Tracking Early Systolic Motion for Assessing Acute Response to Cardiac Resynchronization Therapy in Real Time.

An abnormal systolic motion is frequently observed in patients with left bundle branch block (LBBB), and it has been proposed as a predictor of response to cardiac resynchronization therapy (CRT). Our goal was to investigate if this motion can be monitored with miniaturized sensors feasible for clinical use to identify response to CRT in real time. Motion sensors were attached to the septum and the left ventricular (LV) lateral wall of eighteen anesthetized dogs. Recordings were performed during baseline, after induction of LBBB, and during biventricular pacing. The abnormal contraction pattern in LBBB was quantified by the septal flash index (SFI) equal to the early systolic shortening of the LV septal-to-lateral wall diameter divided by the maximum shortening achieved during ejection. In baseline, with normal electrical activation, there was limited early-systolic shortening and SFI was low (9 ± 8%). After induction of LBBB, this shortening and the SFI significantly increased (88 ± 34%, p < 0.001). Subsequently, CRT reduced it approximately back to baseline values (13 ± 13%, p < 0.001 vs. LBBB). The study showed the feasibility of using miniaturized sensors for continuous monitoring of the abnormal systolic motion of the LV in LBBB and how such sensors can be used to assess response to pacing in real time to guide CRT implantation.

Continuous Estimation of Acute Changes in Preload Using Epicardially Attached Accelerometers.

OBJECTIVE: A miniaturized accelerometer can be incorporated in temporary pacemaker leads which are routinely attached to the epicardium during cardiac surgery and provide continuous monitoring of cardiac motion during and following surgery. We tested if such a sensor could be used to assess volume status, which is essential in hemodynamically unstable patients. METHODS: An accelerometer was attached to the epicardium of 9 pigs and recordings performed during baseline, fluid loading, and phlebotomy in a closed chest condition. Alterations in left ventricular (LV) preload alter myocardial tension which affects the frequency of myocardial acceleration associated with the first heart sound ( fS1). The accuracy of fS1 as an estimate of preload was evaluated using sonomicrometry measured end-diastolic volume (EDV[Formula: see text]). Standard clinical estimates of global end-diastolic volume using pulse index continuous cardiac output (PiCCO) measurements (GEDV[Formula: see text]) and pulmonary artery occlusion pressure (PAOP) were obtained for comparison. The diagnostic accuracy of identifying fluid responsiveness was analyzed for fS1, stroke volume variation (SVV[Formula: see text]), pulse pressure variation (PPV[Formula: see text]), GEDV[Formula: see text], and PAOP. RESULTS: Changes in fS1 correlated well to changes in EDV[Formula: see text] ( r2=0.81, 95%CI: [0.68, 0.89]), as did GEDV[Formula: see text] ( r2=0.59, 95%CI: [0.36, 0.76]) and PAOP ( r2=0.36, 95%CI: [0.01, 0.73]). The diagnostic accuracy [95%CI] in identifying fluid responsiveness was 0.79 [0.66, 0.94] for fS1, 0.72 [0.57, 0.86] for SVV[Formula: see text], and 0.63 (0.44, 0.82) for PAOP. CONCLUSION: An epicardially placed accelerometer can assess changes in preload in real-time. SIGNIFICANCE: This novel method can facilitate continuous monitoring of the volemic status in open-heart surgery patients and help guiding fluid resuscitation.

Automatic detection of valve events by epicardial accelerometer allows estimation of the left ventricular pressure trace and pressure-displacement loop area.

Measurements of the left ventricular (LV) pressure trace are rarely performed despite high clinical interest. We estimated the LV pressure trace for an individual heart by scaling the isovolumic, ejection and filling phases of a normalized, averaged LV pressure trace to the time-points of opening and closing of the aortic and mitral valves detected in the individual heart. We developed a signal processing algorithm that automatically detected the time-points of these valve events from the motion signal of a miniaturized accelerometer attached to the heart surface. Furthermore, the pressure trace was used in combination with measured displacement from the accelerometer to calculate the pressure-displacement loop area. The method was tested on data from 34 animals during different interventions. The accuracy of the accelerometer-detected valve events was very good with a median difference of 2 ms compared to valve events defined from hemodynamic reference recordings acquired simultaneously with the accelerometer. The average correlation coefficient between the estimated and measured LV pressure traces was r = 0.98. Finally, the LV pressure-displacement loop areas calculated using the estimated and measured pressure traces showed very good correlation (r = 0.98). Hence, the pressure-displacement loop area can be assessed solely from accelerometer recordings with very good accuracy.

Left bundle branch block increases left ventricular diastolic pressure during tachycardia due to incomplete relaxation.

