Role of plasma concentration monitoring in the evaluation of response to antiarrhythmic drugs
Identifieur interne : 001F06 ( Istex/Corpus ); précédent : 001F05; suivant : 001F07Role of plasma concentration monitoring in the evaluation of response to antiarrhythmic drugs
Auteurs : Raymond L. WoosleySource :
- The American Journal of Cardiology [ 0002-9149 ] ; 1988.
Abstract
Plasma concentration monitoring of antiarrhythmic agents is valuable, but it is often misused or overemphasized in therapeutic decision-making. There are strict requirements for its appropriate use that are often not met—for both the newer and even the conventional antiarrhythmic drugs. For maximum value, there must be a reliable, accurate relation between the plasma drug concentration and drug action, a relation closer than that between dosage and drug action. The time of sample collection is important—most guidelines are based on “trough” plasma concentrations measured after steady-state equilibrium has been achieved. The use of an accurate, sensitive and specific assay is crucial to the value of plasma concentration monitoring guidelines. However, for agents having active metabolites, monitoring the concentration of only the parent drug can be misleading and limits (but does not necessarily eliminate) the value of plasma concentration monitoring guidelines for these agents. Plasma concentration monitoring of most antiarrhythmic agents is of value for certain specific purposes: to determine compliance to antiarrhythmic therapy, to detect and analyze possible drug interactions, to assess the benefit to risk ratio for increasing the dose of a particular antiarrhythmic agent, to maintain a stable drug effect in the presence of a patient's changing clinical condition and, to a limited extent, to assess the role of an agent in causing an adverse drug reaction. The importance of understanding the assay methods currently in use, as well as how plasma concentration monitoring of individual antiarrhythmic agents is affected by the presence of active metabolites, optical isomers differing in their activity and variations in protein binding, is essential in interpreting data obtained from plasma concentration monitoring.
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DOI: 10.1016/0002-9149(88)90335-9
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There are strict requirements for its appropriate use that are often not met—for both the newer and even the conventional antiarrhythmic drugs. For maximum value, there must be a reliable, accurate relation between the plasma drug concentration and drug action, a relation closer than that between dosage and drug action. The time of sample collection is important—most guidelines are based on “trough” plasma concentrations measured after steady-state equilibrium has been achieved. The use of an accurate, sensitive and specific assay is crucial to the value of plasma concentration monitoring guidelines. However, for agents having active metabolites, monitoring the concentration of only the parent drug can be misleading and limits (but does not necessarily eliminate) the value of plasma concentration monitoring guidelines for these agents. Plasma concentration monitoring of most antiarrhythmic agents is of value for certain specific purposes: to determine compliance to antiarrhythmic therapy, to detect and analyze possible drug interactions, to assess the benefit to risk ratio for increasing the dose of a particular antiarrhythmic agent, to maintain a stable drug effect in the presence of a patient's changing clinical condition and, to a limited extent, to assess the role of an agent in causing an adverse drug reaction. The importance of understanding the assay methods currently in use, as well as how plasma concentration monitoring of individual antiarrhythmic agents is affected by the presence of active metabolites, optical isomers differing in their activity and variations in protein binding, is essential in interpreting data obtained from plasma concentration monitoring.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Raymond L. 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The time of sample collection is important—most guidelines are based on “trough” plasma concentrations measured after steady-state equilibrium has been achieved. The use of an accurate, sensitive and specific assay is crucial to the value of plasma concentration monitoring guidelines. However, for agents having active metabolites, monitoring the concentration of only the parent drug can be misleading and limits (but does not necessarily eliminate) the value of plasma concentration monitoring guidelines for these agents. Plasma concentration monitoring of most antiarrhythmic agents is of value for certain specific purposes: to determine compliance to antiarrhythmic therapy, to detect and analyze possible drug interactions, to assess the benefit to risk ratio for increasing the dose of a particular antiarrhythmic agent, to maintain a stable drug effect in the presence of a patient's changing clinical condition and, to a limited extent, to assess the role of an agent in causing an adverse drug reaction. The importance of understanding the assay methods currently in use, as well as how plasma concentration monitoring of individual antiarrhythmic agents is affected by the presence of active metabolites, optical isomers differing in their activity and variations in protein binding, is essential in interpreting data obtained from plasma concentration monitoring.</abstract><qualityIndicators><score>8</score><pdfVersion>1.3</pdfVersion><pdfPageSize>576 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>1843</abstractCharCount><pdfWordCount>5957</pdfWordCount><pdfCharCount>41622</pdfCharCount><pdfPageCount>9</pdfPageCount><abstractWordCount>268</abstractWordCount></qualityIndicators><title>Role of plasma concentration monitoring in the evaluation of response to antiarrhythmic drugs</title><pii><json:string>0002-9149(88)90335-9</json:string></pii><genre><json:string>research-article</json:string></genre><host><volume>62</volume><pii><json:string>S0002-9149(00)X0703-5</json:string></pii><editor><json:item><name>Raymond L. 