@Article{RSM:Wit2000,
  author =       "H.J. Witchel and J.C. Hancox",
  title =        "Familial and acquired long {QT} syndrome and the cardiac
                 rapid delayed rectifier potassium current.",
  journal =      "Clin Exp Pharmacol Physiol",
  year =         "2000",
  month =        oct,
  volume =       "27",
  number =       "10",
  pages =        "753--766",
  robnote =      "Acquired LQTS has many similar clinical features to
                 congenital LQTS, but typically affects older
                 individuals and is often associated with specific
                 pharmacological agents. 3. A growing number of drugs
                 associated with QT prolongation and its concomitant
                 risks of arrhythmia and sudden death have been shown to
                 block the 'rapid' cardiac delayed rectifier potassium
                 current (IKr) or cloned channels encoded by the human
                 ether-a-go-go-related gene (HERG; the gene believed to
                 encode native IKr). The drugs that produce acquired
                 LQTS are structurally heterogeneous, including
                 anti-arrhythmics, such as quinidine, non-sedating
                 antihistamines, such as terfenadine, and psychiatric
                 drugs, such as haloperidol. Here, clinical observations
                 are associated with cellular data to correlate acquired
                 LQTS with the IKr/HERG potassium (K+) channel. One
                 strategy for developing improved compounds in those
                 drug classes that are currently associated with LQTS
                 could be to design drug structures that preserve
                 clinical efficacy but are modified to avoid
                 pharmacological interactions with IKr.",
  bibdate =      "Tue Oct 30 15:16:38 2001",
}

{"_id":"E2y5PprY5nDYtptFH","bibbaseid":"witchel-hancox-familialandacquiredlongqtsyndromeandthecardiacrapiddelayedrectifierpotassiumcurrent-2000","downloads":0,"creationDate":"2016-07-01T21:38:43.037Z","title":"Familial and acquired long QT syndrome and the cardiac rapid delayed rectifier potassium current.","author_short":["Witchel, H.","Hancox, J."],"year":2000,"bibtype":"article","biburl":"http://www.sci.utah.edu/~macleod/Bibtex/biglit.bib","bibdata":{"bibtype":"article","type":"article","author":[{"firstnames":["H.J."],"propositions":[],"lastnames":["Witchel"],"suffixes":[]},{"firstnames":["J.C."],"propositions":[],"lastnames":["Hancox"],"suffixes":[]}],"title":"Familial and acquired long QT syndrome and the cardiac rapid delayed rectifier potassium current.","journal":"Clin Exp Pharmacol Physiol","year":"2000","month":"October","volume":"27","number":"10","pages":"753–766","robnote":"Acquired LQTS has many similar clinical features to congenital LQTS, but typically affects older individuals and is often associated with specific pharmacological agents. 3. A growing number of drugs associated with QT prolongation and its concomitant risks of arrhythmia and sudden death have been shown to block the 'rapid' cardiac delayed rectifier potassium current (IKr) or cloned channels encoded by the human ether-a-go-go-related gene (HERG; the gene believed to encode native IKr). The drugs that produce acquired LQTS are structurally heterogeneous, including anti-arrhythmics, such as quinidine, non-sedating antihistamines, such as terfenadine, and psychiatric drugs, such as haloperidol. Here, clinical observations are associated with cellular data to correlate acquired LQTS with the IKr/HERG potassium (K+) channel. One strategy for developing improved compounds in those drug classes that are currently associated with LQTS could be to design drug structures that preserve clinical efficacy but are modified to avoid pharmacological interactions with IKr.","bibdate":"Tue Oct 30 15:16:38 2001","bibtex":"@Article{RSM:Wit2000,\n author = \"H.J. Witchel and J.C. Hancox\",\n title = \"Familial and acquired long {QT} syndrome and the cardiac\n rapid delayed rectifier potassium current.\",\n journal = \"Clin Exp Pharmacol Physiol\",\n year = \"2000\",\n month = oct,\n volume = \"27\",\n number = \"10\",\n pages = \"753--766\",\n robnote = \"Acquired LQTS has many similar clinical features to\n congenital LQTS, but typically affects older\n individuals and is often associated with specific\n pharmacological agents. 3. A growing number of drugs\n associated with QT prolongation and its concomitant\n risks of arrhythmia and sudden death have been shown to\n block the 'rapid' cardiac delayed rectifier potassium\n current (IKr) or cloned channels encoded by the human\n ether-a-go-go-related gene (HERG; the gene believed to\n encode native IKr). The drugs that produce acquired\n LQTS are structurally heterogeneous, including\n anti-arrhythmics, such as quinidine, non-sedating\n antihistamines, such as terfenadine, and psychiatric\n drugs, such as haloperidol. Here, clinical observations\n are associated with cellular data to correlate acquired\n LQTS with the IKr/HERG potassium (K+) channel. One\n strategy for developing improved compounds in those\n drug classes that are currently associated with LQTS\n could be to design drug structures that preserve\n clinical efficacy but are modified to avoid\n pharmacological interactions with IKr.\",\n bibdate = \"Tue Oct 30 15:16:38 2001\",\n}\n\n","author_short":["Witchel, H.","Hancox, J."],"key":"RSM:Wit2000","id":"RSM:Wit2000","bibbaseid":"witchel-hancox-familialandacquiredlongqtsyndromeandthecardiacrapiddelayedrectifierpotassiumcurrent-2000","role":"author","urls":{},"metadata":{"authorlinks":{}},"downloads":0,"html":""},"search_terms":["familial","acquired","long","syndrome","cardiac","rapid","delayed","rectifier","potassium","current","witchel","hancox"],"keywords":[],"authorIDs":[],"dataSources":["5HG3Kp8zRwDd7FotB"]}