828 Challenges of artifact in Polysomnography-An LVAD Story

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A323-A323
Author(s):  
Rupa Koothirezhi ◽  
Pratibha Anne ◽  
Ugorji Okorie ◽  
Minh Tam Ho ◽  
Brittany Monceaux ◽  
...  

Abstract Introduction Congestive heart failure and sleep-disordered breathing frequently coexist. Many of these patients are referred for polysomnography(PSG). Left ventricular assist device (LVAD) is increasingly used as a destination therapy or as a bridge to transplant. This can lead to artifacts in EEG and EKG. The artifact can mask pathological waves or over-reading of pathology. We present a case report of a patient who underwent a PSG on LVAD. Report of case(s) Sixty-six-year old male with severe heart failure with reduced ejection fraction (EF) of 15 % presented with snoring and witnessed apnea. The patient was diagnosed with predominant central sleep apnea (92%) but never initiated BPAP/ST due to an unstable heart. He was placed on LVAD (HeartMate III LVAD, oscillatory speed of 5300 rpm/83.3Hz) as the heart status deteriorated. Repeat polysomnography was done for persistent snoring but improved witnessed apneas revealed a newly appearing artifact. EEG showed a diffuse low amplitude,6–7 Hz frequency waves, and a regularly appearing high voltage sharp-peaked wave. The morphology of alpha wave, K wave, spindles, and delta waves could not be appreciated and hence was unable to perform sleep staging. EKG had electrical artifacts. All troubleshooting maneuvers were unsuccessful in eliminating artifacts. The artifact is generated by the impeller rotational speed of LVAD that ranges from 2400 rpm to 10,00 rpm(oscillation frequencies of 40 Hz to 166.7 Hertz,1Hz == 60 rpm). The device’s artificial pulse causes additional minor peaks. EEG artifact can be improved by moving the amplifier away from the heart and repositioning the patient. Adjusting the low-frequency filter can affect the nasal pressure tracing, delta waves, and stage 3 recognition. Reducing the high-frequency filter frequency by 10 from the LVAD oscillation frequency improves the EKG signal. But this may cut off the frequency component of pathologies like left ventricular hypertrophy. Conclusion The LVAD has been increasingly used in the United States. It is important to improve awareness regarding the artifacts among sleep techs and physicians. Unresolved artifacts may lead to missing serious pathologies in EEG and EKG and also can lead to misreading the waves as pathological leading to unnecessary treatment. Support (if any) An image of EEG and EKG

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
H Sekiguchi ◽  
Y Tanaka ◽  
S Tanino ◽  
M Suzuki ◽  
N Hagiwara

Abstract Background Adaptive servo-ventilation (ASV) is reportedly beneficial for the treatment of heart failure in patients with central sleep apnea syndrome. However, the recent SERVE-HF trial reported that ASV treatment increased mortality in these patients. One cause of the negative result was considered to be the low output induced by high expiratory positive airway pressure (EPAP) against the background of low left ventricular ejection fraction (LVEF). Hypothesis We hypothesized that optimized ASV settings can be determined by evaluating outflow by using echocardiography, thereby ensuring benefits for patients with severe heart failure (HF). Methods Between July 2016 and March 2017, we optimized ASV settings by using hemodynamic parameters on echocardiography in hospitalized patients with severe HF treated with catecholamine or who were candidates for heart transplantation. We calculated stroke volume (SV) by using the time-velocity integral in the left ventricular outflow tract and compared the response to ASV with EPAP settings of 2, 4, 6, or 8 mmHg. We determined the optimal setting at which the SV reached the maximum value and compared this with the settings at baseline and discharge. We also compared rehospitalization and all-cause mortality between the patients who used ASV with titration (n=28) and without titration (n=37). Result We evaluated 28 patients with severe HF (mean EF, 32%). ASV treatment improved the SV (from 53.4 to 58.8 ml, P<0.05) when optimal settings were used. However, the SV decreased when ASV was performed with a higher-than-optimal EPAP setting. Moreover, at discharge, the EPAP setting was lower than at baseline (mean EPAP, 4.75 cmH2O decreased to 3.71 cmH2O, P<0.05). During the follow-up (median, 420 days), more hospitalizations and deaths occurred in the patients without ASV titration (48.8% vs 37.8%) than in those with ASV titration (28.6% vs 21.4%, respectively; Figure 1). Conclusion In patients with severe HF, high EPAP decreased the SV and optimal settings were different at baseline and after treatment. The result indicated that the optimal setting for ASV may be beneficial for preventing rehospitalization and death. Whether optimal ASV settings reduce mortality in these patients must be investigated. Figure 1 Funding Acknowledgement Type of funding source: None


