scholarly journals Wearable Cardioverter-Defibrillator Used as a Telemonitoring System in a Real-Life Heart Failure Unit Setting

2021 ◽  
Vol 10 (22) ◽  
pp. 5435
Author(s):  
Christian Blockhaus ◽  
Stephan List ◽  
Hans-Peter Waibler ◽  
Jan-Erik Gülker ◽  
Heinrich Klues ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Real Life ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Specific Patient ◽  
Ventricular Ejection Fraction ◽  
Cardioverter Defibrillator ◽  
Wearable Cardioverter Defibrillator ◽  
Heart Failure Unit

Background: In patients with reduced left ventricular ejection fraction (LVEF) who are at risk of sudden cardiac death, a wearable cardioverter-defibrillator (WCD) is recommended as a bridge to the recovery of LVEF or as a bridge to the implantation of a device. In addition to its function to detect and treat malignant arrhythmia, WCD can be used via an online platform as a telemonitoring system to supervise patients’ physical activity, compliance, and heart rate. Methods: We retrospectively analyzed 173 patients with regard to compliance and heart rate after discharge. Results: Mean WCD wearing time was 59.75 ± 35.6 days; the daily wearing time was 21.19 ± 4.65 h. We found significant differences concerning the patients’ compliance. Men showed less compliance than women, and younger patients showed less compliance than patients who were older. Furthermore, we analyzed the heart rate from discharge until the end of WCD prescription and found a significant decrease from discharge to 4, 8, or 12 weeks. Conclusion: WCD can be used as a telemonitoring system to help the involved heart failure unit or physicians attend to and adjust the medical therapy. Furthermore, specific patient groups should be educated more intensively with respect to compliance.

First clinical trial with etomoxir in patients with chronic congestive heart failure

2000 ◽  
Vol 99 (1) ◽  
pp. 27-35 ◽  
Author(s):  
Stephan SCHMIDT-SCHWEDA ◽  
Christian HOLUBARSCH
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Sarcoplasmic Reticulum ◽  
Left Ventricular Ejection Fraction ◽  
Ejection Fraction ◽  
Stroke Volume ◽  
Left Ventricular ◽  
Ventricular Ejection ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction

In the failing human myocardium, both impaired calcium homoeostasis and alterations in the levels of contractile proteins have been observed, which may be responsible for reduced contractility as well as diastolic dysfunction. In addition, levels of a key protein in calcium cycling, i.e. the sarcoplasmic reticulum Ca2+-ATPase, and of the α-myosin heavy chain have been shown to be enhanced by treatment with etomoxir, a carnitine palmitoyltransferase inhibitor, in normal and pressure-overloaded rat myocardium. We therefore studied, for the first time, the influence of long-term oral application of etomoxir on cardiac function in patients with chronic heart failure. A dose of 80 mg of etomoxir was given once daily to 10 patients suffering from heart failure (NYHA functional class II–III; mean age 55±4 years; one patient with ischaemic heart disease and nine patients with dilated idiopathic cardiomyopathy; all male), in addition to standard therapy. The left ventricular ejection fraction was measured echocardiographically before and after a 3-month period of treatment. Central haemodynamics at rest and exercise (supine position bicycle) were defined by means of a pulmonary artery catheter and thermodilution. All 10 patients improved clinically; no patient had to stop taking the study medication because of side effects; and no patient died during the 3-month period. Maximum cardiac output during exercise increased from 9.72±1.25 l/min before to 13.44±1.50 l/min after treatment (P < 0.01); this increase was mainly due to an increased stroke volume [84±7 ml before and 109±9 ml after treatment (P < 0.01)]. Resting heart rate was slightly reduced (not statistically significant). During exercise, for any given heart rate, stroke volume was significantly enhanced (P < 0.05). The left ventricular ejection fraction increased significantly from 21.5±2.6% to 27.0±2.3% (P < 0.01). In acute studies, etomoxir showed neither a positive inotropic effect nor vasodilatory properties. Thus, although the results of this small pilot study are not placebo-controlled, all patients seem to have benefitted from etomoxir treatment. Etomoxir, which has no acute inotropic or vasodilatory properties and is thought to increase gene expression of the sarcoplasmic reticulum Ca2+-ATPase and the α-myosin heavy chain, improved clinical status, central haemodynamics at rest and during exercise, and left ventricular ejection fraction.