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Woosley, MD, PhD, Georgetown University School of Medicine, 3900 Reservoir Road, NW, Washington, D.C. 20007.</note><affiliation>Address for reprints: Raymond L. Woosley, MD, PhD, Georgetown University School of Medicine, 3900 Reservoir Road, NW, Washington, D.C. 20007.</affiliation><affiliation>From the Department of Pharmacology and Division of Clinical Pharmacology, Department of Medicine and Pharmacology, Georgetown University School of Medicine, Washington D.C., USA</affiliation></author></analytic><monogr><title level="j">The American Journal of Cardiology</title><title level="j" type="abbrev">AJC</title><idno type="pISSN">0002-9149</idno><idno type="PII">S0002-9149(00)X0703-5</idno><meeting><addName>A Symposium: Clinical Evaluation of Response to Antiarrhythmic Therapy, Atlanta, Georgia</addName><date>19880326</date></meeting><editor><persName>Raymond L. Woosley</persName></editor><editor><persName>MD</persName></editor><editor><persName>PhD</persName></editor><imprint><publisher>ELSEVIER</publisher><date type="published" when="1988"></date><biblScope unit="volume">62</biblScope><biblScope unit="issue">12</biblScope><biblScope unit="page" from="H9">H9</biblScope><biblScope unit="page" to="H17">H17</biblScope></imprint></monogr><idno type="istex">1C9DEE0F69494F163672796AFE9E13DC1CA2DF33</idno><idno type="DOI">10.1016/0002-9149(88)90335-9</idno><idno type="PII">0002-9149(88)90335-9</idno><idno type="ArticleID">88903359</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1988</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Plasma concentration monitoring of antiarrhythmic agents is valuable, but it is often misused or overemphasized in therapeutic decision-making. There are strict requirements for its appropriate use that are often not met—for both the newer and even the conventional antiarrhythmic drugs. For maximum value, there must be a reliable, accurate relation between the plasma drug concentration and drug action, a relation closer than that between dosage and drug action. The time of sample collection is important—most guidelines are based on “trough” plasma concentrations measured after steady-state equilibrium has been achieved. The use of an accurate, sensitive and specific assay is crucial to the value of plasma concentration monitoring guidelines. However, for agents having active metabolites, monitoring the concentration of only the parent drug can be misleading and limits (but does not necessarily eliminate) the value of plasma concentration monitoring guidelines for these agents. Plasma concentration monitoring of most antiarrhythmic agents is of value for certain specific purposes: to determine compliance to antiarrhythmic therapy, to detect and analyze possible drug interactions, to assess the benefit to risk ratio for increasing the dose of a particular antiarrhythmic agent, to maintain a stable drug effect in the presence of a patient's changing clinical condition and, to a limited extent, to assess the role of an agent in causing an adverse drug reaction. The importance of understanding the assay methods currently in use, as well as how plasma concentration monitoring of individual antiarrhythmic agents is affected by the presence of active metabolites, optical isomers differing in their activity and variations in protein binding, is essential in interpreting data obtained from plasma concentration monitoring.</p></abstract></profileDesc><revisionDesc><change when="1988">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla" xml:lang="en"><item-info><jid>AJC</jid><aid>88903359</aid><ce:pii>0002-9149(88)90335-9</ce:pii><ce:doi>10.1016/0002-9149(88)90335-9</ce:doi><ce:copyright type="unknown" year="1988"></ce:copyright></item-info><head><ce:title>Role of plasma concentration monitoring in the evaluation of response to antiarrhythmic drugs</ce:title><ce:author-group><ce:author><ce:given-name>Raymond L.</ce:given-name><ce:surname>Woosley</ce:surname><ce:degrees>MD, PhD</ce:degrees><ce:cross-ref refid="COR1"><ce:sup loc="post">∗</ce:sup></ce:cross-ref></ce:author><ce:affiliation><ce:textfn>From the Department of Pharmacology and Division of Clinical Pharmacology, Department of Medicine and Pharmacology, Georgetown University School of Medicine, Washington D.C., USA</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>∗</ce:label><ce:text>Address for reprints: Raymond L. Woosley, MD, PhD, Georgetown University School of Medicine, 3900 Reservoir Road, NW, Washington, D.C. 20007.</ce:text></ce:correspondence></ce:author-group><ce:abstract class="author"><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para view="all" id="simple-para.0010">Plasma concentration monitoring of antiarrhythmic agents is valuable, but it is often misused or overemphasized in therapeutic decision-making. There are strict requirements for its appropriate use that are often not met—for both the newer and even the conventional antiarrhythmic drugs. For maximum value, there must be a reliable, accurate relation between the plasma drug concentration and drug action, a relation closer than that between dosage and drug action. The time of sample collection is important—most guidelines are based on “trough” plasma concentrations measured after steady-state equilibrium has been achieved. The use of an accurate, sensitive and specific assay is crucial to the value of plasma concentration monitoring guidelines. However, for agents having active metabolites, monitoring the concentration of only the parent drug can be misleading and limits (but does not necessarily eliminate) the value of plasma concentration monitoring guidelines for these agents. Plasma concentration monitoring of most antiarrhythmic agents is of value for certain specific purposes: to determine compliance to antiarrhythmic therapy, to detect and analyze possible drug interactions, to assess the benefit to risk ratio for increasing the dose of a particular antiarrhythmic agent, to maintain a stable drug effect in the presence of a patient's changing clinical condition and, to a limited extent, to assess the role of an agent in causing an adverse drug reaction. The importance of understanding the assay methods currently in use, as well as how plasma concentration monitoring of individual antiarrhythmic agents is affected by the presence of active metabolites, optical isomers differing in their activity and variations in protein binding, is essential in interpreting data obtained from plasma concentration monitoring.