Autonomic and antiarrhythmic drug modulation of ST segment elevation in patients with Brugada syndrome
We examined the modulatory effects of autonomic nervous system and antiarrhythmic drugs on the ST segment in patients with Brugada syndrome to gain an insight into the mechanism of ST segment elevation. Right bundle branch block, ST segment elevation and ventricular tachyarrhythmias define a distinc...
Gespeichert in:
| Veröffentlicht in: | Journal of the American College of Cardiology 1996-04, Vol.27 (5), p.1061-1070 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1070 |
|---|---|
| container_issue | 5 |
| container_start_page | 1061 |
| container_title | Journal of the American College of Cardiology |
| container_volume | 27 |
| creator | Miyazaki, Toshihisa Mitamura, Hideo Miyoshi, Shunichiro Soejima, Kyoko Aizawa, Yoshifusa Ogawa, Satoshi |
| description | We examined the modulatory effects of autonomic nervous system and antiarrhythmic drugs on the ST segment in patients with Brugada syndrome to gain an insight into the mechanism of ST segment elevation.
Right bundle branch block, ST segment elevation and ventricular tachyarrhythmias define a distinct clinical and electrocardiographic (ECG) syndrome (Brugada syndrome). However, the mechanism of ST segment elevation and the causes of this syndrome are unknown.
The study included four patients in whom structural heart or coronary artery disease was excluded by noninvasive and invasive tests. High take-off ST segment elevation of either the coved or saddle-back type in precordial leads V1, V2and V3was seen in all patients. Three patients experienced recurrent episodes of syncope or aborted sudden cardiac death, and the remaining patient had palpitation. Autonomic receptor stimulation and blockade and intravenous administration of antiarrhythmic drugs were performed during sinus rhythm while the 12-lead ECG was recorded. Metaiodobenzylguanidine (MIBG) scanning and Holter monitoring were also performed.
Beta-adrenoceptor stimulation by intravenous isoproterenol consistently reduced (≥0.1 mV) ST segment elevation at or 80 ms after the J point in all four patients. Selective alphaadrenoceptor stimulation by intravenous norepinephrine in the presence of propranolol or by intravenous methoxamine consistently augmented, whereas alpha-adrenoceptor blockade reduced, ST segment elevation in three patients. Intracoronary acetylcholine or intravenous edrophonium or neostigmine augmented ST segment elevation without inducing coronary spasm in three of four patients. Class IA antiarrhythmic drugs also consistently augmented (three patients), whereas class IB drugs had no effect on (two patients) ST segment elevation. No abnormality was found on MIBG imaging or heart rate variability in three patients, suggesting that autonomic dysfunction is not a primary disease process. Class IA drugs had no effect on ST segment in three control patients, suggesting that the ST segment elevation seen in patients with Brugada syndrome in response to the drugs is not a nonspecific response.
ST segment elevation in patients with Brugada syndrome was augmented by selective stimulation of alphaadrenoceptors or muscarinic receptors or by class IA drugs but was mitigated by beta-adrenoceptor stimulation or alphaadrenoceptor blockade. These responses might be explained by postulating the presence |