scholarly journals Long-Term clinical outcomes of subcutaneous implantable defibrillator therapy in patients with heart failure and reduced ejection fraction: a single center experience

EP Europace ◽  
2021 ◽  
Vol 23 (Supplement_3) ◽  
Author(s):  
M Ben Kilani ◽  
P Jacon ◽  
A Carabelli ◽  
S Venier ◽  
P Defaye
Keyword(s):  
Ejection Fraction ◽  
Real Life ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Reduced Ejection Fraction ◽  
Cardioverter Defibrillator ◽  
Patients With Heart Failure ◽  
The Mean

Abstract Funding Acknowledgements Type of funding sources: Private company. Main funding source(s): P. JACON consultant: Boston Scientific France Introduction The implantable cardioverter defibrillator (ICD) is the most effective therapy for prevention of sudden cardiac death in high-risk patients with heart failure and reduced ejection fraction (HFrEF). The subcutaneous implantable cardioverter defibrillator (S-ICD) has been considered as a comparable and relatively safer alternative to transvenous ICD in patients (pts) without pacing indication. Purpose Our aim was to assess the clinical "real-life" outcomes of S-ICD in patients with HFrEF and primary or secondary prevention, over a long-term follow-up (FU) period after S-ICD implantation. Methods All pts with HFrEF (left ventricular ejection fraction ≤35%) implanted with a S-ICD and a FU above 6 months were included in a cross-sectional monocentric study. Pts were followed by remote monitoring. Results 88 pts were included (52 ± 12.8 years old, male 87.5%). Indications were: primary 92% and secondary 8% prevention  (ischemic cardiopathy 46%; dilated 46%; hypertrophic 5%; congenital 2%; valvular 1%). The mean left ventricular ejection fraction was 27%. 9 pts had a previous transvenous ICD implanted, but required revision because of infection or lead defects. The mean FU period was 33 ± 18 months with a mortality rate of 10% (S-ICD-related death secondary to inappropriate (inap) shocks for one patient). 5 pts underwent S-ICD system extraction after a mean FU period of 30 ± 21 months. Reasons were infectious complication (1 pt), pacing indication (2 pts) and S-ICD lead dysfunction (2 pts). Extraction after heart transplant was performed in 4 pts. During FU, 18 pts (20.5%) experienced at least one therapy: 8 pts (9%) with appropriate (ap) (3.3% per year) and 11 pts (12%) with inap shocks (4.36% per year). A total number of 24 ap shocks have been observed (3 ± 4 ap shocks per patient, several shocks for 3 pts), the first shock occurred after a mean FU period of 24 ± 14 months. 2 pts were referred to VT ablation and no recurrence of events was observed after medical therapy modification for the other pts. For the 11 pts with inap shocks, time to the first event was 19 ± 20 months. Reasons were: supraventricular arrhythmias (18%), T wave (36%) and noise (54%) oversensing. There was 1.8 ± 1.6 shock per patient with several shocks for 4 pts. Among pts with inap shocks, 2 pts required S-ICD system extraction, 1 pt died, while reprogramming and medical therapy options were efficient in other pts. Conclusion In pts with HFrEF at high risk of sudden cardiac death, S-ICD has proven to be effective in treating ventricular arrhythmias. However, more investigations must be conducted to explain the real-life high rate of inappropriate therapies. Abstract Figure. Survival-free from therapies curve

scholarly journals The Use of Selective Inhibitor of If-Channels Ivabradine in Patients with Ischemic Heart Disease, Heart Failure with High Heart Rate

Kardiologiia ◽  
2019 ◽  
Vol 59 (10) ◽  
pp. 60-65 ◽  
Author(s):  
Yu. N. Belenkov ◽  
I. S. Ilgisonis ◽  
Yu. I. Naymann ◽  
E. A. Privalova ◽  
A. V. Zhito
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Prognostic Significance ◽  
Left Ventricular ◽  
Ischemic Heart ◽  
Left Ventricular Ejection ◽  
High Heart Rate ◽  
Ventricular Ejection Fraction

