Dihydropyridine calcium antagonists increase fibrinolytic activity: a systematic review
Calcium antagonists have been shown to be superior over other antihypertensive drugs to prevent stroke. Because this cannot be fully attributed to blood pressure lowering effects, other mechanisms seem to play a role. Previously we found in patients with subarachnoid hemorrhage that nimodipine enhan...
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| Veröffentlicht in: | Journal of Cerebral Blood Flow & Metabolism 2007-07, Vol.27 (7), p.1293-1308 |
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| container_title | Journal of Cerebral Blood Flow & Metabolism |
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| creator | Di Vergouwen, Mervyn Vermeulen, Marinus de Haan, Rob J Levi, Marcel Roos, Yvo BWEM |
| description | Calcium antagonists have been shown to be superior over other antihypertensive drugs to prevent stroke. Because this cannot be fully attributed to blood pressure lowering effects, other mechanisms seem to play a role. Previously we found in patients with subarachnoid hemorrhage that nimodipine enhances fibrinolytic activity. The purpose of this systematic review was to investigate the fibrinolytic effect of calcium antagonists in general, especially in patients with hypertension. We systematically studied the entire PUBMED and EMBASE database with the search terms ‘calcium antagonist’ combined with ‘fibrinolysis’, ‘(euglobulin) clot lysis time’ (ECLT), ‘tissue plasminogen activator’ (tPA), or ‘plasminogen activator inhibitor’ (PAI). Twenty-six prospective studies were identified and 22 manuscripts were included (802 investigated individuals). The results show that calcium antagonists significantly increase fibrinolysis as shown by a reduction of the ECLT standardized mean differences (SMD) −0.58 (95% confidence interval (CI) −1.05 to −0.11)) and an increase of tPA activity (SMD 0.73 (95% CI 0.25 to 1.21)). This increase of fibrinolysis is apