Dyssynchrony During Acute RV Apex Pacing. Introduction: Patients with heart block have conventionally received a pacemaker that stimulates the right ventricular apex (RVA) to restore heart rate control. While RVA pacing has been shown to create systolic dyssynchrony acutely, dyssynchrony can also occur in diastole. The effects of acute RVA pacing on diastolic synchrony have not been investigated. RVA pacing acutely impairs diastolic function by increasing the time constant of relaxation, decreasing the peak lengthening rate and decreasing peak negative dP/dt. We therefore hypothesized that acute RVA pacing would cause diastolic dyssynchrony in addition to creating systolic dyssynchrony. Methods and Results: Fourteen patients (13 ± 4 years old) with non-preexcited supraventricular tachycardia underwent ablation therapy with subsequent testing to confirm elimination of the tachycardia substrate. Normal cardiac structure and function were then documented on two-dimensional echocardiography and 12-lead electrocardiography prior to enrollment. Tissue Doppler images were collected during normal sinus rhythm (NSR), right atrial appendage pacing (AAI), and VVI-RVA pacing during the postablation waiting interval. Systolic and diastolic dyssynchrony were quantified using cross-correlation analysis of tissue Doppler velocity curves. Systolic dyssynchrony increased 81% during RVA pacing relative to AAI and NSR (P < 0.01). Diastolic synchrony was not affected by the different pacing modes (P = 0.375). Conclusion: Acute dyssynchronous activation of the LV created by RVA pacing resulted in systolic dyssynchrony with preserved diastolic synchrony in pediatric patients following catheter ablation for treatment of supraventricular tachycardia. Our results suggest that systolic and diastolic dyssynchrony are not tightly coupled and may develop through separate mechanisms.
Persistent pressure overload can cause cardiac hypertrophy and progressive heart failure (HF). The authors developed a pressure-overload HF model of juvenile mice to study the cardiac response to pressure overload that may be applicable to clinical processes in children. Severe thoracic aortic banding (sTAB) was performed using a 28-gauge needle for 40 juvenile (age, 3 weeks) and 47 adult (age, 6 weeks) C57BL/6 male mice. To monitor the structural and functional changes, M-mode echocardiography was performed for conscious mice that had undergone sTAB and sham operation. Cardiac hypertrophy, dilation, and HF occurred in both juvenile and adult mice after sTAB. Compared with adults, juvenile HF is characterized by greater impairment of ventricular contractility and less hypertrophy. In addition, juvenile mice had significantly higher rates of survival than adult mice during the early postoperative weeks. Consistent with clinical HF seen in children, juvenile banded mice demonstrated a lower growth rate than either adult banded mice or juvenile control mice that had sham operations. The authors first developed a juvenile murine model of pressure-overload HF. Learning the unique characteristics of pressure-overload HF in juveniles should aid in understanding age-specific pathologic changes for HF development in children.
Background: Left ventricular dyssynchrony is often diagnosed by comparing velocity curves from Doppler tissue images of two or more myocardial regions. Velocity curves are generated by placing sample volumes or regions of interest (ROIs) within the myocardium. ROIs need to be manually relocated to maintain a midmyocardial location as the heart moves, but are frequently left in a stationary position. The error caused by use of a stationary ROI may affect the diagnosis of dyssynchrony, but this has not been quantified.
Objective: We hypothesized that using a stationary ROI to quantify dyssynchrony from Doppler tissue images would affect the diagnosis of dyssynchrony in patients with heart failure.
Methods: We quantified dyssynchrony in 18 patients with heart failure using 4 published dyssynchrony parameters: septal-to-lateral delay, maximum difference in the basal 2- or 4-chamber times to peak, SD of the 12 basal and midwall times to peak, and cross-correlation delay (XCD). Each dyssynchrony parameter was measured using both tracked and stationary ROIs. Results: Use of a stationary ROI did not change the diagnosis of dyssynchrony when using XCD. However, ROI tracking changed the diagnosis of dyssynchrony in 17%, 11%, and 17% of patients when using septal-to-lateral delay, maximum difference in the basal 2- or 4-chamber times to peak, and SD of the 12 basal and midwall times to peak, respectively. XCD showed the lowest percent difference between tracked and stationary ROIs (4 ± 9% vs 22 ± 53%, 50 ± 167%, and 12 ± 30%, respectively, for septal-to-lateral delay, maximum difference in the basal 2- or 4-chamber times to peak, and SD of the 12 basal and midwall times to peak).
Conclusion: Manual ROI tracking is required when using conventional time-to-peak parameters to diagnose dyssynchrony. XCD diagnosis of dyssynchrony can be performed accurately with a stationary ROI.