A molecular formula for heart failure and sudden cardiac death. Focus on “Nav1.5-dependent persistent Na+ influx activates CaMKII in rat ventricular myocytes and N1325S mice”

2011 ◽  
Vol 301 (3) ◽  
pp. C557-C558
Author(s):  
Gregory J. Kaczorowski
Keyword(s):  
Heart Failure ◽  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Ventricular Myocytes ◽  
Molecular Formula ◽  
Rat Ventricular Myocytes

scholarly journals Prognostic implications of troponin T variations in inherited cardiomyopathies using systems biology

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Rameen Shakur ◽  
Juan Pablo Ochoa ◽  
Alan J. Robinson ◽  
Abhishek Niroula ◽  
Aneesh Chandran ◽  
...  
Keyword(s):  
Heart Failure ◽  
Systems Biology ◽  
Sudden Cardiac Death ◽  
Risk Stratification ◽  
Clinical Data ◽  
Cardiac Death ◽  
Troponin T ◽  
Management Options ◽  
Familial Cardiomyopathy ◽  
The Impact

AbstractThe cardiac troponin T variations have often been used as an example of the application of clinical genotyping for prognostication and risk stratification measures for the management of patients with a family history of sudden cardiac death or familial cardiomyopathy. Given the disparity in patient outcomes and therapy options, we investigated the impact of variations on the intermolecular interactions across the thin filament complex as an example of an unbiased systems biology method to better define clinical prognosis to aid future management options. We present a novel unbiased dynamic model to define and analyse the functional, structural and physico-chemical consequences of genetic variations among the troponins. This was subsequently integrated with clinical data from accessible global multi-centre systematic reviews of familial cardiomyopathy cases from 106 articles of the literature: 136 disease-causing variations pertaining to 981 global clinical cases. Troponin T variations showed distinct pathogenic hotspots for dilated and hypertrophic cardiomyopathies; considering the causes of cardiovascular death separately, there was a worse survival in terms of sudden cardiac death for patients with a variation at regions 90–129 and 130–179 when compared to amino acids 1–89 and 200–288. Our data support variations among 90–130 as being a hotspot for sudden cardiac death and the region 131–179 for heart failure death/transplantation outcomes wherein the most common phenotype was dilated cardiomyopathy. Survival analysis into regions of high risk (regions 90–129 and 130–180) and low risk (regions 1–89 and 200–288) was significant for sudden cardiac death (p = 0.011) and for heart failure death/transplant (p = 0.028). Our integrative genomic, structural, model from genotype to clinical data integration has implications for enhancing clinical genomics methodologies to improve risk stratification.

Long-term Clinical Follow-up of Japanese Heart Failure Patients Received ICD Therapy for Primary Prevention of Sudden Cardiac Death

2008 ◽  
Vol 14 (7) ◽  
pp. S140-S141
Author(s):  
Kenji Ando ◽  
Yoshimitsu Soga ◽  
Masahiko Goya ◽  
Shinichi Shirai ◽  
Shinya Nagayama ◽  
...  
Keyword(s):  
Heart Failure ◽  
Primary Prevention ◽  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Icd Therapy ◽  
Heart Failure Patients

scholarly journals Calcium Channel Autoantibodies Predicted Sudden Cardiac Death and All-Cause Mortality in Patients with Ischemic and Nonischemic Chronic Heart Failure

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Haiyun Yu ◽  
Juanhui Pei ◽  
Xiaoyan Liu ◽  
Jingzhou Chen ◽  
Xian Li ◽  
...  
Keyword(s):  
Heart Failure ◽  
Multivariate Analysis ◽  
Sudden Cardiac Death ◽  
Chronic Heart Failure ◽  
Cardiac Death ◽  
Independent Predictor ◽  
All Cause Mortality ◽  
Patient Prognosis ◽  
The Relationship

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.

Sudden Cardiac Death in Patients with Chronic Heart Failure-Epidemiological Findings From the CHART Study

2009 ◽  
Vol 15 (7) ◽  
pp. S141
Author(s):  
Nobuyuki Shiba ◽  
Kotaro Nochioka ◽  
Jun Watanabe ◽  
Tomohiro Tada ◽  
Haruka Kohno ◽  
...  
Keyword(s):  
Heart Failure ◽  
Sudden Cardiac Death ◽  
Chronic Heart Failure ◽  
Cardiac Death

Abstract 2415: Long-Term Baroreflex Activation Therapy Increases the Threshold for the Induction of Lethal Ventricular Arrhythmias in Dogs with Chronic Advanced Heart Failure

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Mengjun Wang ◽  
Valerio Zaca ◽  
Alice Jiang ◽  
Itamar Ilsar ◽  
Matthew Ebinger ◽  
...  
Keyword(s):  
Heart Failure ◽  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Ventricular Arrhythmias ◽  
Lv Function ◽  
Baroreflex Activation Therapy ◽  
Increased Risk ◽  
Lv Remodeling ◽  
Activation Therapy

Heart failure (HF) is associated with a high incidence of ventricular tachycardia (VT) and fibrillation (VF). Patients with HF in whom these lethal arrhythmias can be induced by electrophysiological (EP) testing carry a high risk of sudden cardiac death. We showed that chronic electrical carotid baroreflex activation therapy (BAT) with the Rheos® System (CVRx, Inc.) improves LV function, attenuates LV remodeling and restores autonomic sympathetic-parasympathetic balance in dogs with HF. This study examined the effects of long-term therapy with BAT on the induction of VT or VF in dogs with coronary microembolization-induced HF (LV ejection fraction ~20%). Eleven dogs with HF underwent EP testing at baseline prior to therapy and after 3 and 6 months of therapy with BAT and again 6 weeks after withdrawal of BAT therapy (n = 7) or no therapy at all (Control, n = 4). Programmed ventricular stimulation was performed from the right ventricular apex and included delivery of up to 4 extrastimuli at progressively shorter coupling intervals (in steps of 10 msec). The extrastimuli were delivered following 8 ventricular paced beats with a drive cycle length between 600 and 200 msec. If a sustained monomorphic VT or VF could not be induced, isoproterenol infusion was initiated to increase the sinus rate by ~30% and the EP stimulation protocol was repeated. At baseline, a sustained VT or VF was induced in all 11 dogs (100%). After 3 and 6 months of follow-up, all Control dogs (100%) were induced into sustained VT or VF. After 3 months of BAT, only 3 of 7 dogs (43%) were induced into sustained VT or VF. After 6 months of BAT, only 2 of 7 dogs (29%) were induced into sustained VT or VF. Finally after withdrawal of BAT therapy, all dogs (100%) were again induced into systained VT or VF. In addition to improving LV function and attenuating LV remodeling, long-term monotherapy with BAT markedly increases the threshold for lethal ventricular arrhythmias in dogs with chronic HF. This is a marked improvement over inducibility of lethal arrhythmias seen in historical untreated controls. This benefit of BAT supports the continued exploration of this device as a therapeutic modality for treating patients with chronic HF and increased risk of sudden cardiac death.

Prevention of atrial fibrillation – non-modifiable and modifiable risk factors for AF

2020 ◽  
Vol 2 (55) ◽  
pp. 14-19
Author(s):  
Agnieszka Wojdyła-Hordyńska ◽  
Grzegorz Hordyński
Keyword(s):  
Risk Factors ◽  
Heart Failure ◽  
Atrial Fibrillation ◽  
Cardiovascular Disease ◽  
Cardiovascular Diseases ◽  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Combined Treatment ◽  
Lifestyle Changes ◽  
Modifiable Risk Factors

Atrial fibrillation is one of the most common arrhythmias, with a significant increase in incidence in recent years. AF is a major cause of stroke, heart failure, sudden cardiac death, and cardiovascular disease. Timely intervention and modification of risk factors increase chance to stop the disease. Aggressive, multilevel prevention tactics are a component of combined treatment, including – in addition to lifestyle changes, anticoagulant therapy, pharmacotherapy and invasive anti-arrhythmic treatment – prevention of cardiovascular diseases, hypertension, ischemia, valvular disease and heart failure.

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