scholarly journals Bradycardic variant of sudden cardiac death in patient with left ventricle aneurysm

Cor et Vasa ◽  
2017 ◽  
Vol 59 (5) ◽  
pp. e457-e459
Author(s):  
Oleg Libryk ◽  
Igor Vakaljuk ◽  
Elina Warenytsia ◽  
Andriy Vytryhovskiy
Keyword(s):  
Sudden Cardiac Death ◽  
Left Ventricle ◽  
Cardiac Death

scholarly journals Sudden Cardiac Death in Hereditary Dilated Cardiomyopathy

2020 ◽  
Author(s):  
Marianna Leopoulou ◽  
Jo Ann LeQuang ◽  
Joseph V. Pergolizzi ◽  
Peter Magnusson
Keyword(s):  
Sudden Cardiac Death ◽  
Left Ventricle ◽  
Sudden Death ◽  
Risk Stratification ◽  
Dilated Cardiomyopathy ◽  
Cardiac Death ◽  
Disease Risk ◽  
Systolic Dysfunction ◽  
Preventive Strategies ◽  
Genetic Origin

Dilated cardiomyopathy (DCM) is characterized by the phenotype of a dilated left ventricle with systolic dysfunction. It is classified as hereditary when it is deemed of genetic origin; more than 50 genes are reported to be related to the condition. Symptoms include, among others, dyspnea, fatigue, arrhythmias, and syncope. Unfortunately, sudden cardiac death may be the first manifestation of the disease. Risk stratification regarding sudden death in hereditary DCM as well as preventive management poses a challenge due to the heterogeneity of the disease. The purpose of this chapter is to present the epidemiology, risk stratification, and preventive strategies of sudden cardiac death in hereditary DCM.

scholarly journals CHARACTERISATION OF HYPERTROPHIC CARDIOMYOPATHY BY CARDIAC MAGNETIC RESONANCE IMAGING

2021 ◽  
Vol 9 (11) ◽  
pp. 643-648
Author(s):  
Nava Udaya N.R ◽  
◽  
Ramiah Rajesh Kannan ◽  
Srikanth Moorthy ◽  
Resmi Sekhar ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Sudden Cardiac Death ◽  
Left Ventricle ◽  
Cardiac Mri ◽  
Cardiac Death ◽  
Final Diagnosis ◽  
Left Ventricular ◽  
Categorical Variables ◽  
Diagnostic Parameters ◽  
Septal Hypertrophy

Background: There are many causes of left ventricular hypertrophy which can result in arrhythmias and sudden cardiac death. Hypertrophic cardiomyopathy (HCM) is one of the commonly encountered cause of sudden cardiac death in young adults. Aim: Identifying the role of Cardiac MRI in characterising the diagnostic parameters of HCM. Materials and methods: 125 patients with clinical suspicion or genetic evidence of HCM referred for cardiac MRI between June 2013 to June 2021 were included under the study. Image interpretations were done by fellowship qualified cardiac imaging radiologist. Categorical variables were expressed using frequency and percentage. Numerical variables were presented using mean and standard deviation. Results: Out of the total population, 119 patients (95 %) had LV wall thickness > 13 mm, 48 patients (38.4%) had Left ventricle outflow tract obstruction (LVOTO) and 32 patients (25.6 %) had mid cavity obstruction, 39 patients (37.9 %) had myocardial scar > 15 % and asymmetric septal hypertrophy was the most frequently encountered left ventricle morphology Conclusion: Cardiac MRI detected HCM has a statistically significant association with the final diagnosis (histopathological and genetic correlation). CMRI hence serves as a reliable tool in identifying and characterising the various diagnostic and non- diagnostic parameters of HCM.

scholarly journals Early risk predictors of sudden cardiac death after myocardial infarction: Results of follow up of 881 patients

2006 ◽  
Vol 134 (11-12) ◽  
pp. 482-487 ◽  
Author(s):  
Branislav Milovanovic ◽  
Mirjana Krotin ◽  
Dejana Vukovic ◽  
Vesna Bisenic ◽  
Tijana Mirjanic ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Sudden Cardiac Death ◽  
Left Ventricle ◽  
Cardiac Death ◽  
Systolic Dysfunction ◽  
P Wave ◽  
Late Potentials ◽  
T Wave ◽  
Wave Inversion ◽  
Risk Predictors

