AimsDevice-based pacing-induced diaphragmatic stimulation (PIDS) may have therapeutic potential for chronic heart failure (HF) patients. We studied the effects of PIDS on cardiac function and functional outcomes. Methods and resultsIn 24 chronic HF patients with CRT, an additional electrode was attached to the left diaphragm. Randomized into two groups, patients received the following PIDS modes for 3 weeks in a different sequence: (i) PIDS off (control group); (ii) PIDS 0 ms mode (PIDS simultaneously with ventricular CRT pulse); or (iii) PIDS optimized mode (PIDS with optimized delay to ventricular CRT pulse). For PIDS optimization, acoustic cardiography was used. Effects of each PIDS mode on dyspnoea, power during exercise testing, and LVEF were assessed. Dyspnoea improved with the PIDS 0 ms mode (P = 0.057) and the PIDS optimized mode (P = 0.034) as compared with the control group. Maximal power increased from median 100.5 W in the control group to 104.0 W in the PIDS 0 ms mode (P = 0.092) and 109.5 W in the PIDS optimized mode (P = 0.022). Median LVEF was 33.5% in the control group, 33.0% in the PIDS 0 ms mode, and 37.0% in the PIDS optimized mode (P = 0.763 and P = 0.009 as compared with the control group, respectively).
Introduction: Diaphragmatic Stimulation (DS) is a novel heart failure therapy concept under investigation. Diaphragmatic contractions have been previously shown to alter systolic and diastolic function, venous filling and compliance, and arterial resistance. By electrically stimulating the diaphragm to modulate intrathoracic pressures (ITP), mechanical forces are directly applied to all the organs and vessels within the thoracic cavity including the atria, ventricles, and major vessels. No standard animal instrumentation model exists to study diaphragmatic stimulation as a treatment for heart failure, so a series of experiments were undertaken to identify the most sensitive parameters to ITP modulation using standard cardiovascular hemodynamic parameters. The results will be used to optimize diaphragmatic stimulation effects in an animal heart failure model and human clinical studies. Hypothesis: DS therapy appropriately timed to the cardiac cycle alters hemodynamics. Methods: Sixteen mongrel swine were anesthetized using isoflourane and ventilated. A sutureless, bipolar sensing/ pacing lead was affixed to the left inferior diaphragm via laparoscopy. Milllar pressure catheters were positioned in a variety of locations including the right atrium, right ventricle, left ventricle and aorta. Cardiac output was determined using a thermodilution bolus or continuously via catheter thermistors. ITP was measured using a Millar pressure catheter via the Murphy procedure. Volume overload status was achieved using a 3L intravenous saline venous introduction. Hemodynamic measurements were made at baseline and with diaphragmatic pacing output timing varied relative to sensed R waves. Results: Intrathoracic pressure changes of up to 20% of ITP changes due to respiration were observed when stimulation was applied synchronously upon end diastole. Modifications of early and late LV diastolic filling were reflected in LV pressure traces with cardiac output increases of up to 25% and 10% in LV max dP/dt, with more pronounced effects observed in the volume overload model. Changes in right atrial and right ventricular pressure morphologies occurred contemporaneous to ITP pulsatile alterations suggesting increased venous return. Conclusions: Diaphragmatic stimulation appropriately timed to the cardiac cycle affected hemodynamic waveform morphologies in all chambers instrumented, with changes to cardiac output predominantly through modulation of intrathoracic pressure.
Background: This study evaluated the use of comprehensive geriatric assessment (CGA) in older patients undergoing pacemaker implantation. Methods: In this prospective cohort, CGA was performed in 197 patients ≥75 years at pacemaker implantation and yearly thereafter. CGA embraced the following domains: cognition, mobility, nutrition, activities of daily living (ADLs), and falls (with or without loss of consciousness). Based on comorbidities, the Charlson comorbidity index (CCI) was calculated. For predictive analysis, logistic regression was used. Results: During a mean follow-up duration of 2.4 years, the incidence rates of syncope decreased from 0.46 to 0.04 events per year (p < 0.001), and that of falls without loss of consciousness from 0.27 to 0.15 (p < 0.001) before vs. after implantation. Sixty-three patients (32.0%) died. Impaired mobility (OR 2.60, 95%CI 1.22-5.54, p = 0.013), malnutrition (OR 3.26, 95%CI 1.52-7.01, p = 0.002), and a higher CCI (OR per point increase 1.25, 95%CI 1.04-1.50, p = 0.019) at baseline were significant predictors of mortality. Among 169 patients who survived for more than 1 year and thus underwent follow-up CGA, CGA domains did not deteriorate during follow-up, except for ADLs. This decline in ADLs during follow-up was the strongest predictor of later nursing home admission (OR 9.29, 95%CI 1.82-47.49, p = 0.007). Higher baseline age (OR per year increase 1.10, 95%CI 1.02-1.20, p = 0.018) and a higher baseline CCI (OR per point increase 1.32, 95%CI 1.05-1.65, p = 0.017) were associated with a decline in ADLs during follow-up. Conclusions: CGA is useful to detect functional deficits, which are associated with mortality or nursing home admission after pacemaker implantation. The present study seems to support the use of CGA in older patients undergoing pacemaker implantation as functional deficits and falls are amenable to geriatric interventions.