Ischemic heart disease (IHD) and chronic heart failure (CHF) belong to leading causes of death among patients with cardiovascular diseases (CVD). Modern medical approaches to the treatment of patients with CHF do not always provide a significant improvement in the quality of life, a decrease in the frequency of CHF exacerbations and hospitalizations, and an improvement of the long-term prognosis. According to the neurohumoral theory of IHD and CHF development, the blockade of the sympathoadrenal system with β-adrenoblockers (β-AB) is pathogenetically substantiated, and preparations of this group are recommended as one of the main classes of drugs for the treatment of patients with CHF. However, selection of heart rhythm slowing therapy in patients with CHF of ischemic genesis is often difficult due to the development of undesirable side effects of β-AB, intolerance and/or due to the presence of contraindications for their use. Randomized studies have shown that prescribing a combination of β-AB and If-channel blocker ivabradine for heart rate (HR) reduction or solely ivabradine when use of β-AB is impossible in complex CHF therapy, improves the left ventricle (LV) diastolic function, reducing mortality from CHF decompensation. However, the prognostic significance of the use of ivabradine in patients with CHF with preserved left ventricular ejection fraction of ischemic genesis with heart rate higher than 70 beats/min receiving maximum tolerated doses of β-AB remains not fully investigated.

GENECHOC study: genetic markers of arrhythmic risk in heart failure

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S Anys ◽  
S Rigade ◽  
S Rigade ◽  
E Baron ◽  
E Baron ◽  
...  
Keyword(s):  
Heart Failure ◽  
Genetic Markers ◽  
Left Ventricular ◽  
European Ancestry ◽  
Left Ventricular Ejection ◽  
P Value ◽  
Funding Source ◽  
Ventricular Ejection Fraction ◽  
Cardioverter Defibrillator ◽  
Genome Wide

Abstract Background Ventricular arrhythmic events are responsible for 50% of death in heart failure but no reliable predictive marker is known to discriminate patients at risk of fatal arrhythmia. Interestingly, familial predisposition has been reported suggesting a role of genetic factors. Purpose Identify genetic markers increasing the arrhythmic risk in heart failure population. Method We prospectively included heart failure patients with left ventricular ejection fraction (LVEF) under 35% and a cardioverter defibrillator in primary prevention in 22 French centres between 2009 and 2017. Patients were followed for 72 months and divided into two groups: cases with an arrhythmic event during follow-up and controls. A Genome Wide Association Study (GWAS) was done. Single Nucleotide Polymorphisms (SNPs) genotyping was performed on Affymetrix Axiom Precision Medicine Research Array plates. To complement the directly genotyped SNPs we performed large-scale imputation based on the Haplotype Reference Consortium European ancestry panel leading to a dataset of 7,5 million of SNPs. Results 332 cases and 567 controls were included (86% men, mean age at implantation 52±11 years). 78% of patients had ischaemic cardiopathy, 20% had dilated cardiomyopathy. Mean LVEF was 27±5%. No statistical difference was found between cases and controls on clinical parameters, biological results, electrocardiographic measures. No locus shows genome-wide significant association (p&lt;5.10–8) on the GWAS analysis. However, 16 signals with a p-value between 5.10–8 and 5.10–5 were investigated. eQTL and chromatin conformation point to 35 genes with cardiac expression previously associated with heart failure, cardiomyopathies, cardiogenesis, arrhythmias and inflammation. Variants identified point to regulatory regions of the genome and may then propose a molecular mechanism predisposing patients to arrhythmias. Conclusion No locus raises genome-wide significance, but several signals with a nominal p-value point to relevant genes and pathways. Replication of the GWAS is ongoing on a cohort of 156 new patients with a less severe cardiopathy implanted with a cardioverter defibrillator in secondary prevention. Funding Acknowledgement Type of funding source: Public hospital(s). Main funding source(s): Nantes University Hospital

