Resynchronization therapy optimization by intracardiac impedance.

AIMS: For successful cardiac resynchronization therapy (CRT), an optimization of left ventricular (LV) lead position and stimulation timing is required. The feasibility of optimizing LV lead position, atrioventricular delay (AVd), and interventricular delay (VVd) in CRT using intracardiac impedance measurement was evaluated. METHODS AND RESULTS: Heart failure patients (n = 14, NYHA 13×III, 1×II, ejection fraction: 26 ± 6%, QRS: 165 ± 30 ms) were stimulated by AAI and biventricular (DDD-BiV) pacing in turn. Left ventricular lead site, AVd, and VVd were varied. An external pacemaker measured impedance, and a micromanometer catheter measured LV and aortic pressure. Left ventricular dP/dt(max), pulse pressure (PP), stroke volume (SV), end-systolic impedance (ESZ), and stroke impedance (SZ) were determined. Optimization results achieved by maximum increase in PP, SV, SZ, or ESZ were compared with the reference method (dP/dt(max) increase). Left ventricular lead site variation resulted in a mean optimal dP/dt(max) benefit of 18.2%. Lead site selection by SZ/PP/SV showed benefits of 17.4/17.9/17.2%, respectively. Atrioventricular delay optimization increased the optimal benefit to 22.1%, the methods ESZ/PP/SV achieved 20.1/20.8/19.4%. Interventricular delay optimization resulted in a benefit of 19.1/19.4/19.9% (SZ/PP/SV) with an optimum of 21.8%. The achieved benefit did not differ significantly between impedance, SV, and PP methods. A significant correlation between AVd values selected by dP/dt(max) and by the other methods was observed (r = 0.75/0.67/0.60 for ESZ/PP/SV). CONCLUSION: The feasibility of optimizing LV lead site, AVd, and VVd by intracardiac impedance has been demonstrated for CRT patients with a similar performance as using SV and PP. Application of intracardiac impedance for automatic implant-based CRT optimization appears to be within reach.

Intracardiac impedance monitors stroke volume in resynchronization therapy patients.

AIMS: Monitoring of haemodynamic parameters or surrogate parameters of the left ventricle is especially important for patients under cardiac resynchronization therapy (CRT). Intracardiac impedance reflects left ventricular (LV) volume changes well in animal models. Since it is unknown whether this also holds in humans with heart failure (HF), we examined the correlation of LV intracardiac impedance with haemodynamic parameters in CRT patients for different positions of the LV lead. METHODS AND RESULTS: In 14 HF patients with non-ischaemic cardiomyopathy (four female, age 70 +/- 6 years, NYHA 2.9 +/- 0.3, EF 26 +/- 6%), one or two suitable implantation sites for the LV lead were selected. Following atrial, right ventricular, and LV catheter positioning, a micro-manometer catheter was placed in the ascending aorta. Surface ECG, impedance, and aortic pressure were recorded during graded overdrive bi-ventricular pacing in DDD mode. The correlation between impedance and stroke volume (SV) or pulse pressure (PP) changes was compared for different LV lead positions. In total, 20 overdrive pacing tests were performed at six different LV lead positions. Strong correlations were found between stroke impedance (SZ) and SV (R = 0.82 +/- 0.16) as well as between SZ and PP (R = 0.81 +/- 0.16) without significant influence of LV lead position. CONCLUSION: In HF patients, a strong correlation between changes in intracardiac impedance and LV SV was found. Typical LV lead implant positions have been tested and all appear to be suitable for this method of LV volume monitoring.

Assessing acute ventricular volume changes by intracardiac impedance in a chronic heart failure animal model.

BACKGROUND: Implantable device diagnostics may play an essential role in simplifying the care of heart failure patients by providing fundamental insights into their complex clinical patterns. Early recognition of heart failure progression by a continuous hemodynamic monitoring would allow for timely therapeutic interventions to prevent decompensation and hospitalization. In this study, the feasibility of assessing ventricular volume changes by implant-based measurements of intracardiac impedance was tested in a heart failure animal model. METHODS: Heart failure was induced in five minipigs by high-rate pacing over 3 weeks. During a final open-chest examination a graded dobutamine stress test was performed. Stroke volume (SV) was measured by an ultrasonic flow probe at the ascending aorta. End diastolic pressure (EDP) and maximum pressure slope (dP/dtmax) were calculated from a left ventricular microtip catheter signal. Impedance was measured by an implanted pacemaker between biventricular leads. Stroke impedance (SZ) was calculated as the difference between end-systolic and end-diastolic impedance (EDZ). RESULTS: Administration of dobutamine led to an increase in SV (55+/-16%), dP/dtmax (107+/-89%), and SZ (56+/-30%). EDP changed by 37+/-21% whereas EDZ changed by 7.4+/-4%. Significant correlations were found between SZ and SV (r=0.88), and between EDZ and EDP (r=-0.82). CONCLUSION: The strong correlation with SV allows the application of intracardiac impedance measurements for an implant-based continuous monitoring of cardiac function. Impedance may also be used for hemodynamic optimization of cardiac resynchronization therapy.

Intracardiac impedance monitors hemodynamic deterioration in a chronic heart failure pig model.