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Role of plasma concentration monitoring in the evaluation of response to antiarrhythmic drugs</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Role of plasma concentration monitoring in the evaluation of response to antiarrhythmic drugs</title></titleInfo><name type="personal"><namePart type="given">Raymond L.</namePart><namePart type="family">Woosley</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>From the Department of Pharmacology and Division of Clinical Pharmacology, Department of Medicine and Pharmacology, Georgetown University School of Medicine, Washington D.C., USA</affiliation><description>Address for reprints: Raymond L. 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For maximum value, there must be a reliable, accurate relation between the plasma drug concentration and drug action, a relation closer than that between dosage and drug action. The time of sample collection is important—most guidelines are based on “trough” plasma concentrations measured after steady-state equilibrium has been achieved. The use of an accurate, sensitive and specific assay is crucial to the value of plasma concentration monitoring guidelines. However, for agents having active metabolites, monitoring the concentration of only the parent drug can be misleading and limits (but does not necessarily eliminate) the value of plasma concentration monitoring guidelines for these agents. Plasma concentration monitoring of most antiarrhythmic agents is of value for certain specific purposes: to determine compliance to antiarrhythmic therapy, to detect and analyze possible drug interactions, to assess the benefit to risk ratio for increasing the dose of a particular antiarrhythmic agent, to maintain a stable drug effect in the presence of a patient's changing clinical condition and, to a limited extent, to assess the role of an agent in causing an adverse drug reaction. 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Some stereoselective aspects</title><author><persName><forename type="first">French</forename><forename type="middle">J Ta</forename><surname>Gal</surname></persName></author><author><persName><forename type="middle">T</forename><surname>Zyssert</surname></persName></author><author><persName><surname>Haroldson</surname></persName></author><author><persName><surname>Pe</surname></persName></author></analytic><monogr><title level="j">Drug Metab Dispos</title><imprint><biblScope unit="volume">10</biblScope><biblScope unit="page" from="339" to="404"></biblScope><date type="published" when="1982"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">The pharmacokinetics of R-and S-tocainide in patients with acute vcntriculx arrhythmias</title><author><persName><surname>Thomson</surname></persName></author><author><persName><forename type="first">Murdoch</forename><forename type="middle">G</forename><surname>Ah</surname></persName></author><author><persName><forename type="middle">A</forename><surname>Pottage</surname></persName></author><author><persName><forename type="middle">Aw</forename><surname>Kelman</surname></persName></author><author><persName><forename type="middle">B</forename><surname>Whiting</surname></persName></author><author><persName><surname>Ws</surname></persName></author></analytic><monogr><title level="j">Br J C/in Phormacol</title><imprint><biblScope unit="volume">398621</biblScope><biblScope unit="page" from="149" to="154"></biblScope></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Quinidine therapy in hospitalized palicnts with ventricu-lar arrhythmias</title><author><persName><surname>Carliner Nh</surname></persName></author><author><persName><surname>Wg</surname></persName></author><author><persName><surname>Fisher Ml</surname></persName></author><author><persName><forename type="middle">Ma</forename><surname>Mugmon</surname></persName></author><author><persName><forename type="first">Pk</forename><surname>Vassar Dl</surname></persName></author><author><persName><surname>Plotnik</surname></persName></author><author><persName><surname>Gd</surname></persName></author></analytic><monogr><title level="j">Am Heart J</title><imprint><biblScope unit="volume">98</biblScope><biblScope unit="page" from="708" to="715"></biblScope><date type="published" when="1979"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Steady-state serum levels of quinidine and active metabolitcs in cardiac patients with varying dcgrces of renal function</title><author><persName><surname>Drnycr De</surname></persName></author><author><persName><forename type="first">Rcstivo</forename><forename type="middle">Km</forename><surname>Dt</surname></persName></author><author><persName><forename type="middle">A</forename><surname>Schwartz</surname></persName></author><author><persName><surname>Cook Ce</surname></persName></author><author><persName><surname>Mm</surname></persName></author></analytic><monogr><title level="j">Clin Phamacol Thcr</title><imprint><biblScope unit="volume">24</biblScope><biblScope unit="page" from="31" to="39"></biblScope><date type="published" when="1978"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Quinidine-rifampin inlcraction</title><author><persName><forename type="middle">Y</forename><surname>Twum-Barima</surname></persName></author><author><persName><surname>Sg</surname></persName></author></analytic><monogr><title level="j">N Eng! J :Med</title><imprint><biblScope unit="volume">304</biblScope><biblScope unit="page" from="1466" to="1469"></biblScope><date type="published" when="1981"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Con-trol of lidocaine therapy: new perspectives</title><author><persName><forename type="first">Routledge</forename><forename type="middle">Pa</forename><surname>Stargcl</surname></persName></author><author><persName><forename type="first">Ww</forename><forename type="middle">A</forename><surname>Barchowsky</surname></persName></author><author><persName><surname>Wagner