2021 ◽  
Vol 108 (Supplement_6) ◽  
Author(s):  
A Kumar

Abstract Introduction Heart failure (HF) is a chronic, debilitating and progressive disease(1). Consequently, guidelines recommend heart transplants for patients suffering from end-stage HF, termed destination therapy(2). However, with increasing disparity between the number of donor hearts available and people on the waiting list, identifying the most suitable interim intervention (bridge-to-transplant) therapy is paramount(3,4). Method A scoping search identified controversy surrounding LVAD versus ECMO in end-stage HF. Discussions with an expert in the field at a tertiary centre in the UK (Queen Elizabeth Hospital Birmingham) enabled refinement of the topic. A literature review was conducted, followed by a title and abstract screen. Subsequently, remaining literature was critically appraised. Results First generation LVADs may decrease mortality by 48% in comparison to optimal medical management, although have been associated with disabling stroke. Second and third generation LVADs demonstrate impressive survival at 30 days (>95%), a strong favourable long-term prognostic indicator. Additionally, improvement in HF severity and QoL have been demonstrated. Unlike ECMO, LVAD appears to be feasible as a DT, lasting as long as 8 years. However, the cost of LVADs may be prohibitive, higher than transplantation2. However, ECMO may facilitate multi-organ and right ventricular recovery, enabling transplantation to occur with increased stability. Neither option has conclusive evidence for cost-effectiveness. Conclusions Both LVADs and ECMO can be considered as effective BTT options, suitable in different clinical scenarios. The decision for BTT intervention should be undertaken on a case-by-case basis, in accordance with NICE guidelines, aiming for optimal outcomes in terms of survival, functionality and QoL.


2012 ◽  
Vol 9 (1) ◽  
pp. 90-95 ◽  
Author(s):  
Otto A Smiseth ◽  
Anders Opdahl ◽  
Espen Boe ◽  
Helge Skulstad

Heart failure with preserved left ventricular ejection fraction (HF-PEF), sometimes named diastolic heart failure, is a common condition most frequently seen in the elderly and is associated with arterial hypertension and left ventricular (LV) hypertrophy. Symptoms are attributed to a stiff left ventricle with compensatory elevation of filling pressure and reduced ability to increase stroke volume by the Frank-Starling mechanism. LV interaction with stiff arteries aggravates these problems. Prognosis is almost as severe as for heart failure with reduced ejection fraction (HF-REF), in part reflecting co-morbidities. Before the diagnosis of HF-PEF is made, non-cardiac etiologies must be excluded. Due to the non-specific nature of heart failure symptoms, it is essential to search for objective evidence of diastolic dysfunction which, in the absence of invasive data, is done by echocardiography and demonstration of signs of elevated LV filling pressure, impaired LV relaxation, or increased LV diastolic stiffness. Antihypertensive treatment can effectively prevent HF-PEF. Treatment of HF-PEF is symptomatic, with similar drugs as in HF-REF.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
Y Hsiao ◽  
I Shimizu ◽  
T Wakasugi ◽  
S Jiao ◽  
T Watanabe ◽  
...  

