Electrophysiologic effects of cigarette smoking in patients with and without chronic beta-blocker therapy
After refraining from smoking for at least 8 hours, 22 adult male habitual smokers underwent baseline electrophysiologic study including atrial and ventricular burst pacing and programmed premature stimulation with single extrastimuli. After smoking 2 of their usual brand of cigarettes in rapid succ...
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| Veröffentlicht in: | The American journal of cardiology 1987-11, Vol.60 (13), p.1078-1082 |
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| container_end_page | 1082 |
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| container_issue | 13 |
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| container_title | The American journal of cardiology |
| container_volume | 60 |
| creator | Peters, Robert W. Benowitz, Neal L. Valenti, Steven Modin, Gunnard Fisher, Michael L. |
| description | After refraining from smoking for at least 8 hours, 22 adult male habitual smokers underwent baseline electrophysiologic study including atrial and ventricular burst pacing and programmed premature stimulation with single extrastimuli. After smoking 2 of their usual brand of cigarettes in rapid succession, the electrophysiologic protocol was repeated. Nicotine, catecholamine and carbon monoxide concentrations all increased significantly. Smoking increased heart rate and improved atrioventricular conduction in the 13 patients receiving chronic β-blocker therapy (mostly for angina pectoris); increases in heart rate and improvement in atrioventricular conduction were not different statistically from those seen in patients not receiving β-blocker therapy, suggesting the possibility of a direct effect of nicotine or other components of tobacco smoke. Ventricular refractoriness was not altered and atrial and ventricular arrhythmias were not increased by smoking. Persistent sympathomimetic actions of cigarette smoking may explain in part the failure of β-blocking drugs to reduce cardiac mortality risk in smokers after myocardial infarction. |
| doi_str_mv | 10.1016/0002-9149(87)90356-0 |
| format | Article |
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After smoking 2 of their usual brand of cigarettes in rapid succession, the electrophysiologic protocol was repeated. Nicotine, catecholamine and carbon monoxide concentrations all increased significantly. Smoking increased heart rate and improved atrioventricular conduction in the 13 patients receiving chronic β-blocker therapy (mostly for angina pectoris); increases in heart rate and improvement in atrioventricular conduction were not different statistically from those seen in patients not receiving β-blocker therapy, suggesting the possibility of a direct effect of nicotine or other components of tobacco smoke. Ventricular refractoriness was not altered and atrial and ventricular arrhythmias were not increased by smoking. 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After smoking 2 of their usual brand of cigarettes in rapid succession, the electrophysiologic protocol was repeated. Nicotine, catecholamine and carbon monoxide concentrations all increased significantly. Smoking increased heart rate and improved atrioventricular conduction in the 13 patients receiving chronic β-blocker therapy (mostly for angina pectoris); increases in heart rate and improvement in atrioventricular conduction were not different statistically from those seen in patients not receiving β-blocker therapy, suggesting the possibility of a direct effect of nicotine or other components of tobacco smoke. Ventricular refractoriness was not altered and atrial and ventricular arrhythmias were not increased by smoking. Persistent sympathomimetic actions of cigarette smoking may explain in part the failure of β-blocking drugs to reduce cardiac mortality risk in smokers after myocardial infarction.</description><subject>Adrenergic beta-Antagonists - therapeutic use</subject><subject>Adult</subject><subject>Aged</subject><subject>Arrhythmias, Cardiac - blood</subject><subject>Arrhythmias, Cardiac - drug therapy</subject><subject>Arrhythmias, Cardiac - physiopathology</subject><subject>Atrioventricular Node - physiopathology</subject><subject>Biological and medical sciences</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Sinoatrial Node - physiopathology</subject><subject>Smoking - blood</subject><subject>Smoking - physiopathology</subject><subject>Tobacco, tobacco smoking</subject><subject>Toxicology</subject><issn>0002-9149</issn><issn>1879-1913</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1987</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMFq3DAQhkVpSLZp36AFHUppDk40li1Ll0IJaRMI5JKchSSPd9V4LUfSpuzbV5td9tjTaDTf_AwfIZ-BXQIDccUYqysFjfouuwvFeCsq9o4sQHaqAgX8PVkckTPyIaU_pQVoxSk5raVitYIF8TcjuhzDvNomH8aw9I7iMJS_RMNAnV-aiDkjTevw7Kcl9ROdTfY4FeCvzytqpv7tETaZulUMU0mwmE1lx-CeMdK8wmjm7UdyMpgx4adDPSdPv24er2-r-4ffd9c_7yvHpcgVV63EoePWis7Kvu255Aw5ghQojXNgLTYWJQwCOFe8Zko0Alsh6waMQH5Ovu1z5xheNpiyXvvkcBzNhGGTtASmOtm1BWz2oIshpYiDnqNfm7jVwPTOsN7p0zt9Wnb6zbBmZe3LIX9j19gflw5Ky_zrYW6SM-MQzeR8OmJd2yquZMF-7DEsLl49Rp1cseqw97HY133w_7_jH2MTmKc</recordid><startdate>19871101</startdate><enddate>19871101</enddate><creator>Peters, Robert W.