Nctid:
NCT00001628
Payload:
{"FullStudy"=>{"Rank"=>472866, "Study"=>{"DerivedSection"=>{"MiscInfoModule"=>{"VersionHolder"=>"November 27, 2023"}, "ConditionBrowseModule"=>{"ConditionMeshList"=>{"ConditionMesh"=>[{"ConditionMeshId"=>"D000006333", "ConditionMeshTerm"=>"Heart Failure"}, {"ConditionMeshId"=>"D000009203", "ConditionMeshTerm"=>"Myocardial Infarction"}, {"ConditionMeshId"=>"D000050197", "ConditionMeshTerm"=>"Atherosclerosis"}, {"ConditionMeshId"=>"D000007238", "ConditionMeshTerm"=>"Infarction"}]}, "ConditionAncestorList"=>{"ConditionAncestor"=>[{"ConditionAncestorId"=>"D000014652", "ConditionAncestorTerm"=>"Vascular Diseases"}, {"ConditionAncestorId"=>"D000002318", "ConditionAncestorTerm"=>"Cardiovascular Diseases"}, {"ConditionAncestorId"=>"D000006331", "ConditionAncestorTerm"=>"Heart Diseases"}, {"ConditionAncestorId"=>"D000007511", "ConditionAncestorTerm"=>"Ischemia"}, {"ConditionAncestorId"=>"D000010335", "ConditionAncestorTerm"=>"Pathologic Processes"}, {"ConditionAncestorId"=>"D000009336", "ConditionAncestorTerm"=>"Necrosis"}, {"ConditionAncestorId"=>"D000017202", "ConditionAncestorTerm"=>"Myocardial Ischemia"}, {"ConditionAncestorId"=>"D000001161", "ConditionAncestorTerm"=>"Arteriosclerosis"}, {"ConditionAncestorId"=>"D000001157", "ConditionAncestorTerm"=>"Arterial Occlusive Diseases"}]}, "ConditionBrowseLeafList"=>{"ConditionBrowseLeaf"=>[{"ConditionBrowseLeafId"=>"M9111", "ConditionBrowseLeafName"=>"Heart Failure", "ConditionBrowseLeafAsFound"=>"Heart Failure, Congestive", "ConditionBrowseLeafRelevance"=>"high"}, {"ConditionBrowseLeafId"=>"M9714", "ConditionBrowseLeafName"=>"Hypertension", "ConditionBrowseLeafRelevance"=>"low"}, {"ConditionBrowseLeafId"=>"M11845", "ConditionBrowseLeafName"=>"Myocardial Infarction", "ConditionBrowseLeafAsFound"=>"Myocardial Infarction", "ConditionBrowseLeafRelevance"=>"high"}, {"ConditionBrowseLeafId"=>"M9972", "ConditionBrowseLeafName"=>"Infarction", "ConditionBrowseLeafAsFound"=>"Infarction", "ConditionBrowseLeafRelevance"=>"high"}, {"ConditionBrowseLeafId"=>"M25878", "ConditionBrowseLeafName"=>"Atherosclerosis", "ConditionBrowseLeafAsFound"=>"Atherosclerosis", "ConditionBrowseLeafRelevance"=>"high"}, {"ConditionBrowseLeafId"=>"M17090", "ConditionBrowseLeafName"=>"Vascular Diseases", "ConditionBrowseLeafRelevance"=>"low"}, {"ConditionBrowseLeafId"=>"M9109", "ConditionBrowseLeafName"=>"Heart Diseases", "ConditionBrowseLeafRelevance"=>"low"}, {"ConditionBrowseLeafId"=>"M10233", "ConditionBrowseLeafName"=>"Ischemia", "ConditionBrowseLeafRelevance"=>"low"}, {"ConditionBrowseLeafId"=>"M11974", "ConditionBrowseLeafName"=>"Necrosis", "ConditionBrowseLeafRelevance"=>"low"}, {"ConditionBrowseLeafId"=>"M19196", "ConditionBrowseLeafName"=>"Myocardial Ischemia", "ConditionBrowseLeafRelevance"=>"low"}, {"ConditionBrowseLeafId"=>"M6236", "ConditionBrowseLeafName"=>"Coronary Artery Disease", "ConditionBrowseLeafRelevance"=>"low"}, {"ConditionBrowseLeafId"=>"M4159", "ConditionBrowseLeafName"=>"Arteriosclerosis", "ConditionBrowseLeafRelevance"=>"low"}, {"ConditionBrowseLeafId"=>"M4155", "ConditionBrowseLeafName"=>"Arterial Occlusive Diseases", "ConditionBrowseLeafRelevance"=>"low"}]}, "ConditionBrowseBranchList"=>{"ConditionBrowseBranch"=>[{"ConditionBrowseBranchName"=>"Heart and Blood