| doi_str_mv | 10.1016/0735-1097(95)00613-3 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_77989130</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>0735109795006133</els_id><sourcerecordid>77989130</sourcerecordid><originalsourceid>FETCH-LOGICAL-c421t-8950e1c391c36939b898cd3168c5165f4ed835677d784bc541bbdba75e7ff8483</originalsourceid><addsrcrecordid>eNp9kMFqGzEQhkVocJy0b5CADiWkh20la7WSLgEnpGkg0EPds9BKs7HK7sqVtCl--8i18TGHQeKfb4bhQ-iSkq-U0OYbEYxXlChxo_gXQhrKKnaC5pRzWTGuxAc0PyJn6DylP6RQkqoZmsmGKLZYzFG3nHIYw-AtNqMrlb2Jcb3N613k4vSCh-Cm3mQfRhw6_GuFE7wMMGYMPbzucz_iTfmVMOF_Pq_xXRk0zuC0HV0MA3xEp53pE3w6vBfo9_eH1f2P6vnn49P98rmy9YLmSipOgFqmSjWKqVYqaR2jjbScNryrwUnGGyGckHVreU3b1rVGcBBdJ2vJLtD1fu8mhr8TpKwHnyz0vRkhTEkLoaSijBSw3oM2hpQidHoT_WDiVlOid3r1zp3eudOK6_96NStjV4f9UzuAOw4dfJb-50PfJGv6LprR-nTEGKmlIk3BbvcYFBevHqJOttiz4HwEm7UL_v073gCD1JcB</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>77989130</pqid></control><display><type>article</type><title>Autonomic and antiarrhythmic drug modulation of ST segment elevation in patients with Brugada syndrome</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals Complete</source><source>Free E-Journal (出版社公開部分のみ）</source><creator>Miyazaki, Toshihisa ; Mitamura, Hideo ; Miyoshi, Shunichiro ; Soejima, Kyoko ; Aizawa, Yoshifusa ; Ogawa, Satoshi</creator><creatorcontrib>Miyazaki, Toshihisa ; Mitamura, Hideo ; Miyoshi, Shunichiro ; Soejima, Kyoko ; Aizawa, Yoshifusa ; Ogawa, Satoshi</creatorcontrib><description>We examined the modulatory effects of autonomic nervous system and antiarrhythmic drugs on the ST segment in patients with Brugada syndrome to gain an insight into the mechanism of ST segment elevation.
Right bundle branch block, ST segment elevation and ventricular tachyarrhythmias define a distinct clinical and electrocardiographic (ECG) syndrome (Brugada syndrome). However, the mechanism of ST segment elevation and the causes of this syndrome are unknown.
The study included four patients in whom structural heart or coronary artery disease was excluded by noninvasive and invasive tests. High take-off ST segment elevation of either the coved or saddle-back type in precordial leads V1, V2and V3was seen in all patients. Three patients experienced recurrent episodes of syncope or aborted sudden cardiac death, and the remaining patient had palpitation. Autonomic receptor stimulation and blockade and intravenous administration of antiarrhythmic drugs were performed during sinus rhythm while the 12-lead ECG was recorded. Metaiodobenzylguanidine (MIBG) scanning and Holter monitoring were also performed.
Beta-adrenoceptor stimulation by intravenous isoproterenol consistently reduced (≥0.1 mV) ST segment elevation at or 80 ms after the J point in all four patients. Selective alphaadrenoceptor stimulation by intravenous norepinephrine in the presence of propranolol or by intravenous methoxamine consistently augmented, whereas alpha-adrenoceptor blockade reduced, ST segment elevation in three patients. Intracoronary acetylcholine or intravenous edrophonium or neostigmine augmented ST segment elevation without inducing coronary spasm in three of four patients. Class IA antiarrhythmic drugs also consistently augmented (three patients), whereas class IB drugs had no effect on (two patients) ST segment elevation. No abnormality was found on MIBG imaging or heart rate variability in three patients, suggesting that autonomic dysfunction is not a primary disease process. Class IA drugs had no effect on ST segment in three control patients, suggesting that the ST segment elevation seen in patients with Brugada syndrome in response to the drugs is not a nonspecific response.
