Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Sudden cardiac death due to ventricular fibrillation in a case of giant cell myocarditis.

ABSTRACT: A 70-year-old woman was admitted to our hospital complaining of shortness of breath. She was diagnosed with acute decompensated heart failure due to left ventricular dysfunction. Her symptoms began to improve with standard therapy for heart failure with diuretics, noninvasive pressure ventilation, and inotropes, but paroxysmal atrial fibrillation and premature ventricular contractions (PVCs) occurred. After treatment with amiodarone, the number of PVCs decreased, and the left ventricular wall motion gradually improved. However, on day 28, ventricular fibrillation and cardiopulmonary arrest occurred suddenly, and she could not be resuscitated. She was diagnosed with giant cell myocarditis via an autopsy. The autopsy revealed diffuse inflammatory cells that comprised giant cells and eosinophils as well as cellular degeneration and necrosis. <Learning objective: We herein report a case of sudden cardiac death due to giant cell myocarditis diagnosed at an autopsy.>.

SUBMITTER: Umei TC

PROVIDER: S-EPMC7283290 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

Sudden cardiac death due to ventricular fibrillation in a case of giant cell myocarditis.

Umei Tomohiko C TC Murata Yuya Y Momiyama Yukihiko Y

Journal of cardiology cases 20200312 6

A 70-year-old woman was admitted to our hospital complaining of shortness of breath. She was diagnosed with acute decompensated heart failure due to left ventricular dysfunction. Her symptoms began to improve with standard therapy for heart failure with diuretics, noninvasive pressure ventilation, and inotropes, but paroxysmal atrial fibrillation and premature ventricular contractions (PVCs) occurred. After treatment with amiodarone, the number of PVCs decreased, and the left ventricular wall mo ...[more]

PMID: 32547658

Similar Datasets

Sudden cardiac death risk in contact sports increased by myocarditis: a case series.

Project description:BackgroundMyocarditis is a known cause of sudden cardiac death of the athlete. The impact of direct chest trauma in at-risk sports or activities in patients with a history of myocarditis has never been demonstrated or studied. We report herein two cases of life-threatening ventricular arrhythmia secondary to non-penetrating blunt chest trauma while playing contact sports.Case summaryThe first patient, a 26-year-old man described a brief loss of consciousness after having received blunt impact to the chest (typical intensity) while playing a rugby match. The loss of consciousness was total and proceeded by rapid and regular palpitations. He had a history of viral myocarditis 10 years prior with a fibrotic sequalae in the inferolateral wall on cardiac magnetic resonance imaging (left ventricular ejection fraction 71%). Right apical ventricular pacing induced a sustained monomorphic ventricular tachycardia reproducing the patient's symptoms. A subcutaneous implantable cardioverter-defibrillator was implanted. The second patient is a 22-year-old professional rugby player with no known notable history. During a match, a direct blow to the chest wall was followed by a cardiac arrest. A ventricular fibrillation was cardioverted to pulseless electrical activity. Patient died despite cardiopulmonary resuscitation. An autopsy identified a myocardial sequela of fibrosis with no acute inflammatory remodelling compatible with a previous myocarditis.DiscussionMyocarditis may increase the risk of life-threatening ventricular arrhythmias caused by blunt impact to the chest, particularly in contact sports. Screening and prevention measures should be considered to reduce this risk.

| S-EPMC8185879 | biostudies-literature

Bidirectional Ventricular Tachycardia in a Patient With Fulminant Myocarditis Secondary to Cardiac Sarcoidosis Mimicking Giant Cell Myocarditis.

Project description:Differentiating between sarcoidosis and giant cell myocarditis (GCM) based on clinical presentation is difficult. We present the case of a 57-year-old woman who was initially diagnosed with GCM based on endomyocardial biopsy. The patient was refractory to standard management for GCM and went on to develop bidirectional ventricular tachycardia, a finding suggestive of sarcoidosis. Unfortunately, the patient eventually needed cardiac transplantation. The explanted heart demonstrated cardiac sarcoidosis. Bidirectional ventricular tachycardia has not been demonstrated in GCM, and its presence may help in distinguishing between GCM and cardiac sarcoidosis.

| S-EPMC8712583 | biostudies-literature

Alcohol and the risk of all-cause death, atrial fibrillation, ventricular arrhythmia, and sudden cardiac arrest.

Project description:The risk of having atrial fibrillation (AF) is associated with alcohol intake. However, it is not clear whether sudden cardiac arrest (SCA) and ventricular arrhythmia (VA) including ventricular tachycardia, flutter, or fibrillation have similar associations with alcohol. We aimed to evaluate the association of alcohol intake with all-cause death, new-onset AF, VA, and SCA using single cohort with a sufficient sample size. A total of 3,990,373 people without a prior history of AF, VAs, or SCA was enrolled in this study based on nationwide health check-up in 2009. We classified the participants into four groups according to weekly alcohol consumption, and evaluated the association of alcohol consumption with each outcome. We observed a significant association between mild (hazard ratio [HR] = 0.826; 95% confidence interval [CI] = 0.815-0.838) to moderate (HR = 0.930; 95% CI = 0.912-0.947) drinking with decreased risk of all-cause mortality. However heavy drinking (HR = 1.108; 95% CI = 1.087-1.129) was associated with increased all-cause death. The risk of new-onset AF was significantly associated with moderate (HR = 1.129; 95% CI = 1.097-1.161) and heavy (HR = 1.298; 95% CI = 1.261-1.337) drinking. However, the risk of SCA showed negative association with all degrees of alcohol intake: 20% (HR = 0.803; 95% CI = 0.769-0.839), 15% (HR = 0.853; 95% CI = 0.806-0.902), and 8% (HR = 0.918; 95% CI = 0.866-0.974) lower risk for mild, moderate, and heavy drinkers, respectively. Mild drinking was associated with reduced risk of VA with moderate and heavy drinking having no associations. In conclusion, the association between alcohol and various outcomes in this study were heterogeneous. Alcohol might have different influences on various cardiac disorders.

| S-EPMC10904378 | biostudies-literature

Ventricular fibrillation due to a likely pathogenic <i>SOS1</i> variant: An unrecognized etiology of infantile sudden death?

Project description: Not available

| S-EPMC8377259 | biostudies-literature

First report of sudden death due to myocarditis caused by adenovirus serotype 3.

Project description:Myocarditis is a rare cause of sudden death in childhood. We describe the sudden death of a child from viral myocarditis, which we demonstrate was likely caused by an uncontrolled inflammatory response to a disseminated adenovirus serotype 3 infection originating in the tonsil.

| S-EPMC2815630 | biostudies-literature

Loss of luminal Ca2+ activation in the cardiac ryanodine receptor is associated with ventricular fibrillation and sudden death.

Project description:Different forms of ventricular arrhythmias have been linked to mutations in the cardiac ryanodine receptor (RyR)2, but the molecular basis for this phenotypic heterogeneity is unknown. We have recently demonstrated that an enhanced sensitivity to luminal Ca(2+) and an increased propensity for spontaneous Ca(2+) release or store-overload-induced Ca(2+) release (SOICR) are common defects of RyR2 mutations associated with catecholaminergic polymorphic or bidirectional ventricular tachycardia. Here, we investigated the properties of a unique RyR2 mutation associated with catecholaminergic idiopathic ventricular fibrillation, A4860G. Single-channel analyses revealed that, unlike all other disease-linked RyR2 mutations characterized previously, the A4860G mutation diminished the response of RyR2 to activation by luminal Ca(2+), but had little effect on the sensitivity of the channel to activation by cytosolic Ca(2+). This specific impact of the A4860G mutation indicates that the luminal Ca(2+) activation of RyR2 is distinct from its cytosolic Ca(2+) activation. Stable, inducible HEK293 cells expressing the A4860G mutant showed caffeine-induced Ca(2+) release but exhibited no SOICR. Importantly, HL-1 cardiac cells transfected with the A4860G mutant displayed attenuated SOICR activity compared with cells transfected with RyR2 WT. These observations provide the first evidence that a loss of luminal Ca(2+) activation and SOICR activity can cause ventricular fibrillation and sudden death. These findings also indicate that although suppressing enhanced SOICR is a promising antiarrhythmic strategy, its oversuppression can also lead to arrhythmias.

| S-EPMC2084339 | biostudies-literature

Mutations in calmodulin cause ventricular tachycardia and sudden cardiac death.

Project description:Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a devastating inherited disorder characterized by episodic syncope and/or sudden cardiac arrest during exercise or acute emotion in individuals without structural cardiac abnormalities. Although rare, CPVT is suspected to cause a substantial part of sudden cardiac deaths in young individuals. Mutations in RYR2, encoding the cardiac sarcoplasmic calcium channel, have been identified as causative in approximately half of all dominantly inherited CPVT cases. Applying a genome-wide linkage analysis in a large Swedish family with a severe dominantly inherited form of CPVT-like arrhythmias, we mapped the disease locus to chromosome 14q31-32. Sequencing CALM1 encoding calmodulin revealed a heterozygous missense mutation (c.161A>T [p.Asn53Ile]) segregating with the disease. A second, de novo, missense mutation (c.293A>G [p.Asn97Ser]) was subsequently identified in an individual of Iraqi origin; this individual was diagnosed with CPVT from a screening of 61 arrhythmia samples with no identified RYR2 mutations. Both CALM1 substitutions demonstrated compromised calcium binding, and p.Asn97Ser displayed an aberrant interaction with the RYR2 calmodulin-binding-domain peptide at low calcium concentrations. We conclude that calmodulin mutations can cause severe cardiac arrhythmia and that the calmodulin genes are candidates for genetic screening of individual cases and families with idiopathic ventricular tachycardia and unexplained sudden cardiac death.