Diseases", "ConditionBrowseBranchAbbrev"=>"BC14"}, {"ConditionBrowseBranchName"=>"All Conditions", "ConditionBrowseBranchAbbrev"=>"All"}, {"ConditionBrowseBranchName"=>"Symptoms and General Pathology", "ConditionBrowseBranchAbbrev"=>"BC23"}]}}, "InterventionBrowseModule"=>{"InterventionMeshList"=>{"InterventionMesh"=>[{"InterventionMeshId"=>"D000000804", "InterventionMeshTerm"=>"Angiotensin II"}, {"InterventionMeshId"=>"C000627694", "InterventionMeshTerm"=>"Giapreza"}, {"InterventionMeshId"=>"D000000808", "InterventionMeshTerm"=>"Angiotensinogen"}, {"InterventionMeshId"=>"D000047228", "InterventionMeshTerm"=>"Angiotensin II Type 1 Receptor Blockers"}]}, "InterventionAncestorList"=>{"InterventionAncestor"=>[{"InterventionAncestorId"=>"D000014662", "InterventionAncestorTerm"=>"Vasoconstrictor Agents"}, {"InterventionAncestorId"=>"D000015842", "InterventionAncestorTerm"=>"Serine Proteinase Inhibitors"}, {"InterventionAncestorId"=>"D000011480", "InterventionAncestorTerm"=>"Protease Inhibitors"}, {"InterventionAncestorId"=>"D000004791", "InterventionAncestorTerm"=>"Enzyme Inhibitors"}, {"InterventionAncestorId"=>"D000045504", "InterventionAncestorTerm"=>"Molecular Mechanisms of Pharmacological Action"}, {"InterventionAncestorId"=>"D000057911", "InterventionAncestorTerm"=>"Angiotensin Receptor Antagonists"}]}, "InterventionBrowseLeafList"=>{"InterventionBrowseLeaf"=>[{"InterventionBrowseLeafId"=>"M3822", "InterventionBrowseLeafName"=>"Angiotensin II", "InterventionBrowseLeafAsFound"=>"Dosimetry", "InterventionBrowseLeafRelevance"=>"high"}, {"InterventionBrowseLeafId"=>"M289298", "InterventionBrowseLeafName"=>"Giapreza", "InterventionBrowseLeafAsFound"=>"Dosimetry", "InterventionBrowseLeafRelevance"=>"high"}, {"InterventionBrowseLeafId"=>"M3825", "InterventionBrowseLeafName"=>"Angiotensinogen", "InterventionBrowseLeafAsFound"=>"Dosimetry", "InterventionBrowseLeafRelevance"=>"high"}, {"InterventionBrowseLeafId"=>"M28606", "InterventionBrowseLeafName"=>"Angiotensin Receptor Antagonists", "InterventionBrowseLeafRelevance"=>"low"}, {"InterventionBrowseLeafId"=>"M25479", "InterventionBrowseLeafName"=>"Angiotensin II Type 1 Receptor Blockers", "InterventionBrowseLeafAsFound"=>"NCR", "InterventionBrowseLeafRelevance"=>"high"}, {"InterventionBrowseLeafId"=>"M17099", "InterventionBrowseLeafName"=>"Vasoconstrictor Agents", "InterventionBrowseLeafRelevance"=>"low"}, {"InterventionBrowseLeafId"=>"M14033", "InterventionBrowseLeafName"=>"Protease Inhibitors", "InterventionBrowseLeafRelevance"=>"low"}, {"InterventionBrowseLeafId"=>"M18081", "InterventionBrowseLeafName"=>"Serine Proteinase Inhibitors", "InterventionBrowseLeafRelevance"=>"low"}, {"InterventionBrowseLeafId"=>"M19299", "InterventionBrowseLeafName"=>"HIV Protease Inhibitors", "InterventionBrowseLeafRelevance"=>"low"}, {"InterventionBrowseLeafId"=>"M7641", "InterventionBrowseLeafName"=>"Enzyme Inhibitors", "InterventionBrowseLeafRelevance"=>"low"}, {"InterventionBrowseLeafId"=>"T18", "InterventionBrowseLeafName"=>"Serine", "InterventionBrowseLeafRelevance"=>"low"}]}, "InterventionBrowseBranchList"=>{"InterventionBrowseBranch"=>[{"InterventionBrowseBranchName"=>"Vasoconstrictor Agents", "InterventionBrowseBranchAbbrev"=>"VaCoAg"}, {"InterventionBrowseBranchName"=>"All Drugs and