Gs</surname></persName></author><author><persName><surname>Shand</surname></persName></author><author><persName><surname>Dg</surname></persName></author></analytic><monogr><title level="j">Thcr Drug Monit</title><imprint><biblScope unit="volume">4</biblScope><biblScope unit="page" from="265" to="270"></biblScope><date type="published" when="1982"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Torsades de pointes: the long-short initiating sequence and other clinical fcaturcs: observations in 32 patiems</title><author><persName><forename type="first">Kay</forename><forename type="middle">Gn</forename><surname>Plumb</surname></persName></author><author><persName><forename type="first">Vj</forename><surname>Arcinicgds Jg</surname></persName></author><author><persName><surname>Henthorn Rw</surname></persName></author><author><persName><surname>Waldo</surname></persName></author><author><persName><surname>Al</surname></persName></author></analytic><monogr><title level="j">JACC</title><imprint><biblScope unit="volume">2</biblScope><biblScope unit="page" from="806" to="817"></biblScope><date type="published" when="1983"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Ford 1. Relation of arrhythmias and electrolyte abnormalities to survival in patienls with severe chronic heart failure</title><author><persName><forename type="first">Hj</forename><surname>Dargie</surname></persName></author><author><persName><forename type="first">I</forename><surname>Cleland Jgf</surname></persName></author><author><persName><surname>Bj</surname></persName></author><author><persName><surname>Cg</surname></persName></author><author><persName><surname>East</surname></persName></author></analytic><monogr><title level="j">Circulation</title><imprint><biblScope unit="page" from="75" to="98"></biblScope><date type="published" when="1987"></date></imprint></monogr></biblStruct><biblStruct><monogr><title level="m" type="main">Incidence and clinical features of the quinidine-associated long QT syndrome: implications for patient cart. ,4m Heart J 1986</title><author><persName><forename type="first">Rodcn</forename><forename type="middle">Dm</forename><surname>Woosley Rl</surname></persName></author><author><persName><surname>Primm</surname></persName></author><imprint><biblScope unit="page" from="1088" to="1093"></biblScope></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Anti-arrhythmic prophylaxis with procainamide in acute myocardial infarction</title><author><persName><surname>Koch</surname></persName></author><author><persName><forename type="middle">J</forename><surname>Wescr</surname></persName></author><author><persName><surname>Klein</surname></persName></author><author><persName><surname>Sw</surname></persName></author><author><persName><forename type="first">.</forename><forename type="middle">L</forename><surname>Foe-Canto</surname></persName></author><author><persName><forename type="middle">Ja</forename><surname>Kastor</surname></persName></author><author><persName><surname>Desanctis</surname></persName></author></analytic><monogr><title level="j">N Engl J Med</title><imprint><biblScope unit="volume">28</biblScope><biblScope unit="page" from="1253" to="1260"></biblScope><date type="published" when="1969"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Prccainamide dosage schedules, plasma concentra-tions, and clinical effects</title><author><persName><forename type="first">J</forename><surname>Koch-Wescr</surname></persName></author><author><persName><surname>Klein</surname></persName></author><author><persName><surname>Sw</surname></persName></author></analytic><monogr><title level="j">JAMA</title><imprint><biblScope unit="volume">235</biblScope><biblScope unit="page" from="1454" to="1460"></biblScope><date type="published" when="1973"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Quantitative and qualitative binding characteristics of disopyramidc in serum from patients with decreased renal and hcpatic function</title><author><persName><forename type="first">Le</forename><surname>Pedersen</surname></persName></author><author><persName><forename type="first">Na</forename><forename type="middle">I</forename><surname>Bonde</surname></persName></author><author><persName><forename type="middle">Nv</forename><surname>Backer</surname></persName></author><author><persName><forename type="first">J-Es</forename><surname>Hansen</surname></persName></author><author><persName><surname>Kampmann</surname></persName></author><author><persName><surname>Jp</surname></persName></author></analytic><monogr><title level="j">Br J Clin Pharmacol</title><imprint><biblScope unit="volume">23</biblScope><biblScope unit="page" from="43" to="46"></biblScope><date type="published" when="1987"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Congestive heart failure caused by oral disopyramide</title><author><persName><surname>Podrid Pj</surname></persName></author><author><persName><forename type="middle">A</forename><surname>Schoenberger</surname></persName></author><author><persName><surname>Low</surname></persName></author></analytic><monogr><title level="j">N Engl J Med</title><imprint><biblScope unit="volume">302</biblScope><biblScope unit="page" from="614" to="617"></biblScope><date type="published" when="1980"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Serum tocainide cnantiomer concentrations in human subjects</title><author><persName><forename type="middle">J</forename><surname>Sedman Aj</surname></persName></author><author><persName><forename type="middle">W</forename><surname>Mastropaolo</surname></persName></author><author><persName><forename type="middle">P</forename><surname>Johnson</surname></persName></author><author><persName><forename type="first">Jd</forename><surname>Maloney</surname></persName></author><author><persName><surname>Moyer</surname></persName></author></analytic><monogr><title level="j">Br J Clin Phar-nmol</title><imprint><biblScope unit="volume">17</biblScope><biblScope unit="page" from="113" to="1"></biblScope><date type="published" when="1984"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Plasma lidocdine levels in patients treated with potential inducers of microsomal