Basic Properties And Clinical Applications Of The Intracardiac.

The electric signals detected by intracardiac electrodes provide information on the occurrence and timing of myocardial depolarization, but are not generally helpful to characterize the nature and origin of the sensed event. A novel recording technique referred to as intracardiac ECG (iECG) has overcome this limitation. The iECG is a multipolar signal, which combines the input from both atrial and ventricular electrodes of a dual-chamber pacing system in order to assess the global electric activity of the heart. The tracing resembles a surface ECG lead, featuring P, QRS and T waves. The time-course of the waveform representing ventricular depolarization (iQRS) does correspond to the time-course of the surface QRS with any ventricular activation modality. Morphological variants of the iQRS waveform are specifically associated with each activity pattern, which can therefore be diagnosed by evaluation of the iECG tracing. In the event of tachycardia, SVTs with narrow QRS can be distinguished from other arrhythmia forms based upon the preservation of the same iQRS waveform recorded in sinus rhythm. In ventricular capture surveillance, real pacing failure can be reliably discriminated from fusion beats by the analysis of the area delimited by the iQRS signal. Assessing the iQRS waveform correspondence with a reference template could be a way to check the effectiveness of biventricular pacing, and to discriminate myocardial capture alone from additional His bundle recruitment in para-Hisian stimulation. The iECG is not intended as an alternative to conventional intracavitary sensing, which remains the only tool suitable to drive the sensing function of a pacing device. Nevertheless, this new electric signal can add the benefits of morphological data processing, which might have important implications on the quality of the pacing therapy.

Hemodynamic Surveillance of Ventricular Pacing Effectiveness with the Transvalvular Impedance Sensor.

The Transvalvular Impedance (TVI) is derived between atrial and ventricular pacing electrodes. A sharp TVI increase in systole is an ejection marker, allowing the hemodynamic surveillance of ventricular stimulation effectiveness in pacemaker patients. At routine follow-up checks, the ventricular threshold test was managed by the stimulator with the supervision of a physician, who monitored the surface ECG. When the energy scan resulted in capture loss, the TVI system must detect the failure and increase the output voltage. A TVI signal suitable to this purpose was present in 85% of the tested patients. A total of 230 capture failures, induced in 115 patients in both supine and sitting upright positions, were all promptly recognized by real-time TVI analysis (100% sensitivity). The procedure was never interrupted by the physician, as the automatic energy regulation ensured full patient's safety. The pulse energy was then set at 4 times the threshold to test the alarm specificity during daily activity (sitting, standing up, and walking). The median prevalence of false alarms was 0.336%. The study shows that TVI-based ejection assessment is a valuable approach to the verification of pacing reliability and the autoregulation of ventricular stimulation energy.

Acute effects of right ventricular pacing on cardiac haemodynamics and transvalvular impedance.

AIMS: To assess the acute side-effects of right ventricular (RV) stimulation applied in apex and mid-septum, in order to establish the optimal lead location in clinical practice. METHODS: During pacemaker implantation, the ventricular lead was temporarily fixed in the apex and then moved to mid-septum. In both positions, surface and endocardial electrograms and transvalvular impedance (32 cases), left ventricular (LV) pressure (23), and transthoracic echocardiography (10) were acquired with intrinsic activity and VDD pacing. RESULTS: A larger increase in QRS duration was noticed with apical than septal pacing (65±25 vs. 45±29 ms; P<10(-4)). The proportion of cases where RV stimulation affected the transvalvular impedance waveform was higher with apical lead location (56% vs. 20%; P<0.02). VDD pacing at either site reduced the maximum dP/dt by 6% with respect to intrinsic AV conduction (IAVC; P<0.005). The maximum pressure drop taking place in 100 ms was reduced by 6 and 8%, respectively, with apical and septal pacing (P<0.01 vs. IAVC). Apical VDD decreased mitral annulus velocity in early diastole (E') from 7.5±1.4 to 5.9±0.9 cm/s (P<0.02) and prolonged the E-wave deceleration time (DT) from 156±33 to 199±54 ms (P<0.02), while septal pacing induced non-significant modifications in E' and DT. CONCLUSION: Ventricular stimulation acutely impairs LV systolic and diastolic performance, independent of the pacing site. Septal lead location preserves RV contraction mechanics and reduces the electrical interventricular delay.

Impact of acute changes of left ventricular contractility on the transvalvular impedance: validation study by pressure-volume loop analysis in healthy pigs.