INTRODUCTION: A large number of heart failure (HF) patients benefit from cardiac resynchronization therapy. Measurements of intrathoracic impedance (ITZ) by implantable devices correlate with intrathoracic fluid content and are used for monitoring lung edema formation in HF patients. However, intrathoracic fluid is only an indirect parameter of cardiac function. We hypothesized that changes in intracardiac impedance correlate with left ventricular (LV) volume changes. Therefore, measurements of intracardiac impedance between a right ventricular lead and a LV lead may be used to monitor long-term changes of LV function. METHODS AND RESULTS: HF was successfully induced in nine mini-pigs by continuous high-rate pacing. Hemodynamic parameters as well as intracardiac impedance and ITZ were measured before HF induction and after 20 +/- 5 days of high-rate pacing. After the pacing period, we found a significant deterioration of hemodynamics, reflected by a reduction of ejection fraction from 71+/-11% to 48+/-7% and an increase of LV end diastolic pressure (EDP) from 12 +/- 4 mmHg to 26 +/- 8 mmHg. Worsening of cardiac function correlated with a significant >30% decrease of end diastolic intracardiac impedance, in accordance with a >20% increase of end diastolic volume (EDV). ITZ decreased by more than 8%. We observed a significant inverse correlation between end diastolic intracardiac impedance and EDP (r =-0.81, P < 0.001). CONCLUSIONS: In this animal model, changes of intracardiac impedance revealed hemodynamic deterioration as reflected by EDV and EDP pressure. Thus, intracardiac impedance is a promising new application to monitor heart failure status within implantable devices.

Can transventricular intracardiac impedance measurement discriminate haemodynamically unstable ventricular arrhythmias in human?

AIMS: To measure changes in transventricular impedance during arrhythmias. METHODS AND RESULTS: Patients were studied during electrophysiological studies. A quadrapolar catheter was positioned at the right ventricular apex (RVA) and a decapolar catheter within the coronary sinus (CS). Transventricular impedance was measured by injecting a subthreshold biphasic rectangular pulse of 600 micro A between poles 1 of the CS catheter and pole 1 of the RVA catheter and the voltage measured between CS pole 10 and RVA catheter pole 4. Stroke impedance (SZ), surface ECG, intracardiac electrogram (IEGM), and invasive femoral artery blood pressure (FAP) were recorded. Twenty-eight patients were analysed, 5 with inducible, haemodynamically unstable ventricular tachycardia (VT) (HUSVT), 5 with stable VT (HSVT). During HUSVT, the SZ value reduced to 22% (range 0.15-0.32 P < 0.001) in comparison with sinus rhythm. For HSVT, the SZ value reduced to 58% (range 0.33-0.88) P < 0.01, significantly different from HUSVT (P < 0.01). There was a good correlation between reduction of SZ and arterial pulse pressure (PP) during arrhythmias (r = 0.95). CONCLUSION: Changes in SZ strongly correlated with PP amplitude. Transventricular impedance fell significantly during unstable arrhythmias and may be useful as a sensor capable of haemodynamic discrimination.

The use of unipolar intracardiac impedance for discrimination of haemodynamically stable and unstable arrhythmias in man.

AIMS: To determine the feasibility of discriminating haemodynamically stable from unstable arrhythmias using right ventricular (RV) unipolar intracardiac impedance (Z). METHODS AND RESULTS: A quadrapolar temporary pacing electrode was positioned at the RV apex and unipolar impedance was measured between the tip electrode and a surface patch electrode. Changes in peak-to-peak Z amplitude were measured simultaneously with surface ECG and blood pressure during induced arrhythmias. Haemodynamic instability was defined as a systolic pressure of <90 mmHg. There were 25 episodes of ventricular fibrillation (VF) induced in 15 patients, 18 episodes of ventricular tachycardia in 16 patients, and 33 episodes of supraventricular tachycardia (SVT) in 16 patients. Compared with the baseline rhythm, mean Z amplitude reduced from 51.3+/-7.7 to 11.2+/-7.4 Ohm (P<0.001) during VF, from 52.2+/-6.3 to 21.7+/-10.1 Ohm (P<0.01) during haemodynamically unstable VT, from 55.0+/-6.9 to 39.9+/-11 Ohm (ns) during stable VT, and from 56.4+/-8.4 to 36.9+/-9.3 Ohm during SVT (P<0.001). CONCLUSION: Right ventricular unipolar impedance is an adequate sensor for determining mechanical ventricular contraction and acts as a surrogate marker for a fall in arterial blood pressure during VF. However, for ventricular and supraventricular tachycardias, variations between patients did not allow adequate discrimination between stable and unstable arrhythmias.

Determination of left ventricular volume changes by intracardiac conductance using a biventricular electrode configuration.

AIMS: The feasibility of determining left ventricular (LV) volume changes by LV conductance measurements with an implantable device was investigated in an animal model. METHODS AND RESULTS: The haemodynamic state of six mongrel dogs was altered by overpacing with rates up to 140 bpm and by isoprenaline infusion with dosages up to 0.2 microg/kg/min. The LV conductance, aortic blood flow, and LV and aortic pressure were recorded. Conductance measurements were carried out using the two electrodes of a bipolar right ventricular pacing lead for current injection and two epicardial leads screwed into the mid-lateral LV wall for measuring the resulting voltage. Stroke conductance (SY) was correlated with the LV stroke volume (LVSV), which was computed from the aortic flow. The LVSV rose to 188+/-14% with increasing isoprenaline dosage. A strong correlation between the LV conductance SY and the LVSV was found (mean r=0.97). The LVSV decreased to 68+/-8% with an increasing pacing rate. Again, a strong correlation between SY and LVSV was found (mean r=0.89). CONCLUSION: This animal study confirms the feasibility of assessing changes in LVSV by determining the LV intracardiac conductance. This creates the possibility of continuous haemodynamic monitoring with implantable devices.