It is suggested that amiodarone may also exacerbate the phenotype associated with Long QT-3 syndrome causing mutations such as ∆KPQ. This effect is due to a combination of blocking the peak sodium current, but also contributing to an increased persistent sodium current.Amiodarone chemically resembles thyroxine (thyroid hormone), and its binding to the nuclear thyroid receptor might contribute to some of its pharmacologic and toxic actions. History
The original observation that amiodarones progenitor molecule, khellin, had cardioactive properties, was made by the Russian physiologist Gleb von Anrep while working in Cairo in 1946. Khellin is obtained from a plant extract of Khella or Ammi visnaga, a common plant in north Africa. Anrep noticed that one of his technicians had been cured of anginal symptoms after taking khellin, then used for various, non-cardiac ailments. This led to efforts by European pharmaceutical industries to isolate an active compound. Amiodarone was initially developed in 1961 at the Labaz company, Belgium, by chemists Tondeur and Binon, who were working on preparations derived from khellin. It became popular in Europe as a treatment for angina pectoris.As a doctoral candidate at Oxford University, Bramah Singh determined that amiodarone and sotalol had antiarrhythmic properties and belonged to a new class of antiarrhythmic agents (what would become the class III antiarrhythmic agents). Today the mechanisms of action of amiodarone and sotalol have been investigated in more detail. Both drugs have been demonstrated to prolong the duration of the action potential, prolonging the refractory period, by interacting among other cellular function with K+ channels.
Weill–Marchesani syndrome is a rare genetic disorder characterized by short stature; an unusually short, broad head (brachycephaly) and other facial abnormalities; hand defects, including unusually short fingers (brachydactyly); and distinctive eye (ocular) abnormalities. It was named after ophthalmologists Georges Weill (1866–1952) and Oswald Marchesani (1900–1952) who first described it in 1932 and 1939, respectively. The eye manifestations typically include unusually small, round lenses of the eyes (microspherophakia), which may be prone to dislocating (ectopia lentis), as well as other ocular defects. Due to such abnormalities, affected individuals may have varying degrees of visual impairment, ranging from nearsightedness myopia to blindness. Weill–Marchesani syndrome may have autosomal recessive inheritance involving the ADAMTS10 gene,  or autosomal dominant inheritance involving the FBN1 gene. In some cases there is no association with either of these genes. Diagnosis
Diagnosis is made when several characteristic clinical signs are observed. There is no single test to confirm the presence of Weill–Marchesani syndrome. Exploring family history or examining other family members may prove helpful in confirming this diagnosis. Treatment
Eye surgery has been documented to help those with ocular diseases, such as some forms of glaucoma. Prognosis
However, long term medical management of glaucoma has not proven to be successful for patients with Weill–Marchesani syndrome. Physical therapy and orthopedic treatments are generally prescribed for problems stemming from mobility from this connective tissue disorder. However, this disorder has no cure, and generally, treatments are given to improve quality of life. See also
ADAMTS17
LTBP2

References
External links

GeneReviews/NCBI/NIH/UW entry on Weill-Marchesani Syndrome