enzymes</title><author><persName><forename type="middle">J</forename><surname>Heinoncn</surname></persName></author><author><persName><forename type="middle">S</forename><surname>Takki</surname></persName></author><author><persName><surname>Jarho</surname></persName></author></analytic><monogr><title level="j">Acta Anaesthesiol Stand</title><imprint><biblScope unit="volume">14</biblScope><biblScope unit="page" from="89" to="95"></biblScope><date type="published" when="1970"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Lidocaine pharmacokinctics in advanced heart failure, liver disease and renal failure in humans</title><author><persName><surname>Thomson Pd</surname></persName></author><author><persName><forename type="first">Richardson</forename><forename type="middle">Kl Ja</forename><surname>Mclmon</surname></persName></author><author><persName><forename type="first">K</forename><surname>Cohn</surname></persName></author><author><persName><forename type="middle">W</forename><surname>Stcinbrunn</surname></persName></author><author><persName><forename type="middle">R</forename><surname>Cudihee</surname></persName></author><author><persName><surname>Rowland</surname></persName></author></analytic><monogr><title level="j">Ann Intern Med</title><imprint><biblScope unit="volume">97378</biblScope><biblScope unit="page" from="499" to="508"></biblScope></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Multiple bolus technique. for lidocaine administration in acute ischemic heart disease. II. Treatment of refractory ventricular arrhythmias and the pharmacokinetic significance of severe left ventricular failure</title><author><persName><surname>Wyman Mg</surname></persName></author><author><persName><surname>Slaughter Rl</surname></persName></author><author><persName><forename type="middle">Da</forename><surname>Farolino</surname></persName></author><author><persName><forename type="middle">S</forename><surname>Gore</surname></persName></author><author><persName><surname>Cannom Ds</surname></persName></author><author><persName><forename type="first">Bn</forename><surname>Goldreyer</surname></persName></author><author><persName><surname>Lalka</surname></persName></author></analytic><monogr><title level="j">JACC</title><imprint><biblScope unit="volume">2</biblScope><biblScope unit="page" from="764" to="769"></biblScope><date type="published" when="1983"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Kinelics of antifibrillatory effects of bretylium: correlation with myxardial drug concen-trations</title><author><persName><forename type="first">Anderson</forename><forename type="middle">Jl E</forename><surname>Patterson</surname></persName></author><author><persName><forename type="middle">M</forename><surname>Cordon</surname></persName></author><author><persName><forename type="middle">S</forename><surname>Pasyk</surname></persName></author><author><persName><forename type="middle">B</forename><surname>Pitt</surname></persName></author><author><persName><surname>Lucchesi</surname></persName></author><author><persName><surname>Br</surname></persName></author></analytic><monogr><title level="j">Am J Cardiol</title><imprint><biblScope unit="volume">46</biblScope><biblScope unit="page" from="83" to="592"></biblScope><date type="published" when="1980"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Luc-cheri BR. Serial electrophysiologic effects of brctylium in man and their correla-tion with plasma concentrations</title><author><persName><forename type="first">Anderson</forename><forename type="middle">Jl</forename><surname>Brodine</surname></persName></author><author><persName><forename type="first">Wn</forename><forename type="middle">E</forename><surname>Patterson</surname></persName></author><author><persName><surname>Marshall</surname></persName></author><author><persName><surname>Hw</surname></persName></author><author><persName><surname>Allison</surname></persName></author><author><persName><surname>Sd</surname></persName></author></analytic><monogr><title level="j">J Cardiocosc Pharmacol</title><imprint><biblScope unit="volume">4</biblScope><biblScope unit="page" from="873" to="882"></biblScope><date type="published" when="1982"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Stereoselective analysis of the enan-tiomers of mexiletine by high-performance liquid chromatography using fluores-cence detection and study of their stereosclcctive disposition in man</title><author><persName><forename type="first">L</forename><surname>Mcerhme Km</surname></persName></author><author><persName><surname>Kerr</surname></persName></author></analytic><monogr><title level="j">J Chroma-togr</title><imprint><biblScope unit="volume">19415</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="335" to="346"></biblScope></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Stcreoselective disposition of mexiletinc in man</title><author><persName><forename type="first">Grech</forename><surname>Bclanger</surname></persName></author><author><persName><forename type="middle">J</forename><surname>Turgcon</surname></persName></author><author><persName><surname>Gilbert</surname></persName></author></analytic><monogr><title level="j">Br J Clin Pharmacol</title><imprint><biblScope unit="volume">9821</biblScope><biblScope unit="page" from="481" to="487"></biblScope></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">The clinical pharmacol-ogy of mcxilctine</title><author><persName><forename type="first">Nps</forename><surname>Campbell</surname></persName></author><author><persName><forename type="first">Jg</forename><surname>Kbllcy</surname></persName></author><author><persName><surname>Adgey</surname></persName></author><author><persName><surname>4aj</surname></persName></author><author><persName><surname>Shanks</surname></persName></author></analytic><monogr><title level="j">Br J Clin Pharmacol</title><imprint><biblScope unit="volume">6</biblScope><biblScope unit="page" from="103" to="108"></biblScope><date type="published" when="1978"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">The development and testing of intravenous dosing regimens: application to flecainidc for the suppression of ventricular arrhyrhmias</title><author><persName><forename