We investigated whether tachycardia in left bundle branch block (LBBB) decreases left ventricular (LV) diastolic distensibility and increases diastolic pressures due to incomplete relaxation, and if cardiac resynchronization therapy (CRT) modifies this response. Thirteen canines were studied at baseline heart rate (120 beats/min) and atrial paced tachycardia (180 beats/min) before and after induction of LBBB and during CRT. LV and left atrial pressures (LAP) were measured by micromanometers and dimensions by sonomicrometry. The time constant τ of exponential pressure decay and degree of incomplete relaxation at mitral valve opening (MVO) and end diastole (ED) based on extrapolation of the exponential decay were assessed. Changes in LV diastolic distensibility were investigated using the LV transmural pressure-volume (PV) relation. LBBB caused prolongation of τ (P < 0.03) and increased the degree of incomplete relaxation during tachycardia at MVO (P < 0.001) and ED (P = 0.08) compared with normal electrical activation. This was associated with decreased diastolic distensibility seen as upward shift of the PV relation at MVO by 18.4 ± 7.0 versus 12.0 ± 5.0 mmHg, at ED by 9.8 ± 2.3 versus 4.7 ± 2.3 mmHg, and increased mean LAP to 11.4 ± 2.7 versus 8.5 ± 2.6 mmHg, all P < 0.006. CRT shifted the LV diastolic PV relation downwards during tachycardia, reducing LAP and LV diastolic pressures (P < 0.03). Tachycardia in LBBB reduced LV diastolic distensibility and increased LV diastolic pressures due to incomplete relaxation, whereas CRT normalized these effects. Clinical studies are needed to determine whether a similar mechanism contributes to dyspnea and exercise intolerance in LBBB and if effects of CRT are heart rate dependent.NEW & NOTEWORTHY Compared with normal electrical conduction, tachycardia in left bundle branch block resulted in incomplete relaxation during filling, particularly of the late activated left ventricular lateral wall. This further resulted in reduced left ventricular diastolic distensibility and elevated diastolic pressures and thus amplified the benefits of cardiac resynchronization therapy in this setting.

Dynamic gravity compensation does not increase detection of myocardial ischemia in combined accelerometer and gyro sensor measurements.

Previous studies have shown that miniaturised accelerometers can be used to monitor cardiac function and automatically detect ischemic events. However, accelerometers cannot differentiate between acceleration due to motion and acceleration due to gravity. Gravity filtering is essential for accurate integration of acceleration to yield velocity and displacement. Heart motion is cyclic and mean acceleration over time is zero. Thus, static gravity filtering is performed by subtracting mean acceleration. However, the heart rotates during the cycle, the gravity component is therefore not constant, resulting in overestimation of motion by static filtering. Accurate motion can be calculated using dynamic gravity filtering by a combined gyro and accelerometer. In an animal model, we investigated whether increased accuracy using dynamic filtering, compared to using static filtering, would enhance the ability to detect ischemia. Additionally, we investigated how well the gyro alone could detect ischemia based on the heart's rotation. Dynamic filtering tended towards lower sensitivity and specificity, using receiver operating characteristics analysis, for ischemia-detection compared to static filtering (area under the curve (AUC): 0.83 vs 0.93, p = 0.125). The time-varying gravity component indirectly reflects the heart's rotation. Hence, static filtering has the advantage of indirectly including rotation, which alone demonstrated excellent sensitivity to ischemia (AUC = 0.98).

Mechanism of Abnormal Septal Motion in Left Bundle Branch Block: Role of Left Ventricular Wall Interactions and Myocardial Scar.

OBJECTIVES: This study sought to investigate how regional left ventricular (LV) function modifies septal motion in left bundle branch block (LBBB). BACKGROUND: In LBBB, the interventricular septum often has marked pre-ejection shortening, followed by immediate relengthening (rebound stretch). This motion, often referred to as septal flash, is associated with positive response to cardiac resynchronization therapy (CRT). METHODS: In 10 anesthetized dogs, we induced LBBB by radiofrequency ablation and occluded the circumflex (CX) (n = 10) and left anterior descending (LAD) (n = 6) coronary arteries, respectively. Myocardial dimensions were measured by sonomicrometry and myocardial work by pressure-segment length analysis. In 40 heart failure patients with LBBB, including 20 with post-infarct scar and 20 with nonischemic cardiomyopathy, myocardial strain was measured by speckle-tracking echocardiography and myocardial work by pressure-strain analysis. Scar was assessed by cardiac magnetic resonance imaging with late gadolinium enhancement. RESULTS: During LBBB, each animal showed typical septal flash with pre-ejection shortening and rebound stretch, followed by reduced septal systolic shortening (p < 0.01). CX occlusion caused LV lateral wall dysfunction and abolished septal flash due to loss of rebound stretch (p < 0.0001). Furthermore, CX occlusion restored septal systolic shortening to a similar level as before induction of LBBB and substantially improved septal work (p < 0.001). LAD occlusion, however, accentuated septal flash by increasing rebound stretch (p < 0.05). Consistent with the experimental findings, septal flash was absent in patients with LV lateral wall scar due to lack of rebound stretch (p < 0.001), and septal systolic shortening and septal work far exceeded values in nonischemic cardiomyopathy (p < 0.0001). Septal flash was present in most patients with anteroseptal scar. CONCLUSIONS: LV lateral wall dysfunction and scar abolished septal flash and markedly improved septal function in LBBB. Therefore, function and scar in the LV lateral wall should be taken into account when septal motion is used to evaluate dyssynchrony.