Abstract Background/Introduction Mitochondria are dynamic regulators of cellular metabolism and homeostasis. The dysfunction of mitochondria has long been considered a major contributor to aging and age-related diseases. The prognosis of severe heart failure is still unacceptably poor and it is urgent to establish new therapies for this critical condition. Some patients with heart failure do not respond to established multidisciplinary treatment and they are classified as “non-responders”. The outcome is especially poor for non-responders, and underlying mechanisms are largely unknown. Purpose Studies indicate mitochondrial dysfunction has causal roles for metabolic remodeling in the failing heart, but underlying mechanisms remain to be explored. This study tried to elucidate the role of Mitofusin-1 in a failing heart. Methods We examined twenty-two heart failure patients who underwent endomyocardial biopsy of intraventricular septum. Patients were classified as non-responders when their left-ventricular (LV) ejection fraction did not show more than 10% improvement at remote phase after biopsy. Fourteen patients were classified as responders, and eight as non-responders. Electron microscopy, quantitative PCR, and immunofluorescence studies were performed to explore the biological processes or molecules involved in failure to respond. In addition to studies with cardiac tissue specific knockout mice, we also conducted functional in-vitro studies with neonatal rat ventricular myocytes. Results Twenty-two patients with IDCM who underwent endomyocardial biopsy were enrolled in this study, including 14 responders and 8 non-responders. Transmission electron microscopy (EM) showed a significant reduction in mitochondrial size in cardiomyocytes of non-responders compared to responders. Quantitative PCR revealed that transcript of mitochondrial fusion protein, Mitofusin-1, was significantly reduced in non-responders. Studies with neonatal rat ventricular myocytes (NRVMs) indicated that the beta-1 adrenergic receptor-mediated signaling pathway negatively regulates Mitofusin-1 expression. Suppression of Mitofusin-1 resulted in a significant reduction in mitochondrial respiration of NRVMs. We generated left ventricular pressure overload model with thoracic aortic constriction (TAC) in cardiac specific Mitofusin-1 knockout model (c-Mfn1 KO). Systolic function was reduced in c-Mfn1 KO mice, and EM study showed an increase in dysfunctional mitochondria in the KO group subjected to TAC. Conclusions Mitofusin-1 becomes a biomarker for non-responders with heart failure. In addition, our results suggest that therapies targeting mitochondrial dynamics and homeostasis would become next generation therapy for severe heart failure patients. Funding Acknowledgement Type of funding source: None


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
C Johnsen ◽  
M Sengeloev ◽  
P Joergensen ◽  
N Bruun ◽  
D Modin ◽  
...  

Abstract Background Novel echocardiographic software allows for layer-specific evaluation of myocardial deformation by 2-dimensional speckle tracking echocardiography. Endocardial, epicardial- and whole wall global longitudinal strain (GLS) may be superior to conventional echocardiographic parameters in predicting all-cause mortality in patients with heart failure with reduced ejection fraction (HFrEF). Purpose The purpose of this study was to investigate the prognostic value of endocardial-, epicardial- and whole wall GLS in patients with HFrEF in relation to all-cause mortality. Methods We included and analyzed transthoracic echocardiographic examinations from 1,015 patients with HFrEF. The echocardiographic images were analyzed, and conventional and novel echocardiographic parameters were obtained. A p value in a 2-sided test <0.05 was considered statistically significant. Cox proportional hazards regression models were constructed, and both univariable and multivariable hazard ratios (HRs) were calculated. Results During a median follow-up time of 40 months, 171 patients (16.8%) died. A lower endocardial (HR 1.17; 95% CI (1.11–1.23), per 1% decrease, p<0.001), epicardial (HR 1.20; 95% CI (1.13–1.27), per 1% decrease, p<0.001), and whole wall (HR 1.20; 95% CI (1.14–1.27), per 1% decrease, p<0.001) GLS were all associated with higher risk of death (Figure 1). Both endocardial (HR 1.12; 95% CI (1.01–1.23), p=0.027), epicardial (HR 1.13; 95% CI (1.01–1.26), p=0.040) and whole wall (HR 1.13; 95% CI (1.01–1.27), p=0.030) GLS remained independent predictors of mortality in the multivariable models after adjusting for significant clinical parameters (age, sex, total cholesterol, mean arterial pressure, heart rate, ischemic cardiomyopathy, percutaneous transluminal coronary angioplasty and diabetes) and conventional echocardiographic parameters (left ventricular (LV) ejection fraction, LV mass index, left atrial volume index, deceleration time, E/e', E-velocity, E/A ratio and tricuspid annular plane systolic excursion). No other echocardiographic parameters remained an independent predictors after adjusting. Furthermore, endocardial, epicardial and whole wall GLS had the highest C-statistics of all the echocardiographic parameters. Conclusion Endocardial, epicardial and whole wall GLS are independent predictors of all-cause mortality in patients with HFrEF. Furthermore, endocardial, epicardial and whole wall GLS were superior prognosticators of all-cause mortality compared with all other echocardiographic parameters. Funding Acknowledgement Type of funding source: Public hospital(s). Main funding source(s): Herlev and Gentofte Hospital


