Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/10257
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dc.contributor.authorPowell, A Cen
dc.contributor.authorHorowitz, J Den
dc.contributor.authorKertes, P Jen
dc.contributor.authorHasin, Yen
dc.contributor.authorSyrjanen, M Len
dc.contributor.authorHenry, C Aen
dc.contributor.authorSartor, Daniela Men
dc.contributor.authorLouis, William Jen
dc.date.accessioned2015-05-15T23:38:57Z
dc.date.available2015-05-15T23:38:57Z
dc.date.issued1990-10-01en
dc.identifier.citationJournal of Cardiovascular Pharmacology; 16(4): 572-83en
dc.identifier.govdoc1706798en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/10257en
dc.description.abstractTo examine the relationship between myocardial verapamil content (MVC) and acute effects in humans, coronary sinus catheterization was used in 22 patients to determine myocardial uptake of verapamil after bolus intravenous (i.v.) verapamil (4 mg) injection. Verapamil-induced effects on hemodynamic and electrophysiologic parameters were measured simultaneously and correlated with MVC per unit baseline coronary sinus blood flow (MVC:F). Myocardial uptake of verapamil was rapid: peak MVC (1.2 +/- 0.2% of injected dose) occurred at 5.4 +/- 0.4 min; at 30 min, residual MVC was 71.1 +/- 3.4% of maximum. Peak MVC:F in individual patients was inversely related to the extent of coronary artery disease (p less than 0.005) but not to left ventricular (LV) systolic function. Verapamil produced significant (p less than 0.001) early reductions in arterial pressure and systemic vascular resistance (SVR); cardiac index (CI) increased, left ventricular (LV) positive dP/dt was unchanged. Verapamil prolonged (p less than 0.01) PR and AH intervals (maximum at 12-18 min) and atrioventricular (AV) nodal effective and functional refractory periods (ERP, FRP) (maximum at 30 min). In individual patients, the extent of changes in AH intervals (r = 0.69; p less than 0.05) and LV dP/dt (r = 0.62; p less than 0.05) correlated with peak MVC:F. We conclude that after i.v. injection, verapamil uptake by the human myocardium is rapid and more extensive in patients with minor coronary artery disease. Despite the hysteresis between MVC and drug effects, MCV is a determinant of inotropic and electrophysiologic effects of verapamil.en
dc.language.isoenen
dc.subject.otherAdulten
dc.subject.otherAgeden
dc.subject.otherAnalysis of Varianceen
dc.subject.otherCardiac Catheterizationen
dc.subject.otherClinical Trials as Topicen
dc.subject.otherCoronary Disease.physiopathologyen
dc.subject.otherDrug Evaluationen
dc.subject.otherElectrophysiologyen
dc.subject.otherFemaleen
dc.subject.otherHeart.drug effects.physiopathologyen
dc.subject.otherHemodynamics.drug effectsen
dc.subject.otherHumansen
dc.subject.otherMaleen
dc.subject.otherMiddle Ageden
dc.subject.otherMyocardium.metabolismen
dc.subject.otherVerapamil.blood.pharmacokinetics.pharmacologyen
dc.titleDeterminants of acute hemodynamic and electrophysiologic effects of verapamil in humans: role of myocardial drug uptake.en
dc.typeJournal Articleen
dc.identifier.journaltitleJournal of Cardiovascular Pharmacologyen
dc.identifier.affiliationDepartment of Cardiology, Austin Hospital, Heildelberg, Victoria, Australiaen
dc.description.pages572-83en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/1706798en
dc.type.austinJournal Articleen
local.name.researcherLouis, William J
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptClinical Pharmacology and Therapeutics-
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