Introduction: It has been shown that depolarization disorders, autonomic dysfunction, and systolic dysfunction of the left ventricle are associated with sudden cardiac death after myocardial infarction. Objective: The Objective of study was to examine the prognostic value of the most important predictors in the first week after myocardial infarction. Method: Study included 881 patients who were followed up from 1 to 60 months. During the first week after myocardial infarction, following examination were performed: ECG with standard leads and X, Y, Z orthogonal leads, vectorcardiogram, QT interval, late potentials, short-time spectral analysis of RR variability, nonlinear (Poincare plot) analysis and echocardiogram. Results: In univariate analysis, the following parameters measured on the first day were important predictors of sudden cardiac death: lower LF/HF ratio(<1.5) (p=0.000), T wave inversion in X lead (p=0.000), high P wave in D2 lead (p=0.030), and diminished systolic function (p=0.000). In multivariate analysis, the following parameters were significant risk predictors: T wave inversion in X lead, lower LF/HF ratio, positive late potentials and the left ventricle systolic dysfunction. Conclusion: The parameters of the left ventricle systolic dysfunction with sympathicovagal imbalance and electric instability are the key risk predictors in the first few days after myocardial infarction.

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 Characteristic of fibrotic myocardial lesions associated with life-threatening ventricular tachyarrhythmias in patients with ischemic and non-ischemic cardiomyopathies

2018 ◽  
Vol 90 (9) ◽  
pp. 42-47
Author(s):  
N B Shlevkov ◽  
A A Zhambeev ◽  
A Z Gasparyan ◽  
V N Shitov ◽  
O V Stukalova
Keyword(s):  
Sudden Cardiac Death ◽  
Left Ventricle ◽  
Ejection Fraction ◽  
Cardiac Death ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Tachyarrhythmias ◽  
Ventricular Ejection Fraction ◽  
Contrast Magnetic Resonance ◽  
Magnetic Resonance Imaging Mri

Aim. To identify the features of myocardial scar and fibrosis associated with the occurrence of malignant ventricular tachyarrhythmias (VTs) in high-risk patients with ischemic (ICMP) and non-ischemic cardiomyopathy (NICMP). Materials and methods. This prospective study included 50 patients (41 men, 9 women), age = 60 ± 13 years, 30 patients of them with ICMP and 20 patients with NICMP, who underwent echocardiography (Echo) and contrast magnetic resonance imaging (MRI) of the heart followed by implantation of cardioverter-defibrillators (ICD) or resynchronizing devices with defibrillator (CPTD) to prevent sudden cardiac death. Results. Sustained VTs were reported in 20/30 (67%) patients with ICMP and in 5/20 (25%) patients with NICMP on follow-up [26 (22-37) months]. Successive univariate and ROC-analyses of Echo and MRI-indices between patients with and without recurrence of VTs found different results for ICMP and NICMP patients groups. In ICMP patients the VTs were associated with wide transmural fibrosis on contrast MRI that covered 3 or more segments of left ventricular. These segments were preferably localized in the middle parts of the inferior and inferolateral segments of the left ventricle. The independent predictors of VTs in NICMP patients were non-transmural fibrosis at 4.5% of the left ventricular mass by contrast MRI as well as low left ventricular ejection fraction (less than 26%) by Echo. Conclusion. To determine the indications for implantation of the ICD and CRTD for primary prevention of sudden cardiac death, it is advisable to take into account not only the value of ejection fraction of left ventricular, but also the features of the fibrosis of the left ventricle by contrast MRI of the heart.

Abstract 318: Heterogeneous Remodeling in Diabetic Hearts Leads to Sudden Cardiac Death

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Siva K Panguluri ◽  
Jared Tur ◽  
Srinivas Tipparaju
Keyword(s):  
Ion Channels ◽  
Sudden Cardiac Death ◽  
Left Ventricle ◽  
Cardiac Death ◽  
Transcriptional Factors ◽  
P Value ◽  
Diabetic Mice ◽  
Western Blots ◽  
Arrhythmogenic Substrate ◽  
Repolarization Reserve