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A324-A325
Author(s):  
Pratibha Anne ◽  
Rupa Koothirezhi ◽  
Ugorji Okorie ◽  
Minh Tam Ho ◽  
Brittany Monceaux ◽  
...  

Abstract Introduction Central sleep apnea is commonly seen in patients with heart failure. Here we present a case demonstrating shifting of predominant apneic events from central to obstructive type after placement of left ventricular assist device (LVAD) in end stage heart failure patient. Report of case(s) Case Presentation: 66 year-old African American male has past medical history of chronic congestive heart failure diabetes, hypertension, paroxysmal atrial fibrillation, anemia, hypothyroidism, chronic kidney disease and sleep apnea. Prior to his LVAD placement, his left ventricular ejection fraction (EF) was <10%. Patient was diagnosed with central sleep apnea with AHI of 58 (with 92% of apneic events being central events), oxygen nadir of 74%. Subsequently, patient had LVAD placed for symptomatic heart failure and repeat polysomnogram repeated at six month demonstrated an improved AHI of 45.8 with predominantly obstructive and mixed apneic events, with only 12.5% being central events. Conclusion This case report highlights not only the improvement of the sleep apnea in CHF treated with LVAD but also shows the shift of apneic events from predominantly central to obstructive type post LVAD. Support (if any) 1. Henein MY, Westaby S, Poole-Wilson PA, Cowie MR, Simonds AK. Resolution of central sleep apnoea following implantation of a left ventricular assist device. Int J Cardiol. 2010 Feb 4;138(3):317–9. PMID: 18752859. 2. Köhnlein T, Welte T, Tan LB, Elliott MW. Central sleep apnoea syndrome in patients with chronic heart disease: a critical review of the current literature. Thorax. 2002 Jun;57(6):547–54. PMID: 12037232 3. Monda C, Scala O, Paolillo S, Savarese G, Cecere M, D’Amore C, Parente A, Musella F, Mosca S, Filardi PP. Apnee notturne e scompenso cardiaco: fisiopatologia, diagnosi e terapia [Sleep apnea and heart failure: pathophysiology, diagnosis and therapy]. G Ital Cardiol (Rome). 2010 Nov;11(11):815–22. Italian. PMID: 21348318.


Open Medicine ◽  
2011 ◽  
Vol 6 (1) ◽  
pp. 11-25
Author(s):  
Enrico Vizzardi ◽  
Tania Bordonali ◽  
Elena Tanghetti ◽  
Marco Metra ◽  
Livio Cas

AbstractAnaemia is one of the most frequent co-morbidities in patients with heart failure. Its prevalence increases from 4% to7% in subjects with asymptomatic left ventricular dysfunction to >30% in patients with severe heart failure. Renal insufficiency, activation of inflammatory mediators and treatment with renin-angiotensin antagonists seem to be its main determinants. The results of many studies agree in providing evidence that anaemia is a powerful independent determinant of survival in patients with heart failure. However, the mechanisms of this relation are still not fully understood. Moreover a favourable effect of the correction of anaemia on prognosis has not yet been shown. Also In addition to this, controlled studies assessing its effects on exercise tolerance have yielded controversial results. Further research is needed to assess the effect of correcting anaemia in chronic heart failure (CHF) patients; ongoing reduction of events with RED-HF (Darbepoetin alpha in heart failure) trial will help define the role.


1989 ◽  
Vol 14 (1) ◽  
pp. 127-134 ◽  
Author(s):  
Constantine N. Aroney ◽  
Howard C. Herrmann ◽  
Marc J. Semigran ◽  
G. William ◽  
Charles A. Boucher ◽  
...  

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