854Predictors of ventricular tachyarrhythmia in patients with implantable cardioverter-defibrillator and non-ischaemic systolic heart failure

EP Europace ◽  
2020 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
E Jedrzejczyk-Patej ◽  
M Mazurek ◽  
M Lazar ◽  
P Pruszkowska-Skrzep ◽  
T Podolecki ◽  
...  
Keyword(s):  
Heart Failure ◽  
Atrial Fibrillation ◽  
Ventricular Arrhythmia ◽  
Implantable Cardioverter Defibrillator ◽  
Atrial Flutter ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Urban Region ◽  
Ventricular Ejection Fraction ◽  
Cardioverter Defibrillator

Abstract Funding Acknowledgements none OnBehalf none Background The benefit of an implantable cardioverter-defibrillator (ICD) in patients with ischaemic heart failure (HF) has been well proven but the benefit of ICD in subjects with non-ischaemic systolic HF is less well-established. Consequently, there is very limited evidence which patients with non-ischaemic HF would benefit most from receiving an ICD. Aim To determine the incidence and predictors of ventricular arrhythmia in patients with ICD and non-ischaemic systolic HF. Methods Study population consisted of 420 consecutive patients with ICD and non-ischaemic systolic HF monitored remotely (on a daily basis) between 2010 and 2017 in tertiary care university hospital, in a densely inhabited, urban region of Poland. Sixty-six percentage of patients had cardiac resynchronization therapy with defibrillator (CRT-D). Results During the median follow-up of 1645 days (range: 507-3515) sustained ventricular arrhythmia occurred in 100 patients (23.8%). Of those, ventricular fibrillation (VF), ventricular tachycardia (VT) or VT/VF (combined) occurred in 10 (10.0%), 77 (77.0%) and 13 (13.0%) patients, respectively. Patients with versus without ventricular arrhythmia did differ with respect to baseline variables such as: left ventricular end diastolic diameter (LVEDD) - median of 67 mm [49-82] vs 62 mm [46-78]; post-inflammatory HF (17 vs 9.7%, P = 0.045); atrial fibrillation/atrial flutter - AF/AFL (57 vs. 38.1%, P = 0.0009); supraventricular arrhythmia (SVT) - any supraventricular arrythmia &gt;100/min other than AF/AFL (27 vs. 15.9%, P = 0.01); and left ventricular ejection fraction - EF (25 vs. 28%, P = 0.01). No differences were observed for age, sex, NYHA class, mitral regurgitation, common comorbidities (including diabetes and chronic renal disease) or concomitant medications. On  multivariable regression analysis, LVEDD (HR 1.05, 95% CI 1.004-1.09, P = 0.03), AF/AFL (HR 1.81, 95% CI 1.21-2.72, P = 0.004) and SVT (HR 1.91, 95% CI 1.21-3.01, P = 0.006) were identified as independent predictors of sustained ventricular arrhythmia in patients with ICD and non-ischaemic HF. All-cause mortality in patients with VT/VF was significantly higher than in subjects without sustained ventricular arrhythmias (33% vs. 20%, P = 0.03). Conclusions Ventricular arrhythmia occurred in 23.8% of patients with systolic non-ischaemic HF during 4.5 years of observation and was associated with significantly worse prognosis compared with subjects free of VT/VF. Left ventricular dimension, atrial fibrillation/atrial flutter and supraventricular tachycardia were identified as independent predictors for ventricular arrhythmia.

scholarly journals Baseline and Dynamic Risk Predictors of Appropriate Implantable Cardioverter Defibrillator Therapy

2020 ◽  
Vol 9 (20) ◽  
Author(s):  
Katherine C. Wu ◽  
Shannon Wongvibulsin ◽  
Susumu Tao ◽  
Hiroshi Ashikaga ◽  
Michael Stillabower ◽  
...  
Keyword(s):  
Heart Failure ◽  
Random Forest ◽  
Left Ventricular Ejection Fraction ◽  
Left Atrial ◽  
Left Ventricular ◽  
Ventricular Ejection ◽  
Left Ventricular Ejection ◽  
Time Varying ◽  
Ventricular Ejection Fraction ◽  
Cardioverter Defibrillator

