Disease relevance of Death, Sudden, Cardiac

• Ankyrin-B mutation causes type 4 long-QT cardiac arrhythmia and sudden cardiac death [1].
• It has long been noted that while patients with familial hypertrophic cardiomyopathy due to cardiac troponin T (cTnT) mutations often suffer sudden cardiac death, they do not develop significant ventricular hypertrophy, suggesting that a distinct cellular mechanism apart from alterations in myocardial contractility is responsible [2].
• While iNOS-overexpressing mice infrequently developed overt heart failure, they displayed a high incidence of sudden cardiac death due to bradyarrhythmia [3].
• These results have significant implications for human congenital LQT syndromes because hypokalemia increases the risk of ventricular arrhythmia and cardiac sudden death [4].
• Eight patients were placed on long-term sematilide therapy, and during a mean follow-up period of 7.0 +/- 7.5 months, two patients developed sudden cardiac death, and one additional patient had recurrent sustained ventricular tachycardia [5].
• We found that mice heterozygous for the R2474S mutation in Ryr2 (Ryr2-R2474S mice) exhibited spontaneous generalized tonic-clonic seizures (which occurred in the absence of cardiac arrhythmias), exercise-induced ventricular arrhythmias, and sudden cardiac death [6].

Psychiatry related information on Death, Sudden, Cardiac

• The US FDA recently reported that significant cardiovascular events, including sudden cardiac death, have occurred in men with erectile dysfunction who were taking sildenafil citrate [7].
• Ethanol damage to the heart is evident if alcohol consumption exceeds 90 to 100 g/d. Heavy ethanol consumption leads to increased risk for sudden cardiac death and cardiac arrhythmias [8].

High impact information on Death, Sudden, Cardiac

• FKBP12.6 deficiency and defective calcium release channel (ryanodine receptor) function linked to exercise-induced sudden cardiac death [9].
• Mice deficient for HF-1 b survive to term and exhibit normal cardiac structure and function but display sudden cardiac death and a complete penetrance of conduction system defects, including spontaneous ventricular tachycardia and a high incidence of AV block [10].
• A novel genetic pathway for sudden cardiac death via defects in the transition between ventricular and conduction system cell lineages [10].
• Thus, defects in RyR2 have been linked to heart failure and exercise-induced sudden cardiac death and might provide novel therapeutic targets for the treatment of these common diseases of the heart [11].
• Atopy and sudden cardiac death [12].

Chemical compound and disease context of Death, Sudden, Cardiac

• Overall, there was no evidence of a relation between trans isomers of oleic and linoleic acids combined and sudden cardiac death [13].
• However, trans oleic acid was negatively associated with risk of sudden cardiac death, whereas no association with trans forms of linoleic acid was seen [13].
• This low arrhythmogenicity and the negligible negative inotropic effect of the compound constitute properties that make amiodarone particularly useful in treating high-risk patients prone to sudden cardiac death [14].
• CONCLUSIONS: Clustering of ventricular ectopy, as measured by the fractal dimension, is observed in patients at increased risk of sudden cardiac death [15].
• BACKGROUND: The Cardiac Arrhythmia Suppression Trial has shown that flecainide was associated with an increased incidence of sudden cardiac death in postinfarction patients [16].

Biological context of Death, Sudden, Cardiac

• LQT2 may give rise to severe arrhythmogenic phenotypes leading to sudden cardiac death [17].
• Missense mutations in KCNH2 (HERG) linked to a gain-of-function of the rapidly activating delayed-rectifier current I(Kr) have been identified in the first two reported families with familial sudden cardiac death [18].
• OBJECTIVES: Point mutations in the cardiac ryanodine receptor (RyR2) mediate abnormal intracellular Ca(2+) release and are associated with stress-induced ventricular tachycardia (VT), leading to sudden cardiac death (SCD) [19].
• The predictors of sudden cardiac death were blood pressure, serum cholesterol, serum glucose, cigarette smoking, history of parental heart attack, and electrocardiographic evidence of left ventricular hypertrophy or strain [20].
• Effects of amiodarone on the circadian rhythm and power spectral changes of heart rate and QT interval: significance for the control of sudden cardiac death [21].

Anatomical context of Death, Sudden, Cardiac

• For example, diastolic calcium "leak" via RyR2 channels in the sarcoplasmic reticulum has been identified as an important factor contributing to impaired contractility in heart failure and ventricular arrhythmias that cause sudden cardiac death [22].
• The mechanism by which cocaine produces sudden cardiac death has not been elucidated, but clinical evidence indicates that it may be due to a direct or indirect action on coronary vessels [23].
• CONCLUSION: Accumulation of phytanic acid in myocardial phospholipid membranes is associated with bradycardia and impaired AV nodal and intraventricular impulse conduction, which could provide an explanation for sudden cardiac death in this model [24].
• Based on the fact that high doses of cocaine severely depressed all cardiac parameters and its effect on the isolated heart, cocaine-induced sudden cardiac death appears to be due to a primary effect on the myocardium [25].
• CONCLUSIONS--The percentage content of linoleic acid in adipose tissue was inversely related to the risk of sudden cardiac death [26].

Gene context of Death, Sudden, Cardiac

• MYH7 mutations are one of the most common genetic causes of HCM and have been associated with severe hypertrophy, young age of diagnosis, and high risk of sudden cardiac death [27].
• Currently it is not possible to predict the phenotype in carriers of mutations in these genes, although it is widely accepted that mutations in the MYH7 gene predispose to severe HC, whereas TNNT2 mutations are frequently linked to sudden cardiac death (SCD) in spite of minimal hypertrophy [28].
• KCNJ11 polymorphisms and sudden cardiac death in patients with acute myocardial infarction [29].
• Accordingly, defective KCNE1 and/or KCNQ1 lead to long QT syndrome, a disorder causing fainting and sudden cardiac death [30].
• Role of SCN5A Y1102 polymorphism in sudden cardiac death in blacks [31].

Analytical, diagnostic and therapeutic context of Death, Sudden, Cardiac

• Cost-effectiveness of implantable cardioverter defibrillators relative to amiodarone for prevention of sudden cardiac death [32].
• The diagnosis of AMI was confirmed or ruled out by means of typical electrocardiographic findings, thallium-201 myocardial scintigraphy or autopsy, if death occurred during the hospital period, in 39 primary survivors of sudden cardiac death [33].
• Ambulatory monitoring can be used to identify a subset of patients with coronary disease or cardiomyopathy who are at increased risk for sudden cardiac death [34].
• Losartan-based treatment led to trends toward lower all-cause mortality (30 vs. 49, HR = 0.67, 95% CI 0.42 to 1.06, p = 0.090) and fewer pacemaker implantations (5 vs. 15, p = 0.065), whereas hospitalization for heart failure took place in 15 versus 26 patients and sudden cardiac death in 9 versus 17, respectively (both p = NS) [35].
• In addition, aged Cav-1 null mice may provide a new animal model to study the pathogenesis and treatment of progressive hypertrophic cardiomyopathy and sudden cardiac death syndrome [36].

References