Dual Chamber Rate Responsive Pacing System Driven by Contractility: Final Assessment After 1-Year Follow-up

The aim of this study was to assess the long-term performance of a new dual chamber rate responsive pacing system based on the dynamic measurement of the peak endocardial acceleration (PEA) index of cardiac contractility. Seventy patients who participated in the Multicenter European Clinical Evaluation were studied 1 year after implantation by continuously recording the PEA and the heart rate (HR) during exercise stress testing and during 24 hours of usual activities. A complete examination of standard parameters was also performed to assess the pacing/sensing lead characteristics. Statistical comparisons were performed with the data recorded with the same protocol at 1 month after implant for each patient. A linear correlation coefficient was calculated between PEA and sinus rate when the patient showed predominant atrial tracked rhythm. There were no significant differences between PEA values measured at 1 month and 1 year (PEA = 0.41 ± 0.26 g vs 0.45 ± 0.29 g at rest and PEA = 1.63 ± 0.77 g vs 1.72 ± 0.83 g during peak exercise). The correlation coefficient remained stable (0.67 ± 0.15 vs 0.65 ± 0.14 during daily life and 0.74 ± 0.14 vs 0.77 ± 0.11 during exercise). The PEA signal detected by the sensor was reliable and stable. No long-term complications or adverse effects were observed, and the lead performance was comparable to that of a standard lead.     

A Sensor-based Evaluation of Heart Contractility in Patients with Head-up Tilt-induced Syncope

Studies using the head-up tilt test (HUT) suggest that a reflex increase in sympathetic activity resulting in vigorous myocardial contractions precedes neurally-mediated syncope (NMS), The aim of this study wax to evaluate heart contractility changes during positive HUT. Ten patients with recurrent NMS and positive HUT were investigated. Before HUT we temporarily placed a standard right ventricular pacing electrode incorporating in its tip a recently developed microaccelerometer (Sorin Biomedica, Italy) that measures the peak endocardial acceleration (PEA) during the isovolumetric phase as an index of heart contractility. PEA potential amplitude, heart rate and mean blood pressure were continuously studied during HUT. Syncope occurred 16.7 ± 10.3 min after 60° till, either at baseline (8 patients) or after sublingual nitrate administration (2 patients). PEA value was stable at 0.62 ± 0.34 (1G = 9.8 m/sec²) during the supine phase. It slightly increased to 0.72 ± 0.44 G (p = NS) during the first minutes of 60° tilt and then remained unchanged until a further increase of 71 ± 79% (range 10 to 266 %) as compared to tilt value (p = 0.004) at 2.8 ± 2.4 min (range 0.25 to 6.5 min) before the syncope in 9 patients. The latter increase was not observed in the patient with dilated cardiomyopathy. In conclusion, a significant increase in heart contractility was observed in 9 patients in the minutes preceding HUT-induced NMS. These changes might be used for driving a rate adaptive pacemaker when cardiac pacing is indicated to prevent NMS.     

Detection of acute myocardial ischemia during percutaneous transluminal coronary angioplasty by endocardial acceleration

The first heart sound is generated by vibrations from the myocardium during isovolumic contraction. Peak endocardial acceleration (PEA) has been used previously to measure these vibrations in humans and correlates with myocardial contractility during inotropic interventions. It is unknown if changes in PEA can be used to characterize a reduction in contractility during ischemic episodes. This study was designed to evaluate the use of an endocardial accelerometer for the detection of acute myocardial ischemia. Thirteen patients undergoing routine percutaneous transluminal coronary angioplasty (PTCA) consented to having a single-axis, lead-based accelerometer positioned in the right ventricular apex. PEA was defined as the maximum peak-to-peak amplitude during a window 50 ms before to 200 ms following the peak R wave. Time of endocardial acceleration (TEA) was defined as the time from the peak R wave to the maximum accelerometer signal within this window. To obtain a more robust estimate of the strength of vibrations, a 100-beat template of the accelerometer signal was constructed at baseline and applied as a matched filter during ischemia. The peak magnitude of the filtered endocardial accelerometer signal (Max Filtered EA) was used as an index of signal intensity. Median baseline PEA, TEA, and Max Filtered EA were 0.91 +/- 0.35 g, 75.2 +/- 16.2 ms, and 0.40 +/- 0.20 g, respectively. PEA and Max Filtered EA significantly decreased by 7% during ischemia (0.91 to 0.85 g and 0.40 to 0.37 g, both P < 0.05, respectively). TEA did not significantly change from baseline (77.0 ms, P = ns). The results of this study suggest that acute ischemia can be detected with an endocardial accelerometer in humans.     