| S-EPMC3484646 | biostudies-literature

Risk and Prediction of Sudden Cardiac Death and Ventricular Arrhythmias for Patients with Atrial Fibrillation - A Nationwide Cohort Study.

Project description:Sudden cardiac death (SCD) is the most devastating manifestation of ventricular arrhythmias (VAs), and is the leading cause of mortality among atrial fibrillation (AF) patients. The goal of the present study was to investigate the incidence of SCD/VAs amongst patients with and without AF. We also aimed to identify important risk factors of SCD/VAs among AF patients. Using the "National Health Insurance Research Database" in Taiwan, a total of 352,656 AF and 352,656 non-AF patients without antecedent SCD/VAs were identified. The annual risk of SCD/VAs was higher in AF than non-AF groups (0.97% versus 0.47%) with an adjusted hazard ratio (HR) of 1.64. The increased risk of SCD/VAs in AF patients was consistently observed in different age strata, various comorbidities and patients without use of class I/III anti-arrhythmic drugs or digoxin. Among AF patients, age ≥75 years, congestive heart failure, hypertension, diabetes mellitus, previous stroke/transient ischemic attack, vascular diseases, chronic kidney disease and chronic obstructive pulmonary disease were important risk factors for SCD/VAs. In conclusion, the risk of SCD/VAs amongst AF patients was 1.64-fold higher compared to non-AF patients, which was associated with the number of clinical risk factors associated with the particular AF patient.

| S-EPMC5396069 | biostudies-literature

Antidepressants and the risk of sudden cardiac death and ventricular arrhythmia.

Project description:To examine the association between exposure to antidepressants and emergency department or inpatient admission for sudden cardiac death and ventricular arrhythmia (SD/VA), and to examine the impact of dose and cytochrome P-450 inhibition.A cohort study was conducted using 1999-2003 Medicaid claims data from beneficiaries of five large states, supplemented with Medicare claims for dually eligible individuals. Exposures were prescription claims for antidepressants of interest or a reference antidepressant. Outcomes were incident first-listed emergency department or principal inpatient diagnoses indicative of SD/VA originating in the outpatient setting, an outcome previously found to have a positive predictive value of 85%.In 1.3 million person-years of antidepressant exposure, we identified 4222 SD/VA outcomes for a rate of 3.3/1000 person-years (95%CI, 3.2-3.4). Compared with paroxetine (a referent with a putatively favorable cardiovascular risk profile), adjusted hazard ratios (HRs) were 0.80 (0.67-0.95) for bupropion, 1.24 (0.93-1.65) for doxepin, 0.79 (0.55-1.15) for lithium, and 1.26 (1.11-1.42) for mirtazapine. HRs for amitriptyline, citalopram, fluoxetine, nefazodone, nortriptyline, sertraline, trazodone, and venlafaxine were near unity. For antidepressants having nonnull risks (bupropion and mirtazapine), we observed no relationship with antidepressant dose and some relationships with concomitant cytochrome P-450 inhibition.Of antidepressants studied, only mirtazapine had a statistically significantly greater SD/VA risk versus paroxetine. However, baseline differences between these users suggest that this finding may be attributable to residual confounding. Eleven other antidepressants had SD/VA risks no greater than that of paroxetine, thereby providing reassurance regarding the comparative cardiovascular safety of antidepressants.

| S-EPMC3217297 | biostudies-literature

Cardiac sarcoidosis and giant cell myocarditis after COVID-19 infection.

Project description:Patients infected with SARS-CoV-2 have varying manifestations of cardiac involvement. We report four patients presenting with symptomatic cardiac sarcoidosis (CS) or giant cell myocarditis (GCM) 1-8 months after mild COVID-19. All patients received immunosuppressive therapy and improved gradually within the following months. The possible temporal association between the CS/GCM and COVID-19 infection might suggest that COVID-19 could be a trigger for granulomatous myocarditis.

| S-EPMC9539072 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data