right heart chambers due to significant decreasing of the HR. 6MWT showed that pts of the 2nd gr were able to walk 121,3±17,6 meters more than pts of the 1st gr.Estimating results of SF-36 it was found that pts of 2nd group had significant improvement at such scales as RPF, GH, Vitality, RE and MH comparing to pts of the 1st gr. Conclusion: 6 MWT confirmed efficacy of ivabradin in pts with CCP and RHF. Early prescription of ivabradine in this cohort of pts prevents worsening of RHFimproving the structure-functional data of the right heart chambers, which has a positive influence on life quality of these pts. P3372 | BEDSIDEIs the administration of mineralocorticoid receptor antagonist required in asymptomatic AHA/ACC stage B heart failure patients?T. Okumura, A. Sawamura, Y. Sugiura, H. Hiraiwa, T. Kondo, S. Aoki, N. Watanabe, N. Kano, K. Fukaya, R. Morimoto, Y.K. Bando, T. Murohara. Nagoya University Graduate School of Medicine, Department of Cardiology, Nagoya, Japan Background: Cardiac reverse remodeling (CRR) is considered as a surrogate marker for favorable prognosis of non-ischemic dilated cardiomyopathy (NIDCM). Based on the results of large clinical trials, the current guidelines recommended the administration of mineralocorticoid receptor antagonist (MRA) to reduce mortality and HF hospitalization in all symptomatic heart failure (HF) patients with reduced ejection fraction despite treatment with ACE inhibitors/ARB and beta-blockers. However, the efficacy of the MRA for asymptomatic HF patients (AHA/ACC stage B) has not been established. Purpose: The purpose of this study was 1) to investigate the association between MRA and CRR and 2) the prognostic value of additional MRA administration in asymptomatic NIDCM patients. Methods: We enrolled 122 NIDCM patients classified AHA/ACC stage B HF in this retrospective cohort study. NIDCM was defined by the presence of left ventricular ejection fraction <50% on echocardiography and a dilated LV cavity, in the absence of coronary heart disease, valvular heart disease, or secondary cardiac muscle disease caused by any known systemic condition. All patients were divided into two groups; with-MRA group and without-MRA group. CRR was defined as an absolute increase in left ventricular ejection fraction ≥10% accompanied by a decrease in left ventricular end-diastolic diameter >10% as assessed by echocardiography at 12 months. The cardiac event was defined as composite outcome including cardiac-related death, ICD/CRTD implantation and unplanned hospitalization for worsening HF within 12 months. Results: As for baseline characteristics, the mean of left ventricular ejection fraction and end-diastolic diameter was 33.2% and 62.5 mm, respectively. The administration rate of ACE inhibitors/ARBs and was 84% and 87%. Sixty-three (52%) patients were treated with MRA. The rate of CRR was significantly higher in patients treated with MRA than in patients without MRA (52% vs 29%, p=0.033; Figure A). In Kaplan-Meier survival analysis, the cardiac event-free rates were comparable ...
Introduction: Diaphragmatic Stimulation (DS) is a novel heart failure therapy concept under investigation. Diaphragmatic contractions have been previously shown to alter systolic and diastolic function, venous filling and compliance, and arterial resistance. By electrically stimulating the diaphragm to modulate intrathoracic pressures (ITP), mechanical forces are directly applied to all the organs and vessels within the thoracic cavity including the atria, ventricles, and major vessels. No standard animal instrumentation model exists to study diaphragmatic stimulation as a treatment for heart failure, so a series of experiments were undertaken to identify the most sensitive parameters to ITP modulation using standard cardiovascular hemodynamic parameters. The results will be used to optimize diaphragmatic stimulation effects in an animal heart failure model and human clinical studies. Hypothesis: DS therapy appropriately timed to the cardiac cycle alters hemodynamics. Methods: Sixteen mongrel swine were anesthetized using isoflourane and ventilated. A sutureless, bipolar sensing/ pacing lead was affixed to the left inferior diaphragm via laparoscopy. Milllar pressure catheters were positioned in a variety of locations including the right atrium, right ventricle, left ventricle and aorta. Cardiac output was determined using a thermodilution bolus or continuously via catheter thermistors. ITP was measured using a Millar pressure catheter via the Murphy procedure. Volume overload status was achieved using a 3L intravenous saline venous introduction. Hemodynamic measurements were made at baseline and with diaphragmatic pacing output timing varied relative to sensed R waves. Results: Intrathoracic pressure changes of up to 20% of ITP changes due to respiration were observed when stimulation was applied synchronously upon end diastole. Modifications of early and late LV diastolic filling were reflected in LV pressure traces with cardiac output increases of up to 25% and 10% in LV max dP/dt, with more pronounced effects observed in the volume overload model. Changes in right atrial and right ventricular pressure morphologies occurred contemporaneous to ITP pulsatile alterations suggesting increased venous return. Conclusions: Diaphragmatic stimulation appropriately timed to the cardiac cycle affected hemodynamic waveform morphologies in all chambers instrumented, with changes to cardiac output predominantly through modulation of intrathoracic pressure.
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