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Despite recent reductions in cardiac mortality from other causes, the incidence of SCD remains high with minimal decline in the last decade. The large majority of patients who suffer life-threatening ventricular arrhythmias have advanced left ventricular LV systolic dysfunction.

These patients are often relatively young and have no overt evidence of structural heart disease. For example, the LQTS is a monogenetic disorder associated with prolonged ventricular repolarization, malignant ventricular arrhythmias, typically torsades de pointes, and SCD.

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In this subset of patients, genetic screening is currently available to identify patients at risk for SCD. Linkage analysis in the early s heralded the identification of several mutations responsible for LQTS phenotypes. LQT1 is due to a mutation in KCNQ1, the alpha subunit of the potassium ion channel, and responsible for cardiac slowly activated delayed rectifying potassium current I Ks. Mutation in SCN5a, the alpha subunit of the cardiac sodium channel, is responsible for LQT3 and LQT4 is due to mutation in ankyrin B, a cytoskeletal protein that anchors ion channels to cell membrane.

Although these monogenic disorders would appear to be straightforward causes of SCD i. Identification of abnormal genotype may not be sufficient to identify patients at risk for SCD. Inherited cardiomyopathic disorders can also cause SCD in young individuals and, particularly, athletes. ARVD is a rare disorder characterized by fibro-fatty infiltration of the right ventricle and malignant ventricular arrhythmias. ARVD has been associated with inherited mutations in desmoplakin, plakophilin-2, plakoglobin, and ryanodine receptor.

Therefore, diagnosis and therapy is typically guided by the pattern and severity of the clinical presentation.

Although there have been some recent advances in understanding the genetic basis for coronary vascular disease, 17 the genetic basis for susceptibility to SCD in patients with coronary disease remains elusive. Recent epidemiological studies have demonstrated an interesting clustering of SCD in families where parents or siblings experience SCD. This fact has led to exclusion of such patients in many recent trials aimed at establishing efficacy ICD therapy as primary prevention of SCD.

Elevated plasma levels of brain natriuretic peptide, Creactive protein and troponin T are currently available laboratory indices that are independent predictors of increased mortality in patients with ischemic cardiomyopathy, but have no known role for evaluating risk of SCD. Invasive electrophysiological study EPS uses responses to programmed electrical stimulation to identify patients at risk for SCD.

[Current perspectives in cell therapy in cardiology: an overview of ongoing trials].

Induction of sustained monomorphic ventricular tachycardia is considered highly indicative of risk. With recent advances in digital processing techniques it is now possible to extract information from the electrocardiogram ECG that is not visible on the surface. Several non-invasive electrocardiographic indices are currently available to assess arrhythmia susceptibility in patients at risk for SCD. Various non-invasive indices of sympathovagal tone have also been used to risk-stratify patients. Diminished HRV was associated with a 3. HRV is highly dependent on the ambient conditions under which the measurement is being made, which greatly limits reproducibility in individual patients.

There is also uncertainty as to the best method to assess HRV. Biomechanical forces and atherosclerosis: From mechanism to diagnosis and treatment Vadim V.

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