP and, consequently, upper rate limit.

Lack of interference of electromagnetic navigation bronchoscopy to implanted cardioverter-defibrillator: in-vivo study

AIMS Electromagnetic navigation bronchoscopy (ENB) (Superdimension) is a diagnostic and therapeutic tool in patients with lung lesions. Very small data are available about potential interference of ENB magnetic field to implanted cardioverter-defibrillators (ICDs) and any documentation of ICD behaviour if a ventricular tachyarrhythmia occurs during ENB is lacking. We tested a number of selected ICDs to assess if any interference occurs by ENB magnetic field on detection of clinical ventricular fibrillation and shock delivery. METHODS AND RESULTS Thirteen patients undergoing an ICD implantation or elective replacement with a clinical indication to assess the efficacy of defibrillation underwent: (i) real-time telemetric recording from ICD during ENB activation to detect possible noise; (ii) defibrillation test during exposure to ENB board-generated magnetic field. All tested ICDs showed no noise detection at maximum sensitivity level. Induced ventricular fibrillation was correctly detected and cured by implanted device. No change in programmed ICD parameters was induced by exposure to ENB magnetic field. CONCLUSION All tested ICDs correctly operated and rescued the patients from induced ventricular fibrillation during ENB. Electromagnetic navigation bronchoscopy appears to be safe in heart patients with an ICD; however, close cardiac monitoring of these patients during ENB must be ensured as correct behaviour of all existing ICDs can only be presumed from compliance of the manufacturer to International Standards which establish procedures for electromagnetic interference checking on implantable devices on different ranges of frequency.