Diabetes increases propensity to sudden cardiac death. Although ion channels were implicated, the precise mechanisms leading to arrhythmias remain unclear. We hypothesized that the diabetic heart undergoes heterogeneous remodeling leading to arrhythmogenic substrate and sudden cardiac death. For this, we investigated the expression of cardiac specific microRNAs, key transcriptional factors and their target gene in right (RV) and left ventricle (LV). TaqMan and SYBR green qRT-PCR was used to estimated the transcriptional data and Western blots/ELISA for protein profiles. Our data clearly suggests that miR-1-1a (1.6±0.021; p≤0.00067) and miR-301 (1.36±0.02; p≤0.0201) were up-regulated in epicardium of left ventricle (LV-epi), whereas miR-1-1a (2.9±0.59; p≤0.027), miR-133a (3.7±0.19; p ≤ 0.041) and miR-301 (3.6±0.26; p-value ≤ 0.037) were up-regulated in RV of diabetic (db/db) mice (n=3) hearts compared with wild type (n=3). Out of 30 genes tested we confirmed down-regulation of 14 genes (with p≤0.05) including transcriptional factors NFkB2, GATA6, Irx5, Ezh-2, Six-1, CtBP, SiRT1; ion channels Kv4.2, Scn1b and Scn5a and its protein chaperon Kchip-2, whereas Mef2c was up-regulated significantly in LV-epi in diabetic mice. Similarly, 11 genes including Kv4.2, Mef2c, GATA4, GATA6, Pitx2c, Scn1b, Kchip-2, SiRT1, Nampt and MMP-9 were down-regulated (p≤0.05), whereas 9 genes such as Irx5, Kv2.1, Kv4.3, NFkB1, NFkB2, MHC7, CtBP, NNt, and G6PD were up-regulated significantly in RV of diabetic mice. The Ingenuity Pathway Analysis of the differentially expressed genes in heart revealed hypertrophy, arrhythmias, proliferation, and failure as top toxicology networks in LV-epi, whereas cardiac hypertrophy, hepatic stellate cell activation, oxidative stress, PPAR mediated gene activation, fibrosis and necrosis are among top toxicology networks in RV. The role of miR’s along with transcriptional factors down-regulating Kv4.2 in diabetic LV may be consistent with the idea that repolarization reserve is decreased in diabetic hearts. Moreover, regional differences in potassium current may play vital role in regulating function. These data suggest that the ion channel remodeling in left and right ventricles are modulated via different mechanisms.

Extensive Fibrofatty Infiltration of the Left Ventricle in Two Cases of Sudden Cardiac Death

1994 ◽  
Vol 39 (5) ◽  
pp. 13703J ◽  
Author(s):  
Bobbie Ann Collett ◽  
Gregory James Davis ◽  
William B. Rohr
Keyword(s):  
Sudden Cardiac Death ◽  
Left Ventricle ◽  
Cardiac Death

scholarly journals Noncompaction of Ventricular Wall - A Threat to Life

2012 ◽  
Vol 7 (1) ◽  
pp. 39-41
Author(s):  
Nilufar Fatema ◽  
Ahmed Saiful Bari ◽  
Naznin Sultana ◽  
Mohammad Al Mamun ◽  
SM Mustafa Sultan ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Early Detection ◽  
Left Ventricle ◽  
Cardiac Death ◽  
Ventricular Wall ◽  
Systemic Embolism ◽  
Ventricular Noncompaction ◽  
Noncompaction Cardiomyopathy ◽  
Threat To Life ◽  
Clinical Problems

Ventricular noncompaction is a kind of cardiomyopathy which is called Noncompaction Cardiomyopathy (NCC). In this condition in which the muscular wall of the main pumping chamber of the heart -the left ventricle (LV) appears to be spongy and “non-compacted”, consisting of a meshwork of numerous muscle bands called trabeculations. Here, anatomically LV wall has deep trabeculations. This condition is associated major clinical problems like systolic and diastolic dysfunction, arrhythmia and even systemic embolism. Sudden cardiac death may occur in this group. Early detection of this condition may help to plan the management. DOI: http://dx.doi.org/10.3329/uhj.v7i1.10209 UHJ 2011; 7(1): 39-41

scholarly journals Left sided arrhythmogenic ventricular dysplasia in siblings

Heart ◽  
2001 ◽  
Vol 86 (2) ◽  
pp. 128-130
Author(s):  
C G De Pasquale ◽  
W F Heddle
Keyword(s):  
Sudden Cardiac Death ◽  
Left Ventricle ◽  
Cardiac Death ◽  
Fatty Infiltration ◽  
Ventricular Myocardium ◽  
Arrhythmogenic Right Ventricular Dysplasia ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
The Family ◽  
The Right

A 32 year old man with no previous medical history suffered a sudden cardiac death. Post mortem examination revealed circumferential fibro-fatty infiltration of the left ventricular myocardium. Histological appearance was characteristic of arrhythmogenic right ventricular dysplasia but unusual for its localisation only to the left ventricle. As a result of this sudden cardiac death the family of the deceased was screened for cardiac disease. A brother of the index case was 36 years old and free of cardiac history and symptoms. Cardiac investigations revealed a functionally and electrically abnormal left ventricle with apparent sparing of the right ventricle. The brothers may have a left sided form of arrhythmogenic ventricular dysplasia and illustrate the importance of screening family members of young victims of sudden cardiac death.

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