Is Local Myocardial Contractility Related to Endocardial Acceleration Signals Detected by a Transvenous Pacing Lead?

The availability of sensors monitoring cardiac function parameters may offer many interesting new applications in cardiac pacing. A microaccelerometer sensor (BEST, Biomechanical Endocardial Sorin Transducer) located at the tip of a pacing lead (PL) has been developed by Sorin Biomedica. The signal detected by the accelerometer, peak Endocardial acceleration (PEA), was shown to reflect cardiac contractility and to be related to the dP/dt signal. Whether the PEA detected by the BEST sensor in different cardiac locations is the expression of local acceleration forces or reflects the whole heart contractility has not yet been demonstrated in humans. Endocardial acceleration and PEA were evaluated in five patients (4 males, 1 female, mean age 68 years) who underwent cardiac catheterization. Sinus rhythm was present in four patients and chronic atrial fibrillation was present in one. The BEST PL was introduced through the left subclavian vein and PEA signals were recorded: (1) at the apex of the right ventricle (RV), (2) within the coronary sinus (CS), (3) at the right atrial appendage (RAA), and (4) floating in the right atrium. The PEA signals were recorded simultaneously with surface ECG, intracardiac electrograins, and RV pressure. At each recording site, PEA signals with significant amplitude were always recorded during the preelection period, during the isovolumic contraction phase, independently of the recording site and cardiac rhythm. The PEA amplitude was higher in the RV (mean value 1.32 g) and it decreased in the RAA and CS (0.75 and 0.45 g, respectively). The same behavior of PEA was observed during sinus rhythm or atrial fibrillation. The amplitude and the timing of the PEA signals detected by the BEST accelerometer were independent of the recording site and atrial rhythm; they appeared to be strictly related to the global ventricular contractility. These results suggest that the BEST could be used either as an effective sensor in closed loop pacing systems, or primarily as a diagnostic hemodynamic sensor.     

Relationship between Amplitude and Timing of Heart Sounds and Endocardial Acceleration

Objective: To study the correlation between heart sounds and peak endocardial acceleration (PEA) amplitudes and timings, by modulation of paced atrioventricular (AV) delay in recipients of dual chamber pacemakers.
Methods: Ten recipients of dual chamber pacemakers implanted for high-degree AV block were studied. Endocardial acceleration (EA) and phonocardiographic and electrocardiographic signals were recorded during performance of an AV delay scan in VDD and DDD modes.
Results: First PEA (PEA I) and first heart sound (S1) changed similarly with the AV delay. A close intrapatient correlation was observed between S1 and PEA I amplitudes in all patients (P < 0.0001). The interpatient normalized PEA I to S1 amplitudes correlation was r = 0.89 (P < 0.0001) in DDD mode, and r = 0.81 (P < 0.0001) in VDD mode. The mean cycle-by-cycle PEA I to S1 delay was −4.3 ± 22 ms and second PEA (PEA II) to second heart sound (S2) delay was −7.7 ± 15 ms.
Conclusions: A close correlation was observed between PEA I and S1 amplitudes and timings, and between PEA II and S2 timings. These observations support the hypothesis that PEA and heart sounds are manifestations of the same phenomena. EA might be a useful tool to monitor cardiac function.     

Direct comparison of a contractility and activity pacemaker sensor during treadmill exercise testing

There are limited data about the chronotropic capacity of the peak endocardial acceleration (PEA) sensor. This study directly compared the chronotropic function from the PEA and the activity (ACT) sensor. The study included 18 patients (age 73 ± 7 years) with ≥ 75% pacemaker-driven heart rate (HR) and a PEA sensor and 11 healthy controls (age 67 ± 7 years) underwent a chronotropic assessment exercise protocol (CAEP) exercise test with the pacemaker patients in VVIR mode after programming the sensors in the default setting with adjustment of the upper sensor rate as an age related maximum value (220-age). The ACT sensor was externally strapped on the thorax. Achieved exercise duration for the patients and controls was, respectively, 9.2 ± 3 vs 18.4 ± 4 minutes (P < 0.001). The maximal achieved HR with the PEA sensor was 124 ± 25 beats/min, versus the ACT with 140 ± 23, versus the controls with 153 ± 26 beats/min (P < 0.001 between the groups). For the PEA, ACT, and controls, the time to peak HR was, respectively, 11 ± 3, 7 ± 3.6, and 18 ± 4 (P < 0.001 between groups) and HR after 10 minutes recovery was, respectively, 80 ± 20, 65 ± 15, and 82 ± 4 beats/min (P < 0.001 between groups). The PEA sensor functions hypochonotroop during exercise programmed as a single sensor system. It is, therefore, preferable to combine the PEA sensor with an activity-based sensor in a dual sensor system. Although both groups had normal left ventricular functions, the exercise capacity of pacemaker patients is significantly lower than in the controls.     

