Thus SVT is called supraventricular tachycardia more than twice as often as it is called supraventricular tachyarrhythmia; moreover, those two terms are always completely synonymous—in natural language there is no such term as "healthy/physiologic supraventricular tachycardia". The same themes are also true of AVRT and AVNRT. Thus this pair is an example of when a particular prescription (which may have been tenable 50 or 100 years earlier) can no longer be invariably enforced without violating idiom. But the power to differentiate in an idiomatic way is not lost, regardless, because when the specification of physiologic tachycardia is needed, that phrase aptly conveys it. See also
Postural orthostatic tachycardia syndrome

References


== External links ==
Causes
The vast majority of cases are thought to be due to spontaneous genetic mutations. It can be associated with mutations affecting the cohesin complex.As of 2018, it was confirmed that 500 genetic mutations have been associated with the condition; occurring on 7 different genes. In around 30% of cases of CdLS the genetic cause remains undiscovered. The wide variation in phenotype is attributed to a high degree of somatic mosaicism in CdLS as well as the different genes and type of mutations. For this reason people with CdLS can have very different appearance,  abilities,  and associated health issues. The latter two genes seem to correlate with a milder form of the syndrome.In 2004, researchers at the Childrens Hospital of Philadelphia (United States) and the University of Newcastle upon Tyne (England) identified a gene (NIPBL) on chromosome 5 that causes CdLS when it is mutated. Since then, additional genes have been found (SMC1A, SMC3 and HDAC8, RAD21) that cause CdLS when changed. In July 2012, the fourth "CdLS gene"—HDAC8—was announced. HDAC8 is an X-linked gene, meaning it is located on the X chromosome. Individuals with CdLS who have the gene change in HDAC8 make up just a small portion of all people with CdLS. Evidence of a linkage at chromosome 3q26.3 is mixed.Genetic alterations associated with CdLS have been identified in genes NIPBL, SMC1A and SMC3 as well as the more recently identified genes RAD21 and HDAC8. All of these genetic alterations occurring in CdLS patients affect proteins that function in the cohesin pathway.