ST segment elevation in patients with Brugada syndrome was augmented by selective stimulation of alphaadrenoceptors or muscarinic receptors or by class IA drugs but was mitigated by beta-adrenoceptor stimulation or alphaadrenoceptor blockade. These responses might be explained by postulating the presence of an area of early repolarization or a local “depolarized” area in the ventricle causing ST segment elevation in this syndrome. Because only a small number of patients were studied, these possibilities need further evaluation.</description><identifier>ISSN: 0735-1097</identifier><identifier>EISSN: 1558-3597</identifier><identifier>DOI: 10.1016/0735-1097(95)00613-3</identifier><identifier>PMID: 8609322</identifier><identifier>CODEN: JACCDI</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adult ; Anti-Arrhythmia Agents - therapeutic use ; Biological and medical sciences ; Calcium Channel Blockers - therapeutic use ; Cardiac dysrhythmias ; Cardiology. Vascular system ; Disopyramide - therapeutic use ; Electrocardiography ; Heart ; Humans ; Lidocaine - therapeutic use ; Male ; Medical sciences ; Mexiletine - therapeutic use ; Middle Aged ; Procainamide - therapeutic use ; Syndrome ; Tachycardia, Ventricular - drug therapy ; Tachycardia, Ventricular - physiopathology ; Verapamil - therapeutic use</subject><ispartof>Journal of the American College of Cardiology, 1996-04, Vol.27 (5), p.1061-1070</ispartof><rights>1996 American College of Cardiology</rights><rights>1996 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c421t-8950e1c391c36939b898cd3168c5165f4ed835677d784bc541bbdba75e7ff8483</citedby><cites>FETCH-LOGICAL-c421t-8950e1c391c36939b898cd3168c5165f4ed835677d784bc541bbdba75e7ff8483</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0735-1097(95)00613-3$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>309,310,314,780,784,789,790,3550,23930,23931,25140,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3048906$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8609322$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Miyazaki, Toshihisa</creatorcontrib><creatorcontrib>Mitamura, Hideo</creatorcontrib><creatorcontrib>Miyoshi, Shunichiro</creatorcontrib><creatorcontrib>Soejima, Kyoko</creatorcontrib><creatorcontrib>Aizawa, Yoshifusa</creatorcontrib><creatorcontrib>Ogawa, Satoshi</creatorcontrib><title>Autonomic and antiarrhythmic drug modulation of ST segment elevation in patients with Brugada syndrome</title><title>Journal of the American College of Cardiology</title><addtitle>J Am Coll Cardiol</addtitle><description>We examined the modulatory effects of autonomic nervous system and antiarrhythmic drugs on the ST segment in patients with Brugada syndrome to gain an insight into the mechanism of ST segment elevation.
Right bundle branch block, ST segment elevation and ventricular tachyarrhythmias define a distinct clinical and electrocardiographic (ECG) syndrome (Brugada syndrome). However, the mechanism of ST segment elevation and the causes of this syndrome are unknown.
The study included four patients in whom structural heart or coronary artery disease was excluded by noninvasive and invasive tests. High take-off ST segment elevation of either the coved or saddle-back type in precordial leads V1, V2and V3was seen in all patients. Three patients experienced recurrent episodes of syncope or aborted sudden cardiac death, and the remaining patient had palpitation. Autonomic receptor stimulation and blockade and intravenous administration of antiarrhythmic drugs were performed during sinus rhythm while the 12-lead ECG was recorded. Metaiodobenzylguanidine (MIBG) scanning and Holter monitoring were also performed.
Beta-adrenoceptor stimulation by intravenous isoproterenol consistently reduced (≥0.1 mV) ST segment elevation at or 80 ms after the J point in all four patients. Selective alphaadrenoceptor stimulation by intravenous norepinephrine in the presence of propranolol or by intravenous methoxamine consistently augmented, whereas alpha-adrenoceptor blockade reduced, ST segment elevation in three patients. Intracoronary acetylcholine or intravenous edrophonium or neostigmine augmented ST segment elevation without inducing coronary spasm in three of four patients. Class IA antiarrhythmic drugs also consistently augmented (three patients), whereas class IB drugs had no effect on (two patients) ST segment elevation. No abnormality was found on MIBG imaging or heart rate variability in three patients, suggesting that autonomic dysfunction is not a primary disease process. Class IA drugs had no effect on ST segment in three control patients, suggesting that the ST segment elevation seen in patients with Brugada syndrome in response to the drugs is not a nonspecific response.
ST segment elevation in patients with Brugada syndrome was augmented by selective stimulation of alphaadrenoceptors or muscarinic receptors or by class IA drugs but was mitigated by beta-adrenoceptor stimulation or alphaadrenoceptor blockade. These responses might be explained by postulating the presence of an area of early repolarization or a local “depolarized” area in the ventricle causing ST segment elevation in this syndrome. Because only a small number of patients were studied, these possibilities need further evaluation.</description><subject>Adult</subject><subject>Anti-Arrhythmia Agents - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Calcium Channel Blockers - therapeutic use</subject><subject>Cardiac dysrhythmias</subject><subject>Cardiology. Vascular system</subject><subject>Disopyramide - therapeutic use</subject><subject>Electrocardiography</subject><subject>Heart</subject><subject>Humans</subject><subject>Lidocaine - therapeutic use</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mexiletine - therapeutic use</subject><subject>Middle Aged</subject><subject>Procainamide - therapeutic use</subject><subject>Syndrome</subject><subject>Tachycardia, Ventricular - drug therapy</subject><subject>Tachycardia, Ventricular - physiopathology</subject><subject>Verapamil - therapeutic use</subject><issn>0735-1097</issn><issn>1558-3597</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMFqGzEQhkVocJy0b5CADiWkh20la7WSLgEnpGkg0EPds9BKs7HK7sqVtCl--8i18TGHQeKfb4bhQ-iSkq-U0OYbEYxXlChxo_gXQhrKKnaC5pRzWTGuxAc0PyJn6DylP6RQkqoZmsmGKLZYzFG3nHIYw-AtNqMrlb2Jcb3N613k4vSCh-Cm3mQfRhw6_GuFE7wMMGYMPbzucz_iTfmVMOF_Pq_xXRk0zuC0HV0MA3xEp53pE3w6vBfo9_eH1f2P6vnn49P98rmy9YLmSipOgFqmSjWKqVYqaR2jjbScNryrwUnGGyGckHVreU3b1rVGcBBdJ2vJLtD1fu8mhr8TpKwHnyz0vRkhTEkLoaSijBSw3oM2hpQidHoT_WDiVlOid3r1zp3eudOK6_96NStjV4f9UzuAOw4dfJb-50PfJGv6LprR-nTEGKmlIk3BbvcYFBevHqJOttiz4HwEm7UL_v073gCD1JcB</recordid><startdate>19960401</startdate><enddate>19960401</enddate><creator>Miyazaki, Toshihisa</creator><creator>Mitamura, Hideo</creator><creator>Miyoshi, Shunichiro</creator><creator>Soejima, Kyoko</creator><creator>Aizawa, Yoshifusa</creator><creator>Ogawa, Satoshi</creator><general>Elsevier Inc</general><general>Elsevier Science</general><scope>6I.</scope><scope>AAFTH</scope><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>19960401</creationdate><title>Autonomic and antiarrhythmic drug modulation of ST segment elevation in patients with Brugada syndrome</title><author>Miyazaki, Toshihisa ; Mitamura, Hideo ; Miyoshi, Shunichiro ; Soejima, Kyoko ; Aizawa, Yoshifusa ; Ogawa, Satoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c421t-8950e1c391c36939b898cd3168c5165f4ed835677d784bc541bbdba75e7ff8483</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Adult</topic><topic>Anti-Arrhythmia Agents - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Calcium Channel Blockers - therapeutic use</topic><topic>Cardiac dysrhythmias</topic><topic>Cardiology. Vascular system</topic><topic>Disopyramide - therapeutic use</topic><topic>Electrocardiography</topic><topic>Heart</topic><topic>Humans</topic><topic>Lidocaine - therapeutic use</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mexiletine - therapeutic use</topic><topic>Middle Aged</topic><topic>Procainamide - therapeutic use</topic><topic>Syndrome</topic><topic>Tachycardia, Ventricular - drug therapy</topic><topic>Tachycardia, Ventricular - physiopathology</topic><topic>Verapamil - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Miyazaki, Toshihisa</creatorcontrib><creatorcontrib>Mitamura, Hideo</creatorcontrib><creatorcontrib>Miyoshi, Shunichiro</creatorcontrib><creatorcontrib>Soejima, Kyoko</creatorcontrib><creatorcontrib>Aizawa, Yoshifusa</creatorcontrib><creatorcontrib>Ogawa, Satoshi</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>Journal of the American College of Cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Miyazaki, Toshihisa</au><au>Mitamura, Hideo</au><au>Miyoshi, Shunichiro</au><au>Soejima, Kyoko</au><au>Aizawa, Yoshifusa</au><au>Ogawa, Satoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Autonomic and antiarrhythmic drug modulation of ST segment elevation in patients with Brugada syndrome</atitle><jtitle>Journal of the American College of Cardiology</jtitle><addtitle>J Am Coll Cardiol</addtitle><date>1996-04-01</date><risdate>1996</risdate><volume>27</volume><issue>5</issue><spage>1061</spage><epage>1070</epage><pages>1061-1070</pages><issn>0735-1097</issn><eissn>1558-3597</eissn><coden>JACCDI</coden><abstract>We examined the modulatory effects of autonomic nervous system and antiarrhythmic drugs on the ST segment in patients with Brugada syndrome to gain an insight into the mechanism of ST segment elevation.
Right bundle branch block, ST segment elevation and ventricular tachyarrhythmias define a distinct clinical and electrocardiographic (ECG) syndrome (Brugada syndrome). However, the mechanism of ST segment elevation and the causes of this syndrome are unknown.
The study included four patients in whom structural heart or coronary artery disease was excluded by noninvasive and invasive tests. High take-off ST segment elevation of either the coved or saddle-back type in precordial leads V1, V2and V3was seen in all patients. Three patients experienced recurrent episodes of syncope or aborted sudden cardiac death, and the remaining patient had palpitation. Autonomic receptor stimulation and blockade and intravenous administration of antiarrhythmic drugs were performed during sinus rhythm while the 12-lead ECG was recorded. Metaiodobenzylguanidine (MIBG) scanning and Holter monitoring were also performed.
Beta-adrenoceptor stimulation by intravenous isoproterenol consistently reduced (≥0.1 mV) ST segment elevation at or 80 ms after the J point in all four patients. Selective alphaadrenoceptor stimulation by intravenous norepinephrine in the presence of propranolol or by intravenous methoxamine consistently augmented, whereas alpha-adrenoceptor blockade reduced, ST segment elevation in three patients. Intracoronary acetylcholine or intravenous edrophonium or neostigmine augmented ST segment elevation without inducing coronary spasm in three of four patients. Class IA antiarrhythmic drugs also consistently augmented (three patients), whereas class IB drugs had no effect on (two patients) ST segment elevation. No abnormality was found on MIBG imaging or heart rate variability in three patients, suggesting that autonomic dysfunction is not a primary disease process. Class IA drugs had no effect on ST segment in three control patients, suggesting that the ST segment elevation seen in patients with Brugada syndrome in response to the drugs is not a nonspecific response.
ST segment elevation in patients with Brugada syndrome was augmented by selective stimulation of alphaadrenoceptors or muscarinic receptors or by class IA drugs but was mitigated by beta-adrenoceptor stimulation or alphaadrenoceptor blockade. These responses might be explained by postulating the presence of an area of early repolarization or a local “depolarized” area in the ventricle causing ST segment elevation in this syndrome. Because only a small number of patients were studied, these possibilities need further evaluation.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>8609322</pmid><doi>10.1016/0735-1097(95)00613-3</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0735-1097 |
| ispartof | Journal of the American College of Cardiology, 1996-04, Vol.27 (5), p.1061-1070 |
| issn | 0735-1097 1558-3597 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_77989130 |
| source | MEDLINE; Elsevier ScienceDirect Journals Complete; Free E-Journal (出版社公開部分のみ） |
| subjects | Adult Anti-Arrhythmia Agents - therapeutic use Biological and medical sciences Calcium Channel Blockers - therapeutic use Cardiac dysrhythmias Cardiology. Vascular system Disopyramide - therapeutic use Electrocardiography Heart Humans Lidocaine - therapeutic use Male Medical sciences Mexiletine - therapeutic use Middle Aged Procainamide - therapeutic use Syndrome Tachycardia, Ventricular - drug therapy Tachycardia, Ventricular - physiopathology Verapamil - therapeutic use |
| title | Autonomic and antiarrhythmic drug modulation of ST segment elevation in patients with Brugada syndrome |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-01T10%3A08%3A53IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Autonomic%20and%20antiarrhythmic%20drug%20modulation%20of%20ST%20segment%20elevation%20in%20patients%20with%20Brugada%20syndrome&rft.jtitle=Journal%20of%20the%20American%20College%20of%20Cardiology&rft.au=Miyazaki,%20Toshihisa&rft.date=1996-04-01&rft.volume=27&rft.issue=5&rft.spage=1061&rft.epage=1070&rft.pages=1061-1070&rft.issn=0735-1097&rft.eissn=1558-3597&rft.coden=JACCDI&rft_id=info:doi/10.1016/0735-1097(95)00613-3&rft_dat=%3Cproquest_cross%3E77989130%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=77989130&rft_id=info:pmid/8609322&rft_els_id=0735109795006133&rfr_iscdi=true |