New Concepts in Ischemia Prevention
Transient myocardial ischemia may result from obstruction to flow in the large epicardial coronary arteries or diminshed flow reserve due to small vessel disease or left ventricular hypertrophy. In patients with coronary heart disease, calcium blockers have proven to reduce stress induced ischemia i...
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Veröffentlicht in: | Journal of cardiovascular pharmacology 1991, Vol.18 Suppl 9, p.S7-S14 |
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container_title | Journal of cardiovascular pharmacology |
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creator | Klein, W Eber, B Dusleag, J Rotman, B Gasser, R Weinrauch, V Brussee, H |
description | Transient myocardial ischemia may result from obstruction to flow in the large epicardial coronary arteries or diminshed flow reserve due to small vessel disease or left ventricular hypertrophy. In patients with coronary heart disease, calcium blockers have proven to reduce stress induced ischemia in patients with normal left ventricular function and in those with ischemic cardiomyopathy. However, recent studies indicate a need for caution when giving calcium antagonists to patients with postinfarction left ventricular systolic dysfunction. Moreover, calcium antagonists that reduce heart rate (diltiazem) are able as a monotherapy to reduce total ischemic burden. Calcium antagonists that may increase rate (dihydropiridines) have to be combined with β-blockers to achieve this goal. For 24-h control of ischemia the ischemic threshold should be determined for a differentiated therapy in the individual patient. Is the ischemic threshold of the majority of episodes lower than the exercise threshold, a calcium blocker should work. Angiotensin-converting enzyme (ACE) inhibitors are not effective in stress-induced ischemia, but may reduce total ischemic burden, although this effect is not significant. In patients with left ventricular hypertrophy and/or small vessel disease, calcium blockers and ACE inhibitors are probably effective in regression of left ventricular hypertrophy and vascular hypertrophy. However, it remains to be shown that ischemia is reduced by these drugs. |
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In patients with coronary heart disease, calcium blockers have proven to reduce stress induced ischemia in patients with normal left ventricular function and in those with ischemic cardiomyopathy. However, recent studies indicate a need for caution when giving calcium antagonists to patients with postinfarction left ventricular systolic dysfunction. Moreover, calcium antagonists that reduce heart rate (diltiazem) are able as a monotherapy to reduce total ischemic burden. Calcium antagonists that may increase rate (dihydropiridines) have to be combined with β-blockers to achieve this goal. For 24-h control of ischemia the ischemic threshold should be determined for a differentiated therapy in the individual patient. Is the ischemic threshold of the majority of episodes lower than the exercise threshold, a calcium blocker should work. Angiotensin-converting enzyme (ACE) inhibitors are not effective in stress-induced ischemia, but may reduce total ischemic burden, although this effect is not significant. In patients with left ventricular hypertrophy and/or small vessel disease, calcium blockers and ACE inhibitors are probably effective in regression of left ventricular hypertrophy and vascular hypertrophy. However, it remains to be shown that ischemia is reduced by these drugs.</description><identifier>ISSN: 0160-2446</identifier><identifier>EISSN: 1533-4023</identifier><language>eng</language><publisher>Lippincott-Raven Publishers</publisher><ispartof>Journal of cardiovascular pharmacology, 1991, Vol.18 Suppl 9, p.S7-S14</ispartof><rights>Lippincott-Raven Publishers.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttp://ovidsp.ovid.com/ovidweb.cgi?T=JS&NEWS=n&CSC=Y&PAGE=fulltext&D=ovft&AN=00005344-199106189-00003$$EHTML$$P50$$Gwolterskluwer$$H</linktohtml><link.rule.ids>314,776,780,4010,4595,65206</link.rule.ids></links><search><creatorcontrib>Klein, W</creatorcontrib><creatorcontrib>Eber, B</creatorcontrib><creatorcontrib>Dusleag, J</creatorcontrib><creatorcontrib>Rotman, B</creatorcontrib><creatorcontrib>Gasser, R</creatorcontrib><creatorcontrib>Weinrauch, V</creatorcontrib><creatorcontrib>Brussee, H</creatorcontrib><title>New Concepts in Ischemia Prevention</title><title>Journal of cardiovascular pharmacology</title><description>Transient myocardial ischemia may result from obstruction to flow in the large epicardial coronary arteries or diminshed flow reserve due to small vessel disease or left ventricular hypertrophy. In patients with coronary heart disease, calcium blockers have proven to reduce stress induced ischemia in patients with normal left ventricular function and in those with ischemic cardiomyopathy. However, recent studies indicate a need for caution when giving calcium antagonists to patients with postinfarction left ventricular systolic dysfunction. Moreover, calcium antagonists that reduce heart rate (diltiazem) are able as a monotherapy to reduce total ischemic burden. Calcium antagonists that may increase rate (dihydropiridines) have to be combined with β-blockers to achieve this goal. For 24-h control of ischemia the ischemic threshold should be determined for a differentiated therapy in the individual patient. Is the ischemic threshold of the majority of episodes lower than the exercise threshold, a calcium blocker should work. Angiotensin-converting enzyme (ACE) inhibitors are not effective in stress-induced ischemia, but may reduce total ischemic burden, although this effect is not significant. In patients with left ventricular hypertrophy and/or small vessel disease, calcium blockers and ACE inhibitors are probably effective in regression of left ventricular hypertrophy and vascular hypertrophy. However, it remains to be shown that ischemia is reduced by these drugs.</description><issn>0160-2446</issn><issn>1533-4023</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1991</creationdate><recordtype>article</recordtype><sourceid/><recordid>eNqdi0sKwjAUAIMoWD93CLgOvDQv0ayLohtx4b6U8qTVmEgS7fVV8ATOZmBgRqyQWimBUKoxK0AaECWimbJZSlcAiXptCrY60sCr4Ft65MR7zw-p7ejeN_wU6UU-98Ev2OTSuETLn-cMd9tztRdDcJliurnnQLHuqHG5q-GDVohCWivByI0V36TUn9sb9Ps3Gg</recordid><startdate>1991</startdate><enddate>1991</enddate><creator>Klein, W</creator><creator>Eber, B</creator><creator>Dusleag, J</creator><creator>Rotman, B</creator><creator>Gasser, R</creator><creator>Weinrauch, V</creator><creator>Brussee, H</creator><general>Lippincott-Raven Publishers</general><scope/></search><sort><creationdate>1991</creationdate><title>New Concepts in Ischemia Prevention</title><author>Klein, W ; Eber, B ; Dusleag, J ; Rotman, B ; Gasser, R ; Weinrauch, V ; Brussee, H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-wolterskluwer_health_00005344-199106189-000033</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1991</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Klein, W</creatorcontrib><creatorcontrib>Eber, B</creatorcontrib><creatorcontrib>Dusleag, J</creatorcontrib><creatorcontrib>Rotman, B</creatorcontrib><creatorcontrib>Gasser, R</creatorcontrib><creatorcontrib>Weinrauch, V</creatorcontrib><creatorcontrib>Brussee, H</creatorcontrib><jtitle>Journal of cardiovascular pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Klein, W</au><au>Eber, B</au><au>Dusleag, J</au><au>Rotman, B</au><au>Gasser, R</au><au>Weinrauch, V</au><au>Brussee, H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>New Concepts in Ischemia Prevention</atitle><jtitle>Journal of cardiovascular pharmacology</jtitle><date>1991</date><risdate>1991</risdate><volume>18 Suppl 9</volume><spage>S7</spage><epage>S14</epage><pages>S7-S14</pages><issn>0160-2446</issn><eissn>1533-4023</eissn><abstract>Transient myocardial ischemia may result from obstruction to flow in the large epicardial coronary arteries or diminshed flow reserve due to small vessel disease or left ventricular hypertrophy. In patients with coronary heart disease, calcium blockers have proven to reduce stress induced ischemia in patients with normal left ventricular function and in those with ischemic cardiomyopathy. However, recent studies indicate a need for caution when giving calcium antagonists to patients with postinfarction left ventricular systolic dysfunction. Moreover, calcium antagonists that reduce heart rate (diltiazem) are able as a monotherapy to reduce total ischemic burden. Calcium antagonists that may increase rate (dihydropiridines) have to be combined with β-blockers to achieve this goal. For 24-h control of ischemia the ischemic threshold should be determined for a differentiated therapy in the individual patient. Is the ischemic threshold of the majority of episodes lower than the exercise threshold, a calcium blocker should work. Angiotensin-converting enzyme (ACE) inhibitors are not effective in stress-induced ischemia, but may reduce total ischemic burden, although this effect is not significant. In patients with left ventricular hypertrophy and/or small vessel disease, calcium blockers and ACE inhibitors are probably effective in regression of left ventricular hypertrophy and vascular hypertrophy. However, it remains to be shown that ischemia is reduced by these drugs.</abstract><pub>Lippincott-Raven Publishers</pub></addata></record> |
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title | New Concepts in Ischemia Prevention |
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