Sudden cardiac death in non-ischemic dilated cardiomyopathy: A critical appraisal of existing and potential risk stratification tools

Koutalas, Emmanuel; Kanoupakis, Emmanuel M.; Vardas, Panos

doi:10.1016/j.ijcard.2012.07.014

Cited by 44 publications

(29 citation statements)

References 83 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Recent demonstration and continuous expansion of knowledge regarding arrhythmogenesis genes in DCM open a new field of diagnosis and prognosis of these patients. For example, gadolinium enhancement (Koutalas et al, 2013), LMNA (lamin A/C) gene mutations (Sun et al, 2010), sodium channels SCN5A Arg222Gln missense variant (Mann et al, 2012), and cardiac ryanodine receptor NH 2 -terminal mutation (Tang et al, 2012) are closely related to ventricular arrhythmogenesis. Moreover, matrix metalloproteinase 9, tissue inhibitor of matrix metalloproteinase, procollagen type I carboxyterminal peptide, procollagen type III aminoterminal peptide, and their ratio have been found to be indicative of a deranged equilibrium in myocardial collagen deposition/degradation and collagen I/III synthesis which are related to ventricular arrhythmogenesis (Flevari et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

“…Conduction block in patients with DCM is characterized as multiple types. Additionally, as the disease progresses, the ventricle is markedly enlarged and Purkinje fibers are elongated and damaged, which is the reason for cardiac impulse conduction obstacles (Pruszczyk et al, 2007;Koutalas et al, 2013). To prevent sudden death, an early genetic diagnosis and start of therapy may be important for individuals with a family history.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Torasemide reduces dilated cardiomyopathy, complication of arrhythmia, and progression to heart failure

Han¹,

Guo²,

Lin³

et al. 2014

Genet. Mol. Res.

View full text Add to dashboard Cite

ABSTRACT. The aim of this study was to analyze the incidence and types of arrhythmia and their relationship with the severity and prognosis of chronic heart failure (CHF) in patients with dilated cardiomyopathy (DCM), and to investigate the therapeutic effect of torasemide versus furosemide on CHF and incidence of arrhythmia. DCM patients with NYHA cardiac function II-IV were continuously monitored using a 24-h dynamic electrocardiogram (Holter), and arrhythmia incidence was analyzed by computer automatic analysis combined with manual assessment. In total, 125 participants were evenly divided into two groups: torasemide group which received 10 mg oral torasemide once daily) and regular anti-heart failure treatment (N = 65), and furosemide group which received torasemide (20 mg once daily orally) and regular antiheart failure treatment (N = 60). Another 60 normal healthy persons served as the normal control group. Incidence and severity of arrhythmia increased when degree of CHF was elevated. Size of left atrium was related to atrial fibrillation and size of left ventricle was related to malignant arrhythmia. At 3 months after treatment, cardiac function in both groups improved and incidence and severity of arrhythmia in both groups were reduced. However, left ventricular ejection fraction (LVEF) was higher in the torasemide group than in the furosemide group, while incidence of arrhythmia was lower in the torasemide group. Arrhythmias frequently occurred in patients with DCM and HF. Type of cardiac arrhythmia is closely related to ventricular enlargement and cardiac function grade. Torasemide is better for improving cardiac function to reduce arrhythmia and CHF compared to furosemide.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Torasemide reduces dilated cardiomyopathy, complication of arrhythmia, and progression to heart failure

Han¹,

Guo²,

Lin³

et al. 2014

Genet. Mol. Res.

View full text Add to dashboard Cite

show abstract

“…Moreover, reentrant arrhythmias may arise from the structural changes associated with the development of DCM; sudden cardiac death is a frequent occurrence in all DCM cases irrespective of the underlying genetic defect (30% of all deaths associated with DCM). 32 Distinguishing the contribution of both possibilities was impossible in our cohort because all SCA cases with this mutation also had DCM. Such distinction may come from future studies.…”

Section: Discussionmentioning

confidence: 92%

Sudden Cardiac Arrest and Rare Genetic Variants in the Community

Milano

Blom

Lodder

et al. 2016

Circ Cardiovasc Genet

View full text Add to dashboard Cite

Background— Sudden cardiac arrest (SCA) ranks among the most common causes of death worldwide. Because SCA is most often lethal, yet mostly occurs in individuals without previously known cardiac disease, the identification of patients at risk for SCA could save many lives. In unselected SCA victims from the community, common genetic variants (which are not disease-causing per se, but may increase susceptibility to ventricular fibrillation) are found to be associated with increased SCA risk. However, whether rare genetic variants contribute to SCA risk in the community is largely unexplored. Methods and Results— We here investigated the involvement of rare genetic variants in SCA risk at the population level by studying the prevalence of 6 founder genetic variants present in the Dutch population (PLN-p.Arg14del, MYBPC3-p.Trp792fsX17, MYBPC3-p.Arg943X, MYBPC3-p.Pro955fsX95, PKP2-p.Arg79X, and the Chr7q36 idiopathic ventricular fibrillation risk haplotype) in a cohort of 1440 unselected Dutch SCA victims included in the Amsterdam Resuscitation Study (ARREST). The six studied founder mutations were found to be more prevalent (1.1%) in the ARREST SCA cohort compared with an ethnically and geographically matched set of controls (0.4%, n=1379; P <0.05) or a set of Dutch individuals drawn from the Genome of the Netherlands (GoNL) study (0%, n=500; P <0.02). Conclusions— This finding provides proof-of-concept for the notion that rare genetic variants contribute to some extent to SCA risk in the community.

show abstract

“…These markers include BNP, 66,67 heart-rate variability, 68 spectral turbulence, 69 T-wave alternans, 70,71 baroreflex sensitivity, 72 QT-interval measurements and dispersion, 67,73 and late potentials measured by the signalaveraged ECG. 72,74,75 Electrophysiology Testing…”

Section: What Evaluation Is Necessary To Rule Out a Cardiac Cause Formentioning

confidence: 99%

Syncope in Patients with Organic Heart Disease

Olshansky

Sullivan

2015

Cardiology Clinics

View full text Add to dashboard Cite

Sudden cardiac death in non-ischemic dilated cardiomyopathy: A critical appraisal of existing and potential risk stratification tools

Cited by 44 publications

References 83 publications

Torasemide reduces dilated cardiomyopathy, complication of arrhythmia, and progression to heart failure

Torasemide reduces dilated cardiomyopathy, complication of arrhythmia, and progression to heart failure

Sudden Cardiac Arrest and Rare Genetic Variants in the Community

Syncope in Patients with Organic Heart Disease

Contact Info

Product

Resources

About