BACKGROUND: The real-time and continuous assessment of left ventricular (LV) myocardial contractility through an implanted device is a clinically relevant goal. Transvalvular impedance (TVI) is an impedentiometric signal detected in the right cardiac chambers that changes during stroke volume fluctuations in patients. However, the relationship between TVI signals and LV contractility has not been proven. We investigated whether TVI signals predict changes of LV inotropic state during clinically relevant loading and inotropic conditions in swine normal heart. METHODS: The assessment of RVTVI signals was performed in anesthetized adult healthy anesthetized pigs (n = 6) instrumented for measurement of aortic and LV pressure, dP/dtmax and LV volumes. Myocardial contractility was assessed with the slope (Ees) of the LV end systolic pressure-volume relationship. Effective arterial elastance (Ea) and stroke work (SW) were determined from the LV pressure-volume loops. Pigs were studied at rest (baseline), after transient mechanical preload reduction and afterload increase, after 10-min of low dose dobutamine infusion (LDDS, 10 ug/kg/min, i.v), and esmolol administration (ESMO, bolus of 500 µg and continuous infusion of 100 µg·kg-1·min-1). RESULTS: We detected a significant relationship between ESTVI and dP/dtmax during LDDS and ESMO administration. In addition, the fluctuations of ESTVI were significantly related to changes of the Ees during afterload increase, LDDS and ESMO infusion. CONCLUSIONS: ESTVI signal detected in right cardiac chamber is significantly affected by acute changes in cardiac mechanical activity and is able to predict acute changes of LV inotropic state in normal heart.

Left ventricular mechanical activity detected by impedance recording.

AIMS: Recording and analysing impedance fluctuation along the cardiac cycle in the right (RV) and left ventricles (LV). METHODS AND RESULTS: During a biventricular (BiV) implantation procedure, impedance was sequentially derived between the atrial ring electrode and either electrode (tip or ring) of the RV lead [transvalvular impedance (TVI)], and between the atrial ring and either the tip or ring electrode of a coronary sinus lead, positioned in a cardiac vein [left ventricle impedance (LVI)]. The LVI signal was also recorded by the implanted pacemaker at the 1 day and 3 months follow-ups. With intrinsic conduction, TVI showed an average increase of 53 +/- 29 ohm during ventricular systole, whereas at the same time, LVI decreased by 45 +/- 21 ohm (25 and 23 patients, respectively, out of 28 tested cases). Transvalvular impedance and LVI displayed a similar time course, which appeared to be related to the systolic timing in the RV and LV. Both LVI amplitude and duration decreased as a function of the cardiac rate. The LVI deflection started immediately after LV stimulation, and often anticipated the R-wave sensing after contralateral pacing. At the 3-month follow-up, LVI amplitude was decreased in 70% of cases and increased in the remainder, with a non-significant average change of -5 +/- 85% with respect to the acute recordings. CONCLUSION: Transvalvular impedance properties are consistent with the assumption of an inverse relationship with RV volume. Though LVI requires a different physical interpretation, the waveform duration might reflect the timing of LV myocardial contraction. In this hypothesis, the relationship between TVI and LVI could provide insight into the effects of BiV pacing on mechanical synchronization.

Rate-responsive pacing regulated by cardiac haemodynamics.

AIMS: Trans-valvular impedance (TVI) recording has been proposed for the assessment of cardiac haemodynamics, assuming an inverse relationship between TVI and ventricular volume. We checked whether the TVI sensor can drive the rate-responsive function of a cardiac pacemaker following changes in the inotropic regulation of the heart. METHODS: An external DDD-R pacemaker (Ext Sophos by Medico, Padova, Italy) equipped with the TVI detecting system was tested in 30 patients on the implantation of conventional pacing leads for dual-chamber pacing. Pacing rate regulation was based on the relationship between the stroke volume and the end-diastolic volume, inferred from TVI data. After sensor calibration in basal conditions, beta-adrenergic stimulation was induced by i.v. administration of 2 microg/ml/min isoprenaline (isoproterenol) (IPN). The actual cardiac rate, the TVI waveform, the end-diastolic and systolic TVI in each cardiac cycle and the TVI-indicated rate were stored in memory as a function of time and down-loaded at the end of the session. RESULTS: All patients with intrinsic atrial activity (28/30) showed a positive chronotropic response to IPN, coupled with a significant increase in end-diastolic TVI and a four-times larger increase in end-systolic TVI. The TVI inotropic index mirrored the sinus rate time-course, with a linear correlation between the two parameters (r(2)>0.7 in 25/28 cases). As a result, the TVI-indicated rate closely reproduced the sinus rate. CONCLUSIONS: The study confirms the reliability of the haemodynamic information derived from TVI and supports its application in the regulation of rate-responsive pacing.