</creator><creator>Benowitz, Neal L.</creator><creator>Valenti, Steven</creator><creator>Modin, Gunnard</creator><creator>Fisher, Michael L.</creator><general>Elsevier Inc</general><general>Elsevier</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>7X8</scope></search><sort><creationdate>19871101</creationdate><title>Electrophysiologic effects of cigarette smoking in patients with and without chronic beta-blocker therapy</title><author>Peters, Robert W. ; Benowitz, Neal L. ; Valenti, Steven ; Modin, Gunnard ; Fisher, Michael L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c386t-3958ef73bb67b8d5d3830e3e186e8acc1bbe4be81f613393209646e568241a6e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1987</creationdate><topic>Adrenergic beta-Antagonists - therapeutic use</topic><topic>Adult</topic><topic>Aged</topic><topic>Arrhythmias, Cardiac - blood</topic><topic>Arrhythmias, Cardiac - drug therapy</topic><topic>Arrhythmias, Cardiac - physiopathology</topic><topic>Atrioventricular Node - physiopathology</topic><topic>Biological and medical sciences</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Sinoatrial Node - physiopathology</topic><topic>Smoking - blood</topic><topic>Smoking - physiopathology</topic><topic>Tobacco, tobacco smoking</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Peters, Robert W.</creatorcontrib><creatorcontrib>Benowitz, Neal L.</creatorcontrib><creatorcontrib>Valenti, Steven</creatorcontrib><creatorcontrib>Modin, Gunnard</creatorcontrib><creatorcontrib>Fisher, Michael L.</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>MEDLINE - Academic</collection><jtitle>The American journal of cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Peters, Robert W.</au><au>Benowitz, Neal L.</au><au>Valenti, Steven</au><au>Modin, Gunnard</au><au>Fisher, Michael L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Electrophysiologic effects of cigarette smoking in patients with and without chronic beta-blocker therapy</atitle><jtitle>The American journal of cardiology</jtitle><addtitle>Am J Cardiol</addtitle><date>1987-11-01</date><risdate>1987</risdate><volume>60</volume><issue>13</issue><spage>1078</spage><epage>1082</epage><pages>1078-1082</pages><issn>0002-9149</issn><eissn>1879-1913</eissn><coden>AJCDAG</coden><abstract>After refraining from smoking for at least 8 hours, 22 adult male habitual smokers underwent baseline electrophysiologic study including atrial and ventricular burst pacing and programmed premature stimulation with single extrastimuli. After smoking 2 of their usual brand of cigarettes in rapid succession, the electrophysiologic protocol was repeated. Nicotine, catecholamine and carbon monoxide concentrations all increased significantly. Smoking increased heart rate and improved atrioventricular conduction in the 13 patients receiving chronic β-blocker therapy (mostly for angina pectoris); increases in heart rate and improvement in atrioventricular conduction were not different statistically from those seen in patients not receiving β-blocker therapy, suggesting the possibility of a direct effect of nicotine or other components of tobacco smoke. Ventricular refractoriness was not altered and atrial and ventricular arrhythmias were not increased by smoking. Persistent sympathomimetic actions of cigarette smoking may explain in part the failure of β-blocking drugs to reduce cardiac mortality risk in smokers after myocardial infarction.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>2890291</pmid><doi>10.1016/0002-9149(87)90356-0</doi><tpages>5</tpages></addata></record> |
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| ispartof | The American journal of cardiology, 1987-11, Vol.60 (13), p.1078-1082 |
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| subjects | Adrenergic beta-Antagonists - therapeutic use Adult Aged Arrhythmias, Cardiac - blood Arrhythmias, Cardiac - drug therapy Arrhythmias, Cardiac - physiopathology Atrioventricular Node - physiopathology Biological and medical sciences Humans Male Medical sciences Middle Aged Sinoatrial Node - physiopathology Smoking - blood Smoking - physiopathology Tobacco, tobacco smoking Toxicology |
| title | Electrophysiologic effects of cigarette smoking in patients with and without chronic beta-blocker therapy |
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