scholarly journals Pitfalls of the S-ICD therapy: experiences from a large tertiary centre

Author(s):  
Kevin Willy ◽  
Florian Reinke ◽  
Benjamin Rath ◽  
Christian Ellermann ◽  
Julian Wolfes ◽  
...  

Abstract Aim The subcutaneous ICD (S-ICD) has evolved to a potential first option for many patients who have to be protected from sudden cardiac death. Many trials have underlined a similar performance regarding its effectiveness in relation to transvenous ICDs and have shown the expected benefits concerning infective endocarditis and lead failure. However, there have also been problems due to the peculiarities of the device, such as oversensing and myopotentials. In this study, we present patients from a large tertiary centre suffering from complications with an S-ICD and propose possible solutions. Methods and results All S-ICD patients who experienced complications related to the device (n = 40) of our large-scale single-centre S-ICD registry (n = 351 patients) were included in this study. Baseline characteristics, complications occurring and solutions to these problems were documented over a mean follow-up of 50 months. In most cases (n = 23), patients suffered from oversensing (18 cases with T wave or P wave oversensing, 5 due to myopotentials). Re-programming successfully prevented further oversensing episode in 13/23 patients. In 9 patients, generator or lead-related complications, mostly due to infectious reasons (5/9), occurred. Further problems consisted of ineffective shocks in one patient and need for antibradycardia stimulation in 2 patients and indication for CRT in 2 other patients. In total, the S-ICD had to be extracted in 10 patients. 7 of them received a tv-ICD subsequently, 3 patients refused re-implantation of any ICD. One other patient kept the ICD but had antitachycardic therapy deactivated due to inappropriate shocks for myopotential oversensing. Conclusion The S-ICD is a valuable option for many patients for the prevention of sudden cardiac death. Nonetheless, certain problems are immanent to the S-ICD (limited re-programming options, size of the generator) and should be addressed in future generations of the S-ICD. Graphic abstract

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Larisa G Tereshchenko ◽  
Yiyi Zhang ◽  
Dan E Arking ◽  
Nona Sotoodehnia ◽  
David S Siscovick ◽  
...  

Background: Deep terminal negativity of the P wave in V1 (P prime in V1, PPV1) defined as PPV1 ≤ -0.1mV in amplitude and ≥40 ms in duration (one small box on ECG grid) is sign of a left atrium enlargement, and a component in the Romhilt-Estes score of left ventricular hypertrophy (LVH). LVH is known to be associated with the risk of sudden cardiac death (SCD). Deep PPV1 negativity is also associated with atrial fibrillation (AF) and stroke; both have been linked to SCD as well. However, it is unknown whether or not PPV1 negativity is independently associated with SCD. Method: Baseline resting digital 12-lead ECGs of 13232 ARIC cohort participants (mean age 53.9±5.7 y; 5760 [43.5%] men; 9747 [73.7%] white) were analyzed. Individuals with prevalent baseline coronary heart disease (CHD), heart failure (HF), or QRS ≥ 120 ms were excluded. The ECGs were analyzed using a 12SL TM algorithm (GE Healthcare, Wauwatosa, WI, USA). Amplitude and duration of PPV1 was automatically measured. Results: Deep PPV1 negativity was observed in 97 (0.73%) participants. During a median follow-up of 14 years, 182 participants had SCD. In multivariable competing risks regression analysis, deep PPV1 negativity was significantly associated with SCD after adjustment for baseline risk factors of CHD and SCD (age, sex, race, diabetes, smoking, alcohol consumption, cholesterol, triglycerides, body mass index, serum creatinine, albumin, systolic blood pressure, use of antihypertensive, QT-prolonging medications, level of physical activity, mean heart rate, QTc, QRS duration, ECG-LVH by Cornell product), and incident HF, AF, stroke [subHR 3.8 (95%CI 1.88-7.69); P<0.0001]. Deep PPV1 negativity showed 7% sensitivity and 99% specificity for SCD prediction. Conclusion: In apparently CV healthy, middle-aged individuals, deep terminal negativity of P-wave in V1 is associated with about 4-times higher risk of SCD during 14 years of follow-up. Further studies should explore the cardiac substrate underlying presence of this marker and its use for risk stratification.


2013 ◽  
Vol 61 (S 01) ◽  
Author(s):  
B Sill ◽  
L Eckardt ◽  
C Butter ◽  
M Schlüter ◽  
K Wegscheider ◽  
...  

2012 ◽  
pp. 74-83
Author(s):  
Anh Tien Hoang ◽  
Nhat Quang Nguyen

Background: Decades of research now link TWA with inducible and spontaneous clinical ventricular arrhythmias. This bench-to-bedside foundation makes TWA, NT-ProBNP a very plausible index of susceptibility to ventricular arrythmia, and motivates the need to define optimal combination of TWA and NT-ProBNP in predicting ventricular arrythmia in myocardial infarction patients. We research this study with 2 targets: 1. To evaluate the role of TWA in predicting sudden cardiac death in myocardial infarction patients. 2. To evaluate the role of NT-ProBNP in predicting sudden cardiac death in myocardial infarction patients 3. Evaluate the role of the combined NT-ProBNP and TWA in predicting sudden cardiac death in myocardial infarction patients. Methods: Prospective study with follow up the mortality in 2 years: 71 chronic myocardial infarction patients admitted to hospital from 5/2009 to 5/20011 and 50 healthy person was done treadmill test to caculate TWA; ECG, echocardiography, NT-ProBNP. Results: Cut-off point of NT-ProBNP in predicting sudden cardiac death is 3168 pg/ml; AUC = 0,86 (95% CI: 0,72 - 0,91); Cut-off point of TWA in predicting sudden cardiac death is 107 µV; AUC = 0,81 (95% CI: 0,69 - 0,87); NT-ProBNP can predict sudden cardiac death with OR= 7,26 (p<0,01); TWA can predict sudden cardiac death with OR= 8,45 (p<0,01). The combined NT-ProBNP and TWA in predicting ventricular arrythmia in heart failure patients: OR= 17,91 (p<0,001). Conclusions: The combined NT-ProBNP and TWA have the best predict value of sudden cardiac death in myocardial infarction patients, compare to NT-ProBNP or TWA alone


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
N Soroush ◽  
A Aarnoudse ◽  
F Shokri ◽  
M Van Den Berg ◽  
F Ahmadizar ◽  
...  

Abstract Background Digoxin is one of the oldest cardiovascular medications still used to treat heart failure and atrial fibrillation. Due to its narrow therapeutic window, it is associated with life threatening intoxication and arrhythmias, and with QTc-shortening. Common genetic variation in the nitric oxide synthase-1 adaptor protein (NOS1AP) has been associated with QTc interval prolongation. Purpose We investigated whether the rs10494366 variant of the NOS1AP gene modified the risk of SCD in patients using digoxin. Methods In a prospective population-based cohort study, we included data of the three cohorts, started as of January 1st, 1991 until January 1st 2014. Digoxin current use on the date of cardiac death in cases and the same day of follow-up in the remainder of the cohort was a time-dependent exposure. The main outcome was SCD defined as sudden and unexpected death as a result of cardiac causes, according to international criteria. Identification and adjudication of SCD was performed independently, before the start of this study. We used Cox proportional hazard regression analysis to investigate the associations between NOS1AP rs10494366 variant and incident SCD among digoxin users compared to non-users. Associations were adjusted for age, sex (model 1) in addition to BMI, prevalent diabetes, myocardial infarction, baseline hypertension and smoking status (past, current, never) (model 2). Results We included 14,594 individuals, with a mean age of 65.3 (SD 10.3) years. Almost 59% were female. The cumulative incidence of SCD was 9.5% (609 cases) by the end of follow up. Among them, 98 (16%) individuals were exposed to digoxin at the time of death. In model 1, NOS1AP rs10494366 variant was not associated with SCD in the total study population. However, an interaction term of the gene with the daily dose of digoxin was significantly associated with increased risk of SCD (p-value 0.0001). In model 2, the risk of SCD in current users of digoxin was 4.2 [95% CI 1.3–13.8] for the GG genotype; 2.1 [95% CI 1.1–4.2] for the GT genotype, and 1.5 [95% CI 0.7–3.2] for the TT genotype. Conclusion NOS1AP rs10494366 variant modified the risk of sudden cardiac death in users of digoxin. Our study suggests that individuals with the homozygous minor GG allele have a fourfold increased risk of sudden cardiac death. Funding Acknowledgement Type of funding source: None


2008 ◽  
Vol 14 (7) ◽  
pp. S140-S141
Author(s):  
Kenji Ando ◽  
Yoshimitsu Soga ◽  
Masahiko Goya ◽  
Shinichi Shirai ◽  
Shinya Nagayama ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Haiyun Yu ◽  
Juanhui Pei ◽  
Xiaoyan Liu ◽  
Jingzhou Chen ◽  
Xian Li ◽  
...  

The purpose of this study was to evaluate whether CC-AAbs levels could predict prognosis in CHF patients. A total of 2096 patients with CHF (841 DCM patients and 1255 ICM patients) and 834 control subjects were recruited. CC-AAbs were detected and the relationship between CC-AAbs and patient prognosis was analyzed. During a median follow-up time of 52 months, there were 578 deaths. Of these, sudden cardiac death (SCD) occurred in 102 cases of DCM and 121 cases of ICM. The presence of CC-AAbs in patients was significantly higher than that of controls (bothP<0.001). Multivariate analysis revealed that positive CC-AAbs could predict SCD (HR 3.191, 95% CI 1.598–6.369 for DCM; HR 2.805, 95% CI 1.488–5.288 for ICM) and all-cause mortality (HR 1.733, 95% CI 1.042–2.883 for DCM; HR 2.219, 95% CI 1.461–3.371 for ICM) in CHF patients. A significant association between CC-AAbs and non-SCD (NSCD) was found in ICM patients (HR = 1.887, 95% CI 1.081–3.293). Our results demonstrated that the presence of CC-AAbs was higher in CHF patients versus controls and corresponds to a higher incidence of all-cause death and SCD. Positive CC-AAbs may serve as an independent predictor for SCD and all-cause death in these patients.


Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Di Zhao ◽  
Eliseo Guallar ◽  
Elena Blasco-Colmenares ◽  
Nona Sotoodehnia ◽  
Wendy Post

Background: In hospital-based studies and in studies of participants with pre-existing conditions, African Americans have a higher risk of in- and out-of-hospital sudden cardiac death (SCD) compared with Whites. However, the risk of SCD of African Americans and Whites has never been compared in large-scale community-based cohort studies. Objective: To compare the risk of SCD among African Americans and Whites, and to evaluate the risk factors that may explain racial differences in incidence. Methods: Cohort study of 3,838 African Americans and 11,245 Whites participating in ARIC. Race was self-reported. SCD cases were defined as a sudden pulseless condition from a cardiac cause in a previously stable individual and adjudicated by an expert committee. Mediation effect of covariates was calculated using boot-strapping method. Cox proportional hazards models were adjusted for demographics, social economic status, cardiovascular (CVD), and electrocardiographic risk factors. Results: The mean (SD) age was 53.6 (5.8) for African Americans and 54.4 (5.7) years for Whites. During 25.3 years of follow-up, 215 African Americans and 332 Whites experienced SCD. In multivariable-adjusted models, the HRs (95% CI) for SCD comparing African Americans and Whites were 1.70 (1.37, 2.10) overall, 2.00 (1.40, 2.84) in women, and 1.46 (1.10, 1.92) in men (p-value for race by sex interaction 0.02; Table ). CVD and electrocardiographic risk factors explained 36.6% (21.4, 51.8%) of the excess risk of SCD in African Americans, with a large proportion of racial differences unexplained. Conclusions: The risk of SCD in community-dwelling African Americans was significantly higher than in Whites, particularly among women. CVD risk factors, including higher prevalence of obesity, diabetes, hypertension and LV hypertrophy in African Americans, explained only a small fraction of this difference. Further research is needed to identify factors responsible for race differences in SCD and to implement prevention strategies in high-risk minorities.


2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Erick A. Perez-Alday ◽  
Aron Bender ◽  
David German ◽  
Srini V. Mukundan ◽  
Christopher Hamilton ◽  
...  

Abstract Background The risk of sudden cardiac death (SCD) is known to be dynamic. However, the accuracy of a dynamic SCD prediction is unknown. We aimed to measure the dynamic predictive accuracy of ECG biomarkers of SCD and competing non-sudden cardiac death (non-SCD). Methods Atherosclerosis Risk In Community study participants with analyzable ECGs in sinus rhythm were included (n = 15,716; 55% female, 73% white, age 54.2 ± 5.8 y). ECGs of 5 follow-up visits were analyzed. Global electrical heterogeneity and traditional ECG metrics (heart rate, QRS, QTc) were measured. Adjudicated SCD was the primary outcome; non-SCD was the competing outcome. Time-dependent area under the receiver operating characteristic curve (ROC(t) AUC) analysis was performed to assess the prediction accuracy of a continuous biomarker in a period of 3,6,9 months, and 1,2,3,5,10, and 15 years using a survival analysis framework. Reclassification improvement as compared to clinical risk factors (age, sex, race, diabetes, hypertension, coronary heart disease, stroke) was measured. Results Over a median 24.4 y follow-up, there were 577 SCDs (incidence 1.76 (95%CI 1.63–1.91)/1000 person-years), and 829 non-SCDs [2.55 (95%CI 2.37–2.71)]. No ECG biomarkers predicted SCD within 3 months after ECG recording. Within 6 months, spatial ventricular gradient (SVG) elevation predicted SCD (AUC 0.706; 95%CI 0.526–0.886), but not a non-SCD (AUC 0.527; 95%CI 0.303–0.75). SVG elevation more accurately predicted SCD if the ECG was recorded 6 months before SCD (AUC 0.706; 95%CI 0.526–0.886) than 2 years before SCD (AUC 0.608; 95%CI 0.515–0.701). Within the first 3 months after ECG recording, only SVG azimuth improved reclassification of the risk beyond clinical risk factors: 18% of SCD events were reclassified from low or intermediate risk to a high-risk category. QRS-T angle was the strongest long-term predictor of SCD (AUC 0.710; 95%CI 0.668–0.753 for ECG recorded within 10 years before SCD). Conclusion Short-term and long-term predictive accuracy of ECG biomarkers of SCD differed, reflecting differences in transient vs. persistent SCD substrates. The dynamic predictive accuracy of ECG biomarkers should be considered for competing SCD risk scores. The distinction between markers predicting short-term and long-term events may represent the difference between markers heralding SCD (triggers or transient substrates) versus markers identifying persistent substrate.


Heart Rhythm ◽  
2012 ◽  
Vol 9 (9) ◽  
pp. 1579 ◽  
Author(s):  
Gust Bardy ◽  
Kerry Lee ◽  
Daniel Mark ◽  
Jeanne Poole ◽  
Daniel Fishbein ◽  
...  

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