type="first">Wang</forename><forename type="middle">T La</forename><surname>Siddoway</surname></persName></author><author><persName><forename type="first">Ka</forename><surname>Thompson</surname></persName></author><author><persName><forename type="middle">Gj</forename><surname>Conrad</surname></persName></author><author><persName><forename type="first">Ra</forename><surname>Bcrgstrand</surname></persName></author><author><persName><forename type="first">D</forename><surname>Kvam</surname></persName></author><author><persName><forename type="first">Dm</forename><surname>Roden</surname></persName></author><author><persName><surname>Wooslcy</surname></persName></author></analytic><monogr><title level="j">Clin Pharmocol Ther</title><imprint><biblScope unit="volume">43</biblScope><biblScope unit="page" from="499" to="50"></biblScope><date type="published" when="1988"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Lift-thrcxcaiog flccainide toxicity. A phar-mncodynamic approach</title><author><persName><surname>Winkelman Br</surname></persName></author><author><persName><surname>Leinberger</surname></persName></author></analytic><monogr><title level="j">Ann Intern Med</title><imprint><biblScope unit="volume">106</biblScope><biblScope unit="page" from="807" to="814"></biblScope><date type="published" when="1987"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Pharmacodynamics and side cffccts of flccainidc acclatc</title><author><persName><surname>Salerno Dm</surname></persName></author><author><persName><forename type="middle">G</forename><surname>Granrud</surname></persName></author><author><persName><forename type="first">I</forename><surname>Sharkey</surname></persName></author><author><persName><forename type="middle">J</forename><surname>Krcjci</surname></persName></author><author><persName><forename type="middle">T</forename><surname>Larson</surname></persName></author><author><persName><forename type="middle">D</forename><surname>Erlicn</surname></persName></author><author><persName><forename type="first">D</forename><surname>Berry</surname></persName></author><author><persName><surname>Hodges</surname></persName></author></analytic><monogr><title level="j">Clint Phar-mocol Ther</title><imprint><biblScope unit="volume">40</biblScope><biblScope unit="page" from="101" to="107"></biblScope><date type="published" when="1986"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Influence of genetic polymorphism on the mctabolitcs and disposition of cncainide in man</title><author><persName><forename type="first">Wang</forename><forename type="middle">T</forename><surname>Roden Dm</surname></persName></author><author><persName><forename type="first">Ht</forename><surname>Wolfenden</surname></persName></author><author><persName><forename type="middle">Rl</forename><surname>Wooslcy</surname></persName></author><author><persName><forename type="middle">Ajj</forename><surname>Wood</surname></persName></author><author><persName><surname>Wilkinson</surname></persName></author></analytic><monogr><title level="j">J Pharmacol Exp Ther</title><imprint><biblScope unit="volume">228</biblScope><biblScope unit="page" from="605" to="611"></biblScope><date type="published" when="1984"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Wilkin-son CR. Co-inheritance of the polymorphic metabolism ofcncainide and debriso-quin</title><author><persName><surname>Wooslcy Rl</surname></persName></author><author><persName><forename type="first">Dm</forename><surname>Roden</surname></persName></author><author><persName><surname>Dai</surname></persName></author><author><persName><forename type="first">Wang</forename><forename type="middle">T</forename><surname>Gh</surname></persName></author><author><persName><forename type="middle">D</forename><surname>Altcnbcm</surname></persName></author><author><persName><forename type="middle">J</forename><surname>Oates</surname></persName></author></analytic><monogr><title level="j">Clin Pharmncol Ther</title><imprint><biblScope unit="volume">39</biblScope><biblScope unit="page" from="2" to="2"></biblScope><date type="published" when="1986"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Stereoselective disposition of propafcnonc during chronic oral therapy in man (abstr) Polymorphism ofprupafenone metabolism and disposi-tion in man: clinical and pharmacokinetic consequcnccs</title><author><persName><forename type="first">Roden</forename><forename type="middle">H C Dm</forename><surname>Kroemer</surname></persName></author><author><persName><forename type="first">Wright</forename><forename type="middle">Gili</forename><surname>Wilkinson</surname></persName></author><author><persName><forename type="first">Gr</forename><forename type="middle">M</forename><surname>Eichclbaum</surname></persName></author><author><persName><forename type="first">Rla608</forename><surname>Woosley</surname></persName></author><author><persName><surname>So</surname></persName></author><author><persName><forename type="middle">La</forename><surname>Siddoway</surname></persName></author><author><persName><forename type="first">Ka</forename><surname>Thompson</surname></persName></author><author><persName><surname>Mcallirtcr</surname></persName></author><author><persName><forename type="first">Wang</forename><forename type="middle">T</forename><surname>Cb</surname></persName></author><author><persName><forename type="first">Gr</forename><surname>Wilkinson</surname></persName></author><author><persName><surname>Rodcn Dm</surname></persName></author><author><persName><surname>Woosley</surname></persName></author></analytic><monogr><title level="j">E4SEB .I Circulation</title><imprint><biblScope unit="volume">275</biblScope><biblScope unit="page" from="85" to="791"></biblScope><date type="published" when="1987"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Woos-Icy RL. Beta receplor anldgonism by propafenone in mao: influence of polymor-phic metabolism (abstr</title><author><persName><forename type="first">Lee</forename><forename type="middle">Jt</forename></persName></author><author><persName><forename type="first">C</forename><forename type="middle">Md</forename><surname>Lineberry</surname></persName></author><author><persName><forename