Chemicals", "InterventionBrowseBranchAbbrev"=>"All"}, {"InterventionBrowseBranchName"=>"Anti-Infective Agents", "InterventionBrowseBranchAbbrev"=>"Infe"}, {"InterventionBrowseBranchName"=>"Amino Acids", "InterventionBrowseBranchAbbrev"=>"AA"}]}}}, "ProtocolSection"=>{"DesignModule"=>{"PhaseList"=>{"Phase"=>["Phase 3"]}, "StudyType"=>"Interventional", "DesignInfo"=>{"DesignPrimaryPurpose"=>"Treatment"}, "EnrollmentInfo"=>{"EnrollmentCount"=>"36"}}, "StatusModule"=>{"OverallStatus"=>"Completed", "StartDateStruct"=>{"StartDate"=>"July 1997"}, "ExpandedAccessInfo"=>{"HasExpandedAccess"=>"No"}, "StatusVerifiedDate"=>"June 1999", "CompletionDateStruct"=>{"CompletionDate"=>"September 2000"}, "LastUpdateSubmitDate"=>"March 3, 2008", "StudyFirstSubmitDate"=>"November 3, 1999", "StudyFirstSubmitQCDate"=>"December 9, 2002", "LastUpdatePostDateStruct"=>{"LastUpdatePostDate"=>"March 4, 2008", "LastUpdatePostDateType"=>"Estimate"}, "StudyFirstPostDateStruct"=>{"StudyFirstPostDate"=>"December 10, 2002", "StudyFirstPostDateType"=>"Estimate"}}, "OversightModule"=>{}, "ConditionsModule"=>{"KeywordList"=>{"Keyword"=>["Angiotensin Receptor Antagonist", "Atherosclerosis", "Blood Flow", "Endothelium", "Endothelial Dysfunction"]}, "ConditionList"=>{"Condition"=>["Atherosclerosis", "Heart Failure, Congestive", "Hypertension", "Myocardial Infarction"]}}, "ReferencesModule"=>{"ReferenceList"=>{"Reference"=>[{"ReferencePMID"=>"6736187", "ReferenceType"=>"background", "ReferenceCitation"=>"Ontyd J, Schrader J. Measurement of adenosine, inosine, and hypoxanthine in human plasma. J Chromatogr. 1984 May 11;307(2):404-9. doi: 10.1016/s0378-4347(00)84113-4. No abstract available."}, {"ReferencePMID"=>"7505360", "ReferenceType"=>"background", "ReferenceCitation"=>"Cockcroft JR, Sciberras DG, Goldberg MR, Ritter JM. Comparison of angiotensin-converting enzyme inhibition with angiotensin II receptor antagonism in the human forearm. J Cardiovasc Pharmacol. 1993 Oct;22(4):579-84. doi: 10.1097/00005344-199310000-00011."}, {"ReferencePMID"=>"8403307", "ReferenceType"=>"background", "ReferenceCitation"=>"Gottlieb SS, Dickstein K, Fleck E, Kostis J, Levine TB, LeJemtel T, DeKock M. Hemodynamic and neurohormonal effects of the angiotensin II antagonist losartan in patients with congestive heart failure. Circulation. 1993 Oct;88(4 Pt 1):1602-9. doi: 10.1161/01.cir.88.4.1602."}]}}, "DescriptionModule"=>{"BriefSummary"=>"The renin angiotensin system (RAS) plays an important physiological and pathophysiological role in the control of blood pressure and plasma volume. Inhibition of the RAS is useful in the treatment of hypertension, cardiac failure and in some patients with myocardial infarction. Several recent clinical trials with angiotensin converting enzyme inhibitors (ACEI) have shown that they also reduce the incidence of myocardial infarction, but the mechanisms underlying this anti-ischemic effect are poorly understood. ACEI reduce angiotensin II synthesis and prevent bradykinin degradation. Results from ongoing studies in the Cardiology Branch (Protocol 95-H-0099) designed to investigate the link between ACEI and the vascular endothelium indicate that ACEI improve peripheral endothelial function, an effect that is partially mediated by bradykinin. The current protocol is designed to investigate whether the beneficial effects of ACEI on peripheral endothelial function are also due to inhibition of angiotensin II. The recent development of selective angiotensin II type 1 (AT1) receptor antagonists allows us to specifically examine the effects of angiotensin II on vasomotor activity.", "DetailedDescription"=>"The renin angiotensin system (RAS) plays an important physiological and pathophysiological role in the control of blood pressure and plasma volume. Inhibition of the RAS is useful in the treatment of hypertension, cardiac failure and in some patients with myocardial infarction. Several recent clinical trials with angiotensin converting enzyme inhibitors (ACEI) have shown that they also reduce the incidence of myocardial infarction, but the mechanisms underlying this anti-ischemic effect are poorly understood. ACEI reduce angiotensin II synthesis and prevent bradykinin degradation. Results from ongoing studies in the Cardiology Branch (Protocol 95-H-0099) designed to investigate the link between ACEI and the vascular endothelium indicate that ACEI improve peripheral endothelial function, an effect that is partially mediated by bradykinin. The current protocol is designed to investigate whether the beneficial effects of ACEI on peripheral endothelial function are also due to inhibition of angiotensin II. The recent development of selective angiotensin II type 1 (AT1) receptor antagonists allows us to specifically examine the effects of angiotensin II on vasomotor activity."}, "EligibilityModule"=>{"Gender"=>"All", "StdAgeList"=>{"StdAge"=>["Child", "Adult", "Older Adult"]}, "HealthyVolunteers"=>"Accepts Healthy Volunteers", "EligibilityCriteria"=>"Patients over 18 years with endothelial dysfunction requiring diagnostic cardiac catheterization.\n\nNormal volunteers or patients undergoing catheterization who have normal coronary arteries without risk factors for atherosclerosis will be used as controls.\n\nNo unstable angina.\n\nNo significant left main disease (greater than 50% stenosis).\n\nNo recent myocardial infarction (less than 1 month).\n\nNo pregnancy, lactation.\n\nNo allergy to losartan.\n\nNo renal failure (creatinine greater than 2.5 mg/dl).\n\nAbility to withdraw ACE inhibitors."}, "IdentificationModule"=>{"NCTId"=>"NCT00001628", "BriefTitle"=>"The Role of Angiotensin Type I Receptor in the Regulation of Human Peripheral Vascular Function", "Organization"=>{"OrgClass"=>"NIH", "OrgFullName"=>"National Institutes of Health Clinical Center (CC)"}, "OfficialTitle"=>"The Role of Angiotensin Type I Receptor in the Regulation of Human Peripheral Vascular Function", "OrgStudyIdInfo"=>{"OrgStudyId"=>"970140"}, "SecondaryIdInfoList"=>{"SecondaryIdInfo"=>[{"SecondaryId"=>"97-H-0140"}]}}, "ArmsInterventionsModule"=>{"InterventionList"=>{"Intervention"=>[{"InterventionName"=>"Angiotensin II type 1 receptor antagonists", "InterventionType"=>"Drug"}]}}, "ContactsLocationsModule"=>{"LocationList"=>{"Location"=>[{"LocationZip"=>"20892", "LocationCity"=>"Bethesda", "LocationState"=>"Maryland", "LocationCountry"=>"United States", "LocationFacility"=>"National Heart, Lung and Blood Institute (NHLBI)"}]}}, "SponsorCollaboratorsModule"=>{"LeadSponsor"=>{"LeadSponsorName"=>"National Heart, Lung, and Blood Institute (NHLBI)", "LeadSponsorClass"=>"NIH"}}}}}}
