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SudD inCode®

About

Cardiac Sudden Death (CSD) is an unexpected natural death, usually within the first hour of emergence of symptoms, which have no traumatic cause. The time that elapses between the emergence of symptoms and death is not homogenous and ranges from 1 to 24 hours.

Sudden death is responsible for over 3 million deaths per year worldwide (760,000 deaths per year in the USA (1) and Europe (2)). Its mortality rate is higher than that of lung cancer or AIDS.

SudD inCode® is a personalized medicine service that analyzes a patient’s genetic and clinical data.

SudD inCode® establishes the presence of mutations (new or known) associated with the development of structural and arrhythmogenic heart diseases that can induce cardiac sudden death.

The SudD inCode® service analyzes this genetic information together with the patient’s clinical data to enable healthcare professionals to:

  • Identify the causal mutation in the index case and in first-degree relatives.
  • Establish clinical diagnosis
  • Confirm clinical diagnosis
  • Provide recommendations for the optimum management of patients

Recommendations are supported by an international team of experts in cardiac sudden death that help healthcare professionals provide the best clinical and genetic assessment of patients.

The differential aspect of this service is that it analyzes together the data of 55 genes related to cardiac disease and associated with a high risk of causing sudden death.

We are constantly evolving to offer the most competitive service with an excellent quality-price ratio.





Indications

SudD inCode® is a personalized medicine service that analyzes a patient's genetic and clinical data.

SudD inCode® establishes de presence of mutations (new or known) associated with the development of structural and arrhythmogenic heart diseases that can induce cardiac sudden death.

This service is also available for the relatives of a diagnosed index case.

  • Patients who suffer unexplained syncope, idiopathic ventricular fibrillation, heart arrest and/or torsades de points induced by drugs.
  • Cases of sudden death of unknown origin or with doubtful electrocardiographic signs and suspicion of hereditary sudden death.
  • Patients with underlying arrhythmogenic heart disease:
    • Long QT Syndrome (LQTS)
    • Brugada Syndrome (BrS)
    • Short QT Syndrome (SQTS)
    • Sick sinus Syndrome (SSS)
    • Unexplained Bradycardia
    • Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT)
    • Arrhythmia during exercise
    • Progressive Conduction Defect
  • Patients with underlying structural heart disease:
    • Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)
    • Hypertrophic Cardiomiopathy (HCM)
    • Unexplained cardiac hypertrophy (UCH)
    • Dilated Cardiomiopathy (HCM)
    • Non Compaction Cardiomiopathy (adult and neonatal)
    • Restrictive Cardiomiopathy
  • Patients with other associated syndromes:
    • Marfan Syndrome (MS)
    • Fabry’s Disease (FD)
    • Thoracic aortic aneurysms and aortic dissections (TAAD)
    • Amyloidosis
    • Glycogen deposit disease (GDD)
    • Wolff-Parkinson White Syndrome




Service

The SudD inCode® service includes
SUDD-SEQ

A service based on information related to the existence of a gene or a limited group of genes associated with heart diseases.

SUDD-CLIN

Clinical assessment of genetic analysis performed in our laboratory of reference, by other clinical labs or before requesting a genetic test.

SUDD-NGS

When there are no clinical characteristics that lead to a suspicion of a specific condition, the SUDD-NGS service provides information based on a wide range of genes

  • SudD Global provides information on 55 genes associated with cardiac sudden death.
  • Arrhythmogenic SudD, provides information on 25 genes associated with channelopathies or arrhythmogenic cardiomyopathies.
  • Structural SudD provides information on 42 genes associated with structural heart disease.
  • SudD HCM provides information on 25 genes associated with hypertrophic cardiomyopathies.
  • SudD DCM provides information on 35 genes associated with dilated cardiomyopathies.

The report also states whether the findings have been confirmed by other technologies (Sanger).

Scientific Evidence

Sudden cardiac death (SCD) is one of the main causes of death in the Western World and accounts for approximately 800,000 deaths per year. Its incidence varies depending on the age range and study, but it is estimated to be around 30-200/100,000 inhabitants/year, so it is a major health problem (1).

In Spain, about 9,000 sudden cardiac death cases occur in patients from 25 to 74 years, although they are seldom diagnosed as such in the death statistics bulletin (2).

In individuals under the age of 31, the incidence of sudden cardiac death was estimated in 1.2/100,000 inhabitants in a sample in the Basque Country (3). These deaths are usually linked to doing sports, one of the highest risk factors together with a family history of SD. Sudden cardiac death is difficult to define and, therefore, it is difficult to calculate its incidence. Medical reports are often not available, autopsies are not performed or the cause of death is not specified in the death certificate (4,5).

In 80% of the cases sudden cardiac death is the consequence of coronary disease (infarction). Although in the younger population (< 40 years) the frequency of ischemic SD (atherosclerosis) is slowly increasing, most of the deaths in this population group are non-ischemic.

In this group of young individuals there are two key types of diseases associated with CSD: structural diseases (cardiomyopathies) that may be identified in the autopsy and channelopathies that have negative autopsies in which the cause of death can not be determined. The main problem in both types of diseases is that they often cause SD in seemingly healthy individuals. Unfortunately, sudden cardiac death may be the first sign of a heart disorder. 

Cardiomyopathies (hypertrophic cardiomyopathy [HCM], dilated cardiomyopathy [DCM], or arrhythmogenic right ventricular cardiomyopathy  [ARVC], among others) as well as channelopathies (Brugada syndrome [BrS], long QT syndrome [LQTS], short QT syndrome [SQTC], catecholaminergic polymorphic ventricular tachycardia [CPVT],  among others) may be hereditary and, therefore, have a genetic basis. It is worth noting that in an important percentage of sudden cardiac death cases the genetic analysis showed the presence of double or even triple mutations located in the same genes or in different genes associated with different phenotypes (6-8).


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