type="first">Pi</forename><surname>Chaffin</surname></persName></author></analytic><monogr><title level="j">Hrs</title><imprint><biblScope unit="volume">36</biblScope><biblScope unit="page">294</biblScope><date type="published" when="1988"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Clinical pharmacology of propafc-none: pharmacokinetics. metabolism and concentration-response rclalions</title><author><persName><forename type="first">La</forename><surname>Siddoway</surname></persName></author><author><persName><surname>Roden Dm</surname></persName></author><author><persName><surname>Wooslcy</surname></persName></author></analytic><monogr><title level="j">Ant J Cardiol I</title><imprint><biblScope unit="volume">98454</biblScope><biblScope unit="page">12</biblScope></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Inhibition of propafenonc metabolism by low doses of quinidinc in man (abstr)</title><author><persName><surname>Funck-Brentanoc</surname></persName></author><author><persName><forename type="first">H</forename><surname>Krocmcr</surname></persName></author><author><persName><surname>Pavlou</surname></persName></author><author><persName><forename type="first">Wright</forename><forename type="middle">Gm</forename><surname>Ii</surname></persName></author><author><persName><surname>Wooslcy Rl</surname></persName></author><author><persName><surname>Dm</surname></persName></author></analytic><monogr><title level="j">Clin Res</title><imprint><biblScope unit="volume">36</biblScope><biblScope unit="page">363</biblScope><date type="published" when="1988"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Amiodaronc and its desethyl metabolitc: tissue distribution and morphologic changes during long-term therapy</title><author><persName><forename type="first">Adams</forename><forename type="middle">Pc</forename><surname>Holt</surname></persName></author><author><persName><forename type="first">Dw</forename><surname>Storey</surname></persName></author><author><persName><surname>Cc</surname></persName></author><author><persName><forename type="middle">4r</forename><surname>Morley</surname></persName></author><author><persName><forename type="middle">J</forename><surname>Callaghan</surname></persName></author><author><persName><forename type="middle">Mrc</forename><surname>Path</surname></persName></author><author><persName><surname>Campbell</surname></persName></author></analytic><monogr><title level="j">Circulation</title><imprint><biblScope unit="volume">72</biblScope><biblScope unit="page" from="1064" to="1075"></biblScope><date type="published" when="1985"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Amiodaronc phdrmacoki-netics</title><author><persName><surname>Holt</surname></persName></author><author><persName><surname>Dw</surname></persName></author><author><persName><forename type="middle">Gt</forename><surname>Tucker</surname></persName></author><author><persName><forename type="middle">Pr</forename><surname>Jackson</surname></persName></author><author><persName><surname>Mckenna</surname></persName></author></analytic><monogr><title level="j">Br J Clin Pratt</title><imprint><biblScope unit="volume">44</biblScope><biblScope unit="page" from="109" to="14"></biblScope><date type="published" when="1986"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Pharmacokinct-its of amiodarone in rats</title><author><persName><forename type="first">Riva</forename><forename type="middle">E M</forename><surname>Gerna</surname></persName></author><author><persName><forename type="middle">P</forename><surname>Neyroz</surname></persName></author><author><persName><forename type="first">R</forename><surname>Ur~o</surname></persName></author><author><persName><forename type="middle">I</forename><surname>Bartosck</surname></persName></author><author><persName><surname>Guaitani</surname></persName></author></analytic><monogr><title level="j">I Cardiocosc Pharmacol</title><imprint><biblScope unit="volume">4</biblScope><biblScope unit="page" from="270" to="27"></biblScope><date type="published" when="1982"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">In vitro metabolism of amiodaronc bq' rabbit and rat liver and small intestine</title><author><persName><forename type="first">Young</forename><forename type="middle">Ra</forename><surname>Mchcndale</surname></persName></author><author><persName><surname>Hm</surname></persName></author></analytic><monogr><title level="j">Drug Metab Dispos</title><imprint><biblScope unit="volume">4</biblScope><biblScope unit="page" from="423" to="429"></biblScope><date type="published" when="1986"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Pharmacodynamic studies of amiodaronc and its active N-desethyl mctabolite</title><author><persName><forename type="first">S</forename><surname>Nattel</surname></persName></author></analytic><monogr><title level="j">J Cardior;asc Pharmacol</title><imprint><biblScope unit="volume">8</biblScope><biblScope unit="page" from="771" to="777"></biblScope><date type="published" when="1986"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Electro-physiologic effects of desethylammdarone, an active mctnbolitc of amiodxone: comparison with amiodaronc during chronic administration in rabbi&. An?</title><author><persName><forename type="middle">R</forename><surname>Kato</surname></persName></author><author><persName><forename type="middle">N</forename><surname>Venkatcsh</surname></persName></author><author><persName><forename type="middle">K</forename><surname>Kamiya</surname></persName></author><author><persName><forename type="middle">S</forename><surname>Yabek</surname></persName></author><author><persName><forename type="middle">R</forename><surname>Kannan</surname></persName></author><author><persName><surname>Singh</surname></persName></author></analytic><monogr><title level="j">Heart J</title><imprint><biblScope unit="volume">115</biblScope><biblScope unit="page" from="321" to="359"></biblScope><date type="published" when="1988"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Comparative electrophysiologic cffccls of intravenous amiodarone and desethylamiodarone in dogs: Evidence for clinically relevant activity of the metabolilc</title><author><persName><forename