Acute hemodynamic and neurohumoral effects of moxonidine in congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy
Elevated plasma norepinephrine (PNE) has been shown to be an important predictor of morbidity and mortality in patients with congestive heart failure (CHF). Moxonidine selectively stimulates imidazoline receptors located in the medulla, which centrally inhibit sympathetic outflow. PNE is suppressed...
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| Veröffentlicht in: | The American journal of cardiology 1999-06, Vol.83 (12), p.1638-1644 |
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| creator | Dickstein, Kenneth Manhenke, Cord Aarsland, Torbjørn Køpp, Ulf McNay, John Wiltse, Curtis |
| description | Elevated plasma norepinephrine (PNE) has been shown to be an important predictor of morbidity and mortality in patients with congestive heart failure (CHF). Moxonidine selectively stimulates imidazoline receptors located in the medulla, which centrally inhibit sympathetic outflow. PNE is suppressed and peripheral vasodilation reduces systemic blood pressure. This study evaluated the acute neurohumoral and hemodynamic effects of a single dose of oral moxonidine in 32 patients (22 men, mean ± SD age 66 ± 10 years) with CHF. All patients were in New York Heart Association functional class III and stabilized on chronic therapy with diuretics, digitalis, and angiotensin-converting enzyme inhibitors. The mean PNE concentration was 509 ± 304 pg/ml at baseline. Patients underwent invasive hemodynamic monitoring after double-blind randomization to either placebo (n = 12), moxonidine 0.4 mg (n = 9), or moxonidine 0.6 mg (n = 11). Moxonidine produced a dose-dependent, vasodilator response compared with placebo. Analysis of the time-averaged change from baseline over 6 hours demonstrated that moxonidine 0.6 mg caused significant reductions in mean systemic arterial pressure (p |
| doi_str_mv | 10.1016/S0002-9149(99)00170-8 |
| format | Article |
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Moxonidine selectively stimulates imidazoline receptors located in the medulla, which centrally inhibit sympathetic outflow. PNE is suppressed and peripheral vasodilation reduces systemic blood pressure. This study evaluated the acute neurohumoral and hemodynamic effects of a single dose of oral moxonidine in 32 patients (22 men, mean ± SD age 66 ± 10 years) with CHF. All patients were in New York Heart Association functional class III and stabilized on chronic therapy with diuretics, digitalis, and angiotensin-converting enzyme inhibitors. The mean PNE concentration was 509 ± 304 pg/ml at baseline. Patients underwent invasive hemodynamic monitoring after double-blind randomization to either placebo (n = 12), moxonidine 0.4 mg (n = 9), or moxonidine 0.6 mg (n = 11). Moxonidine produced a dose-dependent, vasodilator response compared with placebo. Analysis of the time-averaged change from baseline over 6 hours demonstrated that moxonidine 0.6 mg caused significant reductions in mean systemic arterial pressure (p <0.0001), mean pulmonary arterial pressure (p <0.005), systemic vascular resistance (p <0.05), pulmonary vascular resistance (p <0.01), and heart rate (p <0.05). Stroke volume was unchanged. PNE was reduced substantially (−180 pg/ml at 4 hours, p <0.005) and the reduction was highly correlated with the baseline level (r = −0.968). Moxonidine was well tolerated in this single-dose study and resulted in a modest, dose-dependent, vasodilator response, with substantial reductions in systemic and pulmonary arterial blood pressure. Trials designed to evaluate the clinical efficacy of chronic moxonidine therapy in CHF added to conventional therapy would be appropriate.]]></description><identifier>ISSN: 0002-9149</identifier><identifier>EISSN: 1879-1913</identifier><identifier>DOI: 10.1016/S0002-9149(99)00170-8</identifier><identifier>PMID: 10392868</identifier><identifier>CODEN: AJCDAG</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Administration, Oral ; Aged ; Analysis of Variance ; Antihypertensive Agents - blood ; Antihypertensive Agents - pharmacokinetics ; Antihypertensive Agents - therapeutic use ; Biological and medical sciences ; Cardiology. Vascular system ; Cardiomyopathy, Dilated - complications ; Dose-Response Relationship, Drug ; Double-Blind Method ; Drug therapy ; Heart ; Heart failure ; Heart Failure - drug therapy ; Heart Failure - etiology ; Heart Failure - physiopathology ; Heart failure, cardiogenic pulmonary edema, cardiac enlargement ; Hemodynamics - drug effects ; Humans ; Imidazoles - blood ; Imidazoles - pharmacokinetics ; Imidazoles - therapeutic use ; Male ; Medical sciences ; Myocardial Ischemia - complications ; Norepinephrine - blood ; Prescription drugs</subject><ispartof>The American journal of cardiology, 1999-06, Vol.83 (12), p.1638-1644</ispartof><rights>1999 Excerpta Medica Inc.