scholarly journals Dissociation of hemodynamic and electrocardiographic indexes of myocardial ischemia in pigs with hibernating myocardium and sudden cardiac death

2013 ◽  
Vol 304 (12) ◽  
pp. H1697-H1707 ◽  
Author(s):  
Matthew F. Pizzuto ◽  
Gen Suzuki ◽  
Michael D. Banas ◽  
Brendan Heavey ◽  
James A. Fallavollita ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Hibernating Myocardium ◽  
Sympathetic Activation ◽  
Premature Ventricular Contractions ◽  
Severe Coronary Artery ◽  
Artery Disease

Many survivors of sudden cardiac death (SCD) have normal global ventricular function and severe coronary artery disease but no evidence of symptomatic ischemia or infarction before the development of lethal ventricular arrhythmias, and the trigger for ventricular tachycardia (VT)/ventricular fibrillation (VF) remains unclear. We sought to identify the role of spontaneous ischemia and temporal hemodynamic factors preceding SCD using continuous telemetry of left ventricular (LV) pressure and the ECG for periods up to 5 mo in swine ( n = 37) with hibernating myocardium who experience spontaneous VT/VF in the absence of heart failure or infarction. Hemodynamics and ST deviation at the time of VT/VF were compared with survivors with hibernating myocardium as well as sham controls. All episodes of VT/VF occurred during sympathetic activation and were initiated by single premature ventricular contractions, and the VT degenerated into VF in ∼ 30 s. ECG evidence of ischemia was infrequent and no different from those that survived. Baseline hemodynamics were no different among groups, but LV end-diastolic pressure during sympathetic activation was higher at the time of SCD (37 ± 4 vs. 26 ± 4 mmHg, P < 0.05) and the ECG demonstrated QT shortening (155 ± 4 vs. 173 ± 5 ms, P < 0.05). The week before SCD, both parameters were no different from survivors. These data indicate that there are no differences in the degree of sympathetic activation or hemodynamic stress when VT/VF develops in swine with hibernating myocardium. The transiently elevated LV end-diastolic pressure and QT shortening preceding VT/VF raises the possibility that electrocardiographically silent subendocardial ischemia and/or mechanoelectrical feedback serve as a trigger for the development of SCD in chronic ischemic heart disease.

Supplementary role of left ventricular global longitudinal strain for predicting sudden cardiac death in hypertrophic cardiomyopathy

2021 ◽  
Author(s):  
Hyun-Jung Lee ◽  
Hyung-Kwan Kim ◽  
Sang Chol Lee ◽  
Jihoon Kim ◽  
Jun-Bean Park ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Sudden Cardiac Death ◽  
Risk Score ◽  
Primary Endpoint ◽  
Cardiac Death ◽  
Longitudinal Strain ◽  
Global Longitudinal Strain ◽  
Left Ventricular ◽  
C Statistic

Abstract Aims We investigated the prognostic role of left ventricular global longitudinal strain (LV-GLS) and its incremental value to established risk models for predicting sudden cardiac death (SCD) in patients with hypertrophic cardiomyopathy (HCM). Methods and results LV-GLS was measured with vendor-independent software at a core laboratory in a cohort of 835 patients with HCM (aged 56.3 ± 12.2 years) followed-up for a median of 6.4 years. The primary endpoint was SCD events, including appropriate defibrillator therapy, within 5 years after the initial evaluation. The secondary endpoint was a composite of SCD events, heart failure admission, heart transplantation, and all-cause mortality. Twenty (2.4%) and 85 (10.2%) patients experienced the primary and secondary endpoints, respectively. Lower absolute LV-GLS quartiles, especially those worse than the median (−15.0%), were associated with progressively higher SCD event rates (P = 0.004). LV-GLS was associated with an increased risk for the primary endpoint, independent of the LV ejection fraction, apical aneurysm, and 2014 European Society of Cardiology (ESC) risk score [adjusted hazard ratio (aHR) 1.14, 95% confidence interval (CI) 1.02–1.28] or 2011 American College of Cardiology/American Heart Association (ACC/AHA) risk factors (aHR 1.18, 95% CI 1.05–1.32). LV-GLS was also associated with a higher risk for the composite secondary endpoint (aHR 1.06, 95% CI 1.01–1.12). The addition of LV-GLS enhanced the performance of the ESC risk score (C-statistic 0.756 vs. 0.842, P = 0.007) and the 2011 ACC/AHA risk factor strategy (C-statistic 0.743 vs. 0.814, P = 0.007) for predicting SCD. Conclusion LV-GLS is an important prognosticator in patients with HCM and provides additional information to established risk stratification strategies for predicting SCD.