Monitoring cardiac function by accelerometer - detecting start systole from the acceleration signal makes additional ECG recordings for R-peak detection redundant.

A miniaturized accelerometer attached to the heart has been used for monitoring functional parameters such as early systolic velocity and displacement. Currently, processing of the accelerometer signal for derival of these functional parameters depends on determining start systole by detecting the ECG R-peaks. This study proposes an alternative method using only the accelerometer signal to detect start systole, making additional ECG recordings for this purpose redundant. A signal processing method for automatic detection of start systole by accelerometer alone was developed and compared with detected R-peaks in 15 pigs during 5 different interventions showing a difference of 30 ± 17 ms. Furthermore, the derived early systolic velocity and displacement using only accelerometer measurements correlated well (r2=0.91 and 0.82, respectively) with minor differences compared to the current method using ECG R-peaks as time reference. The results show that an accelerometer can be used to monitor cardiac function without the need to measure ECG which can simplify the monitoring system.

Left ventricular end-systolic volume is a more sensitive marker of acute response to cardiac resynchronization therapy than contractility indices: insights from an experimental study.

AIMS: There are conflicting data and no consensus on how to measure acute response to cardiac resynchronization therapy (CRT). This study investigates, which contractility indices are best markers of acute CRT response. METHODS AND RESULTS: In eight anaesthetized dogs with left bundle branch block, we measured left ventricular (LV) pressure by micromanometer and end-diastolic volume (EDV) and end-systolic volume (ESV) by sonomicrometry. Systolic function was measured as LV ejection fraction (EF), peak rate of LV pressure rise (LV dP/dtmax) and as a gold standard of contractility, LV end-systolic elastance (Ees), and volume axis intercept (V0) calculated from end-systolic pressure-volume relations (ESPVR). Responses to CRT were compared with inotropic stimulation by dobutamine. Both CRT and dobutamine caused reduction in ESV (P < 0.01) and increase in LV dP/dtmax (P < 0.05). Both interventions shifted the ESPVR upwards indicating increased contractility, but CRT which reduced V0 (P < 0.01), caused no change in Ees. Dobutamine markedly increased Ees, which is the typical response to inotropic stimulation. Preload (EDV) was decreased (P < 0.01) by CRT, and there was no change in EF. When adjusting for the reduction in preload, CRT increased EF (P = 0.02) and caused a more marked increase in LV dP/dtmax (P < 0.01). CONCLUSION: Increased contractility by CRT could not be identified by Ees, which is a widely used reference method for contractility. Furthermore, reduction in preload by CRT attenuated improvement in contractility indices such as EF and LV dP/dtmax. These results suggest that changes in LV volume may be more sensitive markers of acute CRT response than conventional contractility indices.

Gravity Compensation Method for Combined Accelerometer and Gyro Sensors Used in Cardiac Motion Measurements.

A miniaturized accelerometer fixed to the heart can be used for monitoring of cardiac function. However, an accelerometer cannot differentiate between acceleration caused by motion and acceleration due to gravity. The accuracy of motion measurements is therefore dependent on how well the gravity component can be estimated and filtered from the measured signal. In this study we propose a new method for estimating the gravity, based on strapdown inertial navigation, using a combined accelerometer and gyro. The gyro was used to estimate the orientation of the gravity field and thereby remove it. We compared this method with two previously proposed gravity filtering methods in three experimental models using: (1) in silico computer simulated heart motion; (2) robot mimicked heart motion; and (3) in vivo measured motion on the heart in an animal model. The new method correlated excellently with the reference (r 2 > 0.93) and had a deviation from reference peak systolic displacement (6.3 ± 3.9 mm) below 0.2 ± 0.5 mm for the robot experiment model. The new method performed significantly better than the two previously proposed methods (p < 0.001). The results show that the proposed method using gyro can measure cardiac motion with high accuracy and performs better than existing methods for filtering the gravity component from the accelerometer signal.