Peak endocardial acceleration reflects heart contractility also in atrial fibrillation

Previous studies demonstrated that peak endocardial acceleration (PEA) in sinus rhythm is related to LV dP/dtmax. Until now, PEA was never evaluated during R-R interval variations in AF. The aim of this study was to establish the behavior of PEA in AF and the relationship of PEA versus LV dP/dtmax. Six sheep (65 +/- 6 kg) were instrumented with a LV Millar catheter and with an accelerometer lead. AF was induced and PEA, LV dP/dtmax, and ECG were monitored. AF persisted for 5 +/- 1.3 minutes. From sinus rhythm to AF, the heart rate went from 92 +/- 3 to 130 +/- 35 beats/min (P < 0.05), LV dP/dtmax from 684 +/- 18 to 956 +/- 344 mmHg/s (P = NS) and PEA from 0.82 +/- 0.06 to 0.94 +/- 0.33 g (P = NS). The correlation between PEA and LV dP/dtmax was significative in sinus rhythm (r = 0.7, P < 0.05) and in AF (r = 0.8, P < 0.05). A positive relationship was found between the preceding interval and PEA (r = 0.4 +/- 0.07, P < 0.05) and LV dP/dtmax (r = 0.61 +/- 0.08, P < 0.05), while a negative one was found between the prepreceding interval and both PEA (r = -0.39 +/- 0.11, P < 0.05) and LV dP/dtmax (r = -0.64 +/- 0.05, P < 0.05). At the onset of AF, LV dP/dtmax and PEA showed similar changes: beat-to-beat correlation between PEA and LV dP/dtmax was high. As for LV dP/dtmax, PEA is positively related to the preceding interval and negatively related to the prepreceding interval. These data confirm that PEA reflects heart contractility also during AF and hold promise for the use of this sensor in therapeutic implantable devices.     

Recording of Peak Endocardial Acceleration in the Atrium

Background: The important role played by peak endocardial acceleration (PEA or sonR) in hemodynamic monitoring of cardiac resynchronization therapy (CRT) was recently highlighted in several studies with the sensor embedded in a right ventricular (RV) lead tip. This study examined the short- and long-term reliability of a right atrial (RA) sonR sensor.
Methods: RA and RV sonR signals were measured from RA and RV leads respectively, at implant and up to 12 months of follow-up, in 19 recipients of either single chamber pacemakers or CRT systems. At 1 month of follow up, RA sonR signals and heart rate were simultaneously recorded during exercise.
Results: A reliable RA sonR signal amplitude was measured at implant, proportional to the RV amplitude. We observed in both the right atrium and right ventricle (1) a similar signal noise ratio at implant, (2) a similar evolution of the sonR signal amplitude up to 12 months of follow-up, and (3) a high correlation between heart rate and RA sonR signal amplitude during exercise.
Conclusions: The RA sonR signal was reliable and proportional to the RV signal on the short and long term, and reflected changes in activity. These observations suggest that the sonR sensor could be placed in the atrium for the hemodynamic monitoring of CRT system recipients.     

Autonomic Nervous System-Controlled Cardiac Pacing: A Comparison Between Intracardiac Impedance Signal and Muscle Sympathetic Nerve Activity