</rights><rights>1999 INIST-CNRS</rights><rights>Copyright Elsevier Sequoia S.A. 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Moxonidine selectively stimulates imidazoline receptors located in the medulla, which centrally inhibit sympathetic outflow. PNE is suppressed and peripheral vasodilation reduces systemic blood pressure. This study evaluated the acute neurohumoral and hemodynamic effects of a single dose of oral moxonidine in 32 patients (22 men, mean ± SD age 66 ± 10 years) with CHF. All patients were in New York Heart Association functional class III and stabilized on chronic therapy with diuretics, digitalis, and angiotensin-converting enzyme inhibitors. The mean PNE concentration was 509 ± 304 pg/ml at baseline. Patients underwent invasive hemodynamic monitoring after double-blind randomization to either placebo (n = 12), moxonidine 0.4 mg (n = 9), or moxonidine 0.6 mg (n = 11). Moxonidine produced a dose-dependent, vasodilator response compared with placebo. Analysis of the time-averaged change from baseline over 6 hours demonstrated that moxonidine 0.6 mg caused significant reductions in mean systemic arterial pressure (p <0.0001), mean pulmonary arterial pressure (p <0.005), systemic vascular resistance (p <0.05), pulmonary vascular resistance (p <0.01), and heart rate (p <0.05). Stroke volume was unchanged. PNE was reduced substantially (−180 pg/ml at 4 hours, p <0.005) and the reduction was highly correlated with the baseline level (r = −0.968). Moxonidine was well tolerated in this single-dose study and resulted in a modest, dose-dependent, vasodilator response, with substantial reductions in systemic and pulmonary arterial blood pressure. Trials designed to evaluate the clinical efficacy of chronic moxonidine therapy in CHF added to conventional therapy would be appropriate.]]></description><subject>Administration, Oral</subject><subject>Aged</subject><subject>Analysis of Variance</subject><subject>Antihypertensive Agents - blood</subject><subject>Antihypertensive Agents - pharmacokinetics</subject><subject>Antihypertensive Agents - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Cardiomyopathy, Dilated - complications</subject><subject>Dose-Response Relationship, Drug</subject><subject>Double-Blind Method</subject><subject>Drug therapy</subject><subject>Heart</subject><subject>Heart failure</subject><subject>Heart Failure - drug therapy</subject><subject>Heart Failure - etiology</subject><subject>Heart Failure - physiopathology</subject><subject>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</subject><subject>Hemodynamics - drug effects</subject><subject>Humans</subject><subject>Imidazoles - blood</subject><subject>Imidazoles - pharmacokinetics</subject><subject>Imidazoles - therapeutic use</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocardial Ischemia - complications</subject><subject>Norepinephrine - blood</subject><subject>Prescription drugs</subject><issn>0002-9149</issn><issn>1879-1913</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkdtqFTEUhoNU7G71EZRQpOjFaDKHTHIlpXiCghf2PmSSle6UmWSbzBT3U_jKrn1AizfeJKyVb_38Kz8hLzl7xxkX778zxupK8Va9UeotY7xnlXxCVlz2quKKNydk9Qc5JWel3GPJeSeekVPOGlVLIVfk15VdZqBrmJLbRjMFS010NMKS03qZUjYjBe_BzoUmT6f0M8XgQgQaIrUp3kGZw8NOwOSZehPGJQMtgE_O5C2dEw3FojwKp0xxNG3MvMbKhdHM4Kg1GZvTdt_fPidPvRkLvDje5-T208fb6y_VzbfPX6-vbirb8n6unLfCdsK3rofB1dyaFlwrmcFTid5ZY_kgau4lHzrftU0vmrYewAzOKKaac3J5kN3k9GPBHfSENmEcTYS0FC2U7BlvGYIX_4D3ackRrem6YU2HbjqEugNkcyolg9ebHCZcX3Omd2npfVp6F4VWSu_T0hLnXh3Fl2EC92jqEA8Cr4-AKdaMPptoQ_nLSYmJCsQ-HDDAH3sIkHWxAaIFFzImp10K_3HyGyd0tSE</recordid><startdate>19990615</startdate><enddate>19990615</enddate><creator>Dickstein, Kenneth</creator><creator>Manhenke, Cord</creator><creator>Aarsland, Torbjørn</creator><creator>Køpp, Ulf</creator><creator>McNay, John</creator><creator>Wiltse, Curtis</creator><general>Elsevier Inc</general><general>Elsevier</general><general>Elsevier Limited</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TS</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>M7Z</scope><scope>NAPCQ</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>19990615</creationdate><title>Acute hemodynamic and neurohumoral effects of moxonidine in congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy</title><author>Dickstein, Kenneth ; Manhenke, Cord ; Aarsland, Torbjørn ; Køpp, Ulf ; McNay, John ; Wiltse, Curtis</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-dfc6c56f4d7ebd21ca4ed480aed4967dcac1b621f81b5f54376342beabda9093</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Administration, Oral</topic><topic>Aged</topic><topic>Analysis of Variance</topic><topic>Antihypertensive Agents - blood</topic><topic>Antihypertensive Agents - pharmacokinetics</topic><topic>Antihypertensive Agents - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Cardiomyopathy, Dilated - complications</topic><topic>Dose-Response Relationship, Drug</topic><topic>Double-Blind Method</topic><topic>Drug therapy</topic><topic>Heart</topic><topic>Heart failure</topic><topic>Heart Failure - drug therapy</topic><topic>Heart Failure - etiology</topic><topic>Heart Failure - physiopathology</topic><topic>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</topic><topic>Hemodynamics - drug effects</topic><topic>Humans</topic><topic>Imidazoles - blood</topic><topic>Imidazoles - pharmacokinetics</topic><topic>Imidazoles - therapeutic use</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocardial Ischemia - complications</topic><topic>Norepinephrine - blood</topic><topic>Prescription drugs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dickstein, Kenneth</creatorcontrib><creatorcontrib>Manhenke, Cord</creatorcontrib><creatorcontrib>Aarsland, Torbjørn</creatorcontrib><creatorcontrib>Køpp, Ulf</creatorcontrib><creatorcontrib>McNay, John</creatorcontrib><creatorcontrib>Wiltse, Curtis</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Physical Education Index</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biochemistry Abstracts 1</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The American journal of cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dickstein, Kenneth</au><au>Manhenke, Cord</au><au>Aarsland, Torbjørn</au><au>Køpp, Ulf</au><au>McNay, John</au><au>Wiltse, Curtis</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Acute hemodynamic and neurohumoral effects of moxonidine in congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy</atitle><jtitle>The American journal of cardiology</jtitle><addtitle>Am J Cardiol</addtitle><date>1999-06-15</date><risdate>1999</risdate><volume>83</volume><issue>12</issue><spage>1638</spage><epage>1644</epage><pages>1638-1644</pages><issn>0002-9149</issn><eissn>1879-1913</eissn><coden>AJCDAG</coden><abstract><![CDATA[Elevated plasma norepinephrine (PNE) has been shown to be an important predictor of morbidity and mortality in patients with congestive heart failure (CHF). Moxonidine selectively stimulates imidazoline receptors located in the medulla, which centrally inhibit sympathetic outflow. PNE is suppressed and peripheral vasodilation reduces systemic blood pressure. This study evaluated the acute neurohumoral and hemodynamic effects of a single dose of oral moxonidine in 32 patients (22 men, mean ± SD age 66 ± 10 years) with CHF. All patients were in New York Heart Association functional class III and stabilized on chronic therapy with diuretics, digitalis, and angiotensin-converting enzyme inhibitors. The mean PNE concentration was 509 ± 304 pg/ml at baseline. Patients underwent invasive hemodynamic monitoring after double-blind randomization to either placebo (n = 12), moxonidine 0.4 mg (n = 9), or moxonidine 0.6 mg (n = 11). Moxonidine produced a dose-dependent, vasodilator response compared with placebo. Analysis of the time-averaged change from baseline over 6 hours demonstrated that moxonidine 0.6 mg caused significant reductions in mean systemic arterial pressure (p <0.0001), mean pulmonary arterial pressure (p <0.005), systemic vascular resistance (p <0.05), pulmonary vascular resistance (p <0.01), and heart rate (p <0.05). Stroke volume was unchanged. PNE was reduced substantially (−180 pg/ml at 4 hours, p <0.005) and the reduction was highly correlated with the baseline level (r = −0.968). Moxonidine was well tolerated in this single-dose study and resulted in a modest, dose-dependent, vasodilator response, with substantial reductions in systemic and pulmonary arterial blood pressure. Trials designed to evaluate the clinical efficacy of chronic moxonidine therapy in CHF added to conventional therapy would be appropriate.]]></abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>10392868</pmid><doi>10.1016/S0002-9149(99)00170-8</doi><tpages>7</tpages></addata></record> |
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| subjects | Administration, Oral Aged Analysis of Variance Antihypertensive Agents - blood Antihypertensive Agents - pharmacokinetics Antihypertensive Agents - therapeutic use Biological and medical sciences Cardiology. Vascular system Cardiomyopathy, Dilated - complications Dose-Response Relationship, Drug Double-Blind Method Drug therapy Heart Heart failure Heart Failure - drug therapy Heart Failure - etiology Heart Failure - physiopathology Heart failure, cardiogenic pulmonary edema, cardiac enlargement Hemodynamics - drug effects Humans Imidazoles - blood Imidazoles - pharmacokinetics Imidazoles - therapeutic use Male Medical sciences Myocardial Ischemia - complications Norepinephrine - blood Prescription drugs |
| title | Acute hemodynamic and neurohumoral effects of moxonidine in congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy |
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