type="middle">M</forename><surname>Talajic</surname></persName></author><author><persName><forename type="first">Mr</forename><surname>Deroodc</surname></persName></author><author><persName><surname>Nattel</surname></persName></author></analytic><monogr><title level="j">Circulation</title><imprint><biblScope unit="volume">987</biblScope><biblScope unit="page" from="75" to="265"></biblScope></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Interaction of amiodaronc and dcsclhyldmiodarone with solubilized nuclear thyroid hormone receptors</title><author><persName><surname>Latham Kr</surname></persName></author><author><persName><forename type="middle">Df</forename><surname>Sellitti</surname></persName></author><author><persName><surname>Goldstein</surname></persName></author></analytic><monogr><title level="j">JACC</title><imprint><biblScope unit="volume">19879</biblScope><biblScope unit="page" from="872" to="876"></biblScope></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Comparison of the cytotoxicity ofamicdarone and dcscthyl amiodarone to human lymphwytes in vitro (abslr)</title><author><persName><forename type="first">Wright</forename><forename type="middle">G</forename><surname>Wooslcy Rl</surname></persName></author><author><persName><forename type="first">J</forename><forename type="middle">J</forename><surname>Wooslcy</surname></persName></author><author><persName><surname>Kennedy</surname></persName></author></analytic><monogr><title level="j">FASEB J</title><imprint><biblScope unit="volume">988</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page">1557</biblScope></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Amiodarone dosing: a proposal based on its pharmacokinetics</title><author><persName><forename type="middle">La</forename><surname>Siddoway</surname></persName></author><author><persName><forename type="middle">Cr</forename><surname>Mchllister</surname></persName></author><author><persName><forename type="first">Roden</forename><forename type="middle">Gr Dm</forename><surname>Wilkinson</surname></persName></author><author><persName><surname>Wooslcq</surname></persName></author></analytic><monogr><title level="j">Am Heart J</title><imprint><biblScope unit="volume">106</biblScope><biblScope unit="page" from="95" to="956"></biblScope><date type="published" when="1983"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Pharmacokinctic approach to amiodaronc dosage selection</title><author><persName><forename type="first">Barbey</forename><forename type="middle">Jt</forename><surname>Woosley</surname></persName></author></analytic><monogr><title level="j">Clin Prog Electrophy.riol Pacing</title><imprint><biblScope unit="volume">4</biblScope><biblScope unit="page" from="0" to="317"></biblScope><date type="published" when="1986"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Absolulc bio-availability ofamiodaronc in normal subjects</title><author><persName><forename type="middle">S</forename><surname>Pourbaix</surname></persName></author><author><persName><forename type="first">Y</forename><surname>Bergcr</surname></persName></author><author><persName><forename type="first">J-P</forename><surname>Desager</surname></persName></author><author><persName><forename type="first">M</forename><surname>Pacco</surname></persName></author><author><persName><surname>Harvcngt</surname></persName></author></analytic><monogr><title level="j">Clin Pharmacol Ther</title><imprint><biblScope unit="volume">98537118</biblScope><biblScope unit="page">133</biblScope></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">The possible effect of long-term high plasma Icvels of phenytoin on mortality after acute myocardial infarc-tion</title><author><persName><forename type="first">Prineas</forename><forename type="middle">Rj</forename><surname>Vajda Fje</surname></persName></author><author><persName><surname>Lovcll</surname></persName></author><author><persName><surname>Sloman</surname></persName></author></analytic><monogr><title level="j">Eur J Clin Pharmacol</title><imprint><biblScope unit="volume">5</biblScope><biblScope unit="page" from="138" to="144"></biblScope><date type="published" when="1973"></date></imprint></monogr></biblStruct><biblStruct><monogr><author><persName><surname>Woosley Rl</surname></persName></author><author><persName><forename type="first">Fogoros</forename><forename type="middle">J Rn</forename><surname>Morganroth</surname></persName></author><author><persName><forename type="middle">Fg</forename><surname>Mcmahon</surname></persName></author><author><persName><surname>Humphries</surname></persName></author><author><persName><surname>Jo</surname></persName></author></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Pharmacokinetics of moricizine HCI</title><author><persName><surname>Mason</surname></persName></author><author><persName><surname>Dt</surname></persName></author><author><persName><surname>Williams</surname></persName></author></analytic><monogr><title level="j">Am J Cardiol I987</title><imprint><biblScope unit="page" from="35" to="39"></biblScope></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Eflicdcy. safety, hcmodynamic effects. and pharmacokinctics of high-dose moricizinc during short-and long-lerm therapy</title><author><persName><surname>Salerno Dm</surname></persName></author><author><persName><forename type="first">Pj</forename><surname>Sharkey</surname></persName></author><author><persName><forename type="middle">Ga</forename><surname>Granrud</surname></persName></author><author><persName><surname>Asinger</surname></persName></author></analytic><monogr><title level="j">Clin Pharmacol l'her</title><imprint><biblScope unit="volume">42</biblScope><biblScope unit="page" from="201" to="209"></biblScope><date type="published" when="1987"></date></imprint></monogr></biblStruct><biblStruct><analytic></analytic><monogr><title level="j">THE AMERICAN JOURNAL OF CARDIOLOGY OCTOBER</title><imprint><biblScope unit="volume">19</biblScope><date type="published" when="1988"></date></imprint></monogr></biblStruct></listBibl></back></text></istex:refBibTEI></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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