BINGGELI, C., et al. : Autonomic Nervous System‐Controlled Cardiac Pacing: A Comparison Between Intracardiac Impedance Signal and and Muscle Sympathetic Nerve Activity. A recently introduced rate responsive cardiac pacing system is based on information derived from the intracardiac impedance signal containing information on the inotropic state of the ventricle. This study compared the inotropic state index (ISI) with muscle sympathetic activity (MSA), both being modulated by the autonomic nervous system. Nine patients (66 ± 3 years, mean ± SEM ) with Inos2DR pacemakers were included. Each patient was studied at rest and during cold pressor test (CPT). Microneurography of the peroneal nerve was performed to measure MSA continuously, which was digitally stored along with continuous surface ECG and blood pressure. The intracardiac impedance signal was transmitted by the pacemaker and stored simultaneously. Linear correlation between ISI and MSA was calculated for the period of the CPT. During CPT, mean systolic blood pressure increased from 122 ± 4 to 149 ± 6 mmHg (P < 0.0001), diastolic blood pressure increased from 74 ± 8 to 86 ± 4 mmHg (P = 0.02 ), and intrinsic heart rate increased from 69 ± 7 to 75 ± 7 beats/mill (P = 0.019 ). ISI increased by 21 ± 7% (P = 0.018 ), MSA by 26 ± 6% (P = 0.004 ). ISI and MSA were positively correlated during the CPT in eight of nine patients (R2 = 0.86–0.99, P < 0.0001 ). Negative correlation was found in one patient (R2 = 0.94 ). This study demonstrates parallel increases of the ISI and MSA during CPT. ISI and MSA showed a close linear relationship during provoked changes of sympathetic activity. These results provide further evidence that the sympathetic nervous system is responsible for the observed ISI changes.     

Atrial transseptal left ventricular lead implantation for cardiac resynchronization therapy using arteriovenous loop technique

To date, several techniques for transseptal left ventricular (LV) endocardial pacing for cardiac resynchronization therapy (CRT) have been proposed in patients for whom routine transvenous LV pacing is infeasible. These techniques are of varying difficulty and complexity, and some requires devices not easily accessible. We herein report a simple, safe and effective approach of atrial transseptal LV lead implantation using arteriovenous loop technique in a patient for whom transvenous LV implantation lead had failed.     

Alternative Techniques for Left Ventricular Pacing in Cardiac Resynchronization Therapy

Cardiac resynchronization therapy (CRT) is an important treatment modality for a well‐defined subgroup of heart failure patients. Coronary sinus (CS) lead placement is the first‐line clinical approach but the insertion is unsuccessful in about 5–10% of the patients. In recent years, the number of CRT recipients and the considerable need for left ventricular (LV) lead revisions increased enormously. Numerous techniques and technologies have been specifically developed to provide alternatives for the CS LV pacing. Currently, the surgical access is most frequently used as a second choice by either minithoracotomy or especially the video‐assisted thoracoscopy. The transseptal or transapical endocardial LV lead implantations are being developed but there are no longer follow‐up data in larger patient cohorts. These new techniques should be reserved for patients failing conventional or surgical CRT implants. In the future, randomized studies are needed to asses the potential benefits of some alternative LV pacing techniques and other new technologies for LV lead placement are expected.     

Feasibility of Using Intracardiac Impedance Measurements for Capture Detection

Energy consumption and longevity of modern pacemakers are determined by the controlling electronic circuitry and by the stimulation energy. While with technological progress the electronics' energy consumption has been reduced significantly, clinical practice shows that many cardiac pacemakers are programmed to suboptimal settings with regard to minimization of pacing energy consumption. Several methods for optimizing pacemaker output settings have been proposed in the past. The most promising concept is an output parameter optimizing pacemaker with automatic capture detection. We examined whether it is possible to distinguish between effective and ineffective pacemaker stimulus capture by analyzing high pass filtered intracardiac impedance signals that are derived from standard bipolar pacing leads. In one series of 11 patients undergoing replacement or implantation of chronic bipolar pacemakers, four patients during electrophysiology studies, and eight volunteers undergoing invasive electrophysiology trials, we examined intracardiac impedance signals obtained with various stimulation rates and output parameter settings. Additionally we analyzed a series of five patients with implanted pacemakers that can measure and telemeter intracardiac impedance signals. Several evaluation concepts have been analyzed regarding their ability to discriminate between effective and ineffective stimuli. We developed an adequate algorithm that detects capture or loss of capture at different output parameter settings based on intracardiac impedance analysis. The sensitivity is 98.5% and specificity is 91% to loss of capture for the currently investigated algorithm and this can be used to determine the optimal setting of pulse width and amplitude with regard to energy consumption. This concept is currently under realization in the external programmer and in the future an implementation of these algorithms within the pacemaker itself is intended.     