Background Current approaches fail to separate patients at high versus low risk for ventricular arrhythmias owing to overreliance on a snapshot left ventricular ejection fraction measure. We used statistical machine learning to identify important cardiac imaging and time‐varying risk predictors. Methods and Results Three hundred eighty‐two cardiomyopathy patients (left ventricular ejection fraction ≤35%) underwent cardiac magnetic resonance before primary prevention implantable cardioverter defibrillator insertion. The primary end point was appropriate implantable cardioverter defibrillator discharge or sudden death. Patient characteristics; serum biomarkers of inflammation, neurohormonal status, and injury; and cardiac magnetic resonance‐measured left ventricle and left atrial indices and myocardial scar burden were assessed at baseline. Time‐varying covariates comprised interval heart failure hospitalizations and left ventricular ejection fractions. A random forest statistical method for survival, longitudinal, and multivariable outcomes incorporating baseline and time‐varying variables was compared with (1) Seattle Heart Failure model scores and (2) random forest survival and Cox regression models incorporating baseline characteristics with and without imaging variables. Age averaged 57±13 years with 28% women, 66% white, 51% ischemic, and follow‐up time of 5.9±2.3 years. The primary end point (n=75) occurred at 3.3±2.4 years. Random forest statistical method for survival, longitudinal, and multivariable outcomes with baseline and time‐varying predictors had the highest area under the receiver operating curve, median 0.88 (95% CI, 0.75‐0.96). Top predictors comprised heart failure hospitalization, left ventricle scar, left ventricle and left atrial volumes, left atrial function, and interleukin‐6 level; heart failure accounted for 67% of the variation explained by the prediction, imaging 27%, and interleukin‐6 2%. Serial left ventricular ejection fraction was not a significant predictor. Conclusions Hospitalization for heart failure and baseline cardiac metrics substantially improve ventricular arrhythmic risk prediction.

scholarly journals Efficacy Profile of Ivabradine in Patients with Heart Failure plus Angina Pectoris

Cardiology ◽  
2016 ◽  
Vol 136 (2) ◽  
pp. 138-144 ◽  
Author(s):  
Jeffrey S. Borer ◽  
Karl Swedberg ◽  
Michel Komajda ◽  
Ian Ford ◽  
Luigi Tavazzi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Systolic Heart Failure ◽  
Cardiovascular Death ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
End Point ◽  
Artery Disease ◽  
The Impact

Objectives: In the Systolic Heart Failure Treatment with the If Inhibitor Ivabradine Trial (SHIFT), slowing of the heart rate with ivabradine reduced cardiovascular death or heart failure hospitalizations among patients with systolic chronic heart failure (CHF). Subsequently, in the Study Assessing the Morbidity-Mortality Benefits of the If Inhibitor Ivabradine in Patients with Coronary Artery Disease (SIGNIFY) slowing of the heart rate in patients without CHF provided no benefit for cardiovascular death or nonfatal myocardial infarction (primary composite end point), with secondary analyses suggesting possible harm in the angina subgroup. Therefore, we examined the impact of ivabradine in the patients with CHF plus angina in SHIFT. Methods: SHIFT enrolled adults with stable, symptomatic CHF, a left ventricular ejection fraction ≤35% and a sinus rhythm with a resting heart rate ≥70 bpm. Outcomes were the SHIFT and SIGNIFY primary composite end points and their components. Results: Of 6,505 patients in SHIFT, 2,220 (34%) reported angina at randomization. Ivabradine numerically, but not significantly, reduced the SIGNIFY primary composite end point by 8, 11 and 11% in the SHIFT angina subgroup, nonangina subgroup and overall population, respectively. Ivabradine also reduced the SHIFT primary composite end point in all 3 subgroups. Conclusions: In SHIFT, ivabradine showed consistent reduction of cardiovascular outcomes in patients with CHF; similar results were seen in the subgroup of SHIFT patients with angina.

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