Prevention of sudden cardiac death in persons living with HIV infection

2021 ◽  
Vol 19 ◽  
Author(s):  
Jean-Jacques Monsuez ◽  
Marilucy Lopez-Sublet
Keyword(s):  
Sudden Cardiac Death ◽  
Hiv Infection ◽  
Cardiac Death ◽  
Left Ventricular ◽  
Qt Interval Prolongation ◽  
Increased Risk ◽  
Persons Living With Hiv ◽  
Artery Disease ◽  
Optimized Treatment ◽  
Living With Hiv

: Persons living with HIV infection (PLWH) have been recognized to have an increased risk of sudden cardiac death (SCD). Prevention of this risk should theoretically be included in their long-term management. However, only a few approaches have been proposed to optimize such interventions. Targeting detection of the commonly associated conditions such as coronary artery disease, left ventricular dysfunction, heart failure, QT interval prolongation and ventricular arrhythmias is the first step of this prevention. However, although detection of the risk of SCD is a suitable challenge in PLWH, it remains uncertain whether optimized treatment of the identified risks would unequivocally translate into a decrease in SCD rates.

P1247FLNC pathogenic variants in patients with various cardiomyopathies:prevalence and genotype-phenotype correlations

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
F Ader ◽  
P De Groote ◽  
P Reant ◽  
D Dupin-Deguine ◽  
C Rambaud ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Left Ventricular ◽  
Pathogenic Variant ◽  
Pathogenic Variants ◽  
History Of ◽  
Custom Panel ◽  
Few Data ◽  
First Time

Abstract Background/Introduction Pathogenic variants FLNC encoding filamin C have been firstly reported to cause myopathies, and were recently linked to isolated cardiac phenotypes.However, few data on phenotype-genotype correlation are available. Purpose Our aim was to estimate the prevalence of FLNC pathogenic variants in cardiomyopathies and to study the relations between phenotype and genotype. Methods DNAs from a cohort of 1150 unrelated index-patients with an isolated cardiomyopathy (700 hypertrophic, 300 dilated, 50 restrictive cardiomyopathies, and 100 left ventricle non-compactions) have been sequenced on a custom panel of 52 cardiomyopathy disease-causing genes. Results A FLNC pathogenic variant was identified in 28 patients corresponding to a prevalence ranging from 1 to 8% depending on the cardiomyopathy subtypes. Truncating variants were always identified in patients with dilated cardiomyopathy, while missense or in-frame variants were found in other phenotypes. This work reported for the first time a left ventricular non-compaction associated with FLNC pathogenic variant. In the cohort, nine patients (32%) were implanted with an automatic defibrillator. In 7 families (25%), history of sudden cardiac death (SCD) before 50 years was reported. A personal or family history of sudden cardiac death (SCD) was significantly higher in patients with truncating variants than in patients carrying missense variants (p=0.01). Four patients died of cardiac cause including 3 from SCD and 1 from heart failure. Conclusion This work highlights the role of FLNC in cardiomyopathies. A correlation between the type of the variant and the cardiomyopathy subtype was observed as well as with SCD risk. These new data should be taken into consideration for patient's management and primary prevention of sudden cardiac death. Acknowledgement/Funding La ligue contre la Cardiomyopathie

Causes of sudden cardiac death in young athletes and nonathletes: systematic review and meta-analysis