An Active Optical Sensor for Monitoring Mixed Venous Oxygen-Saturation for an Implantable Rate-Regulating Pacing System

Les stimuJateurs dits "physiologiques" qui sont actuellement disponibles ne restaurent pos la fréquence optimale dans les cos de défaillance auriculaire. Ďautres paramètres biologiques doivent servir de stimulus physiologique pour determiner ľouto-reglage de la fréquence. La saturation veineuse mesurée par capteur optique serait probablement le paramètre idéal pour ce système de sfimulation. Des recherches supplémentaires sont nécessaires pour bien déterminer les modalités des reponse du système.
Presently available physiologic pacing systems do not fully restore rate regulation, especially in respect to little or no atrial response to activity. Other biologic parameters, detected by sensors, may provide the physiologic responsiveness necessary to rate-regulating pacemakers. An optical sensor using mixed venous oxygen saturation may be the ideal parameter for such a pacing system. At present, further research is necessary to elaborate a suitable algorithm for optimal rate control.     

Comparison of the efficacy of two surgical alternatives for cardiac resynchronization therapy: trans-apical versus epicardial left ventricular pacing

Background: Epicardial pacing lead implantation is the currently preferred surgical alternative for left ventricular (LV) lead placement. For endocardial LV pacing, we developed a fundamentally new surgical method. The trans‐apical lead implantation is a minimally invasive technique that provides access to any LV segments. The aim of this prospective randomized study was to compare the outcome of patients undergoing either trans‐apical endocardial or epicardial LV pacing. Methods: In group I, 11 end‐stage heart failure (HF) patients (mean age 59.7 ± 7.9 years) underwent trans‐apical LV lead implantation. Epicardial LV leads were implanted in 12 end‐stage HF patients (group II; mean age 62.8 ± 7.3 years). Medical therapy was optimized in all patients. The following parameters were compared during an 18‐month follow‐up period: LV ejection fraction (LVEF), LV end‐diastolic diameter (LVEDD), LV end‐systolic diameter, and New York Heart Association (NYHA) functional class. Results: Nine out of 11 patients responded favorably to the treatment in group I (LVEF 39.7 ± 12.5 vs 26.0 ± 7.8%, P < 0.01; LVEDD 70.4 ± 13.6 mm vs 73.7 ± 10.5 mm, P = 0.002; NYHA class 2.2 ± 0.4 vs 3.5 ± 0.4, P < 0.01) and eight out of 12 in group II (LVEF 31.5 ± 11.5 vs 26.4 ± 8.9%, P = < 0.001; NYHA class 2.7 ± 0.4 vs 3.6 ± 0.4, P < 0.05). During the follow‐up period, one patient died in group I and three in group II. There was one intraoperative LV lead dislocation in group I and one early postoperative dislocation in each group. None of the patients developed thromboembolic complications. Conclusions: Our data suggest that trans‐apical endocardial LV lead implantation is an alternative to epicardial LV pacing. PACE 2012; 35:124–130)     

Feasibility of Long-Term Electrocardiographic Monitoring with an Implanted Device for Syncope Diagnosis

Patients with infrequent recurrent syncope undiagnosed after extensive noninvasive and invasive testing pose a diagnostic and therapeutic dilemma. The purpose of this pilot study was to assess the feasibility of using an implanted, long-term monitor as an aid to diagnosis in these patients. This was done using commercially available pacemakers with monitoring functions. Sixteen patients (eight males and eight femaiesj, aged 59.7 ± 17 years who had unexplained syncope despite a 12-lead electrocardiogram, repeated Holter monitoring, exercise testing, echocardiography, an eJectro-physioJogical study, and a tiJf test (n = 6), were entered into the study. Patients had experienced a mean of 3.3 ± 1 episodes of syncope in the 12 months prior to the study. All provided a history suggestive of Stokes-Adams attacks and were referred for consideration of pacemaker implantation. Two patients had ischemic heart disease and one patient had a long QT interval. Patients had an Intermedics Nova II or Medtronic Quintech DPG pulse generator capable of recording sensed and paced events implanted with a single right ventricular lead. Syncope or presyncope occurred in ten patients (62%) 4.9 ± 4.2 months after pacemaker implantation. Bradycardia was detected in six patients and four patients had no arrhythmia. In addition to bradycardia, one patient also had tachycardia detected. Pacing therapy resulted in symptom relief in all six patients with syncope or presyncope due to bradycardia. Complications of pacemaker implantation (lead insulation failure) occurred in two patients. One of these patients subsequently had an infection of the generator pocket with associated systemic sepsis. Although the devices used in this study have serious limitations, the results suggest that continuous long-term electrocardiographic monitoring can be useful in patients with recurrent syncope and a negative diagnostic work-up. A smaller device with self-contained electrodes designed for this purpose would be required for wider applicability.