2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
F D"ascenzi ◽  
F Valentini ◽  
S Pistoresi ◽  
F Frascaro ◽  
P Pietro ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Ventricular Hypertrophy ◽  
Total Population ◽  
Meta Analysis ◽  
Left Ventricular ◽  
Normal Heart ◽  
Funding Sources ◽  
Artery Disease ◽  
Funding Acknowledgements

Abstract Funding Acknowledgements Type of funding sources: None. Introduction. The etiology of sudden cardiac death (SCD) in young people is still debated. The aim of this meta-analysis was to identify the most frequent causes of SCD in individuals aged ≤35 years, the differences between athletes and nonathletes and among geographic areas. Methods.  Studies published between 01/01/1990 and 01/31/2020 and evaluating post-mortem the etiology of SCD in young individuals (≤35 years) were included. Individuals were divided in athletes and nonathletes. Studies that did not report separately data between athletes and nonathletes were excluded. Results. Thirty-four studies met the inclusion criteria and a total population of 5,060 victims of SCD were analysed (2,890 athletes, 2,170 nonathletes). Structurally normal heart, hypertrophic cardiomyopathy (HCM), idiopathic left ventricular hypertrophy, and anomalous origin of coronary arteries (AOCA) were the most frequent causes of SCD in athletes while coronary artery disease (CAD), arrhythmogenic cardiomyopathy (ACM), and channelopathies were frequent causes of SCD in nonathletes. The number of SCDs due to ischemic heart disease (19.6% vs. 9.1%, p = 0.009), ACM (11.5% vs. 4.7%, p = 0.03) and channelopathies (8.4% vs. 1.9%, p = 0.02) was higher in nonathletes comparing with athletes. SCD due to non-ischemic left ventricular scar (5.1% vs. 1.1%, p = 0.01) was more frequent in athletes. HCM (p = 0.01) and AOCA (p = 0.004) were more frequently cause of SCD in US while ACM (p = 0.001), structurally normal heart (p = 0.02), and channelopathies (p = 0.02) in Europe. Conclusions. Structurally normal heart, HCM, AOCA were frequent causes of SCD in athletes while CAD, ACM and channelopathies in nonathletes. The causes of SCD differ between US and Europe.

scholarly journals 683 Cor in memoria posterorum: role of familial screening in sudden death syndrome

2021 ◽  
Vol 23 (Supplement_G) ◽  
Author(s):  
Chiara Chiti ◽  
Vanda Parisi ◽  
Maddalena Graziosi ◽  
Elena Biagini
Keyword(s):  
Sudden Cardiac Death ◽  
Left Ventricle ◽  
Cardiac Death ◽  
Structural Damage ◽  
Family Members ◽  
Anterior Wall ◽  
Left Ventricular ◽  
Arrhythmogenic Cardiomyopathy ◽  
Therapeutic Implications

Abstract A 14-year-old boy suddenly died during a school lesson. His familial history was negative for sudden cardiac death and no comorbidities were reported. As part of Emilia Romagna regional network for sudden cardiac death, the heart was examined at our Cardiovascular Pathology Unit. The molecular autopsy revealed extensive lymphocytic macrophage left ventricle myocarditis (infero-lateral and anterior wall) in various evolutive stages. Genetic testing with next-generation sequencing was performed on DNA isolated from explanted heart samples (178 candidate genes for channelopathies and cardiomyopathies were analysed) and it showed a frameshift pathological mutation in the filamine C gene (FLNC c.8034delC p. Cys2679fsTer6) which induces protein premature termination. In order to screen family members, we evaluated the father, 53-year-old, asymptomatic and with an unremarkable cardiology history. The ECG showed sinus rhythm, HR 60 b.p.m., normal atrioventricular conduction, QRS fragmentation and negative T waves in the inferior leads. The echocardiogram revealed left ventricle mild dilation (79 mL/m2) with global hypokinesia (EF 45%), while right ventricle was normal for size and kinetics. A cardiac MRI confirmed left ventricular dilation and hypokinesia with diffuse LGE with circumferential mesocardial distribution mainly in the middle-baseline site, which reflected structural damage (fibrosis). The 24-h Holter ECG did not record arrhythmias. The genetic test was then performed and the same FLNC frameshift mutation was identified. We thus suspected familial arrhythmogenic cardiomyopathy involving left ventricle with pathological filamine C mutation and an ICD was recommended. Other family members had no pathological findings. Filamine C mutations are associated with many type of cardiomyopathy. A possible association between some mutated variants and certain subtypes of cardiomyopathy has been highlighted. In particular, the frameshift variant is associated with an increased arrhythmic risk, particularly when dilated forms are considered. Recent studies have identified a correlation with arrhythmogenic cardiomyopathy, although the role of these mutated variants has not yet been fully defined. This clinical case underlines the importance of multidisciplinary approach in cases of sudden cardiac death, consisting of autopsy, genetic and clinical evaluation, in order to identify any forms of familial cardiomyopathy and activate a systematic screening in family members with important prognostic and therapeutic implications. Data about our regional structural network for sudden cardiac death will also be shown.

scholarly journals Sudden Cardiac Death

2021 ◽  
pp. 32-41
Author(s):  
Omar Elsaka
Keyword(s):  
Heart Disease ◽  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Public Health Problem ◽  
The United States ◽  
Left Ventricular ◽  
Future Research ◽  
Large Size ◽  
Artery Disease ◽  
Lake Size

Background: Sudden cardiac death (SCD) remains a major open clinical and public health problem, with an estimated 300,000 deaths per year in the United States. The possibility of identifying potential SCD victims is limited by the large size of the large number of SCD victims and the apparent time-dependent risk of sudden death. The latter refers to the tendency of SCDs to detect other cardiovascular events during the most dangerous period of 6–18 months following a major cardiovascular event and the risk of subsequent collapse. The combination of time and lake size provides the basis for future research to find more vulnerable people. Pathologically, SCD can be seen as an interaction between some electrophysiological events that causes abnormalities in cardiac structure, temporal dysfunction, and malignant arrhythmias. Structural deformities represent an anatomical matrix of chronic risk and include the effects of electrophysiological anatomical abnormalities such as coronary artery disease, left ventricular hypertrophy, myopathic ventricles, and bypass leaflets in the myocardium. Conclusion: Macroscopic cardiac features are common in about one-third of young SCD victims. However, in 79% of them, histological studies reveal hidden pathological features such as local myocarditis, heart disease and motor system disorders. A total of 16 (6%) victims had no evidence of systemic heart disease and the mechanism of SCD was not described.

The role of implantable cardioverter-defibrillators and sudden cardiac death prevention: indications, device selection, and outcome

2019 ◽  
Vol 41 (21) ◽  
pp. 2003-2011 ◽  
Author(s):  
Ilan Goldenberg ◽  
David T Huang ◽  
Jens Cosedis Nielsen
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Current Knowledge ◽  
Left Ventricular ◽  
Cardiac Resynchronization ◽  
Implantable Cardioverter Defibrillators ◽  
Icd Implantation ◽  
Device Selection ◽  
Cardioverter Defibrillators

Abstract Multiple randomized multicentre clinical trials have established the role of the implantable cardioverter-defibrillator (ICD) as the mainstay in the treatment of ventricular tachyarrhythmias and sudden cardiac death (SCD) prevention. These trials have focused mainly on heart failure patients with advanced left ventricular dysfunction and were mostly conducted two decades ago, whereas a more recent trial has provided conflicting results. Therefore, much remains to be determined on how best to balance the identification of patients at high risk of SCD together with who would benefit most from ICD implantation in a contemporary setting. Implantable cardioverter-defibrillators have also evolved from the simple, defibrillation-only devices implanted surgically to more advanced technologies of multi-chamber devices, with physiologic bradycardic pacing, including cardiac resynchronization therapy, atrial and ventricular therapeutic pacing algorithms, and subcutaneous ICDs. These multiple options necessitate individualized approach to device selection and programming. This review will focus on the current knowledge on selection of patients for ICD treatment, device selection and programming, and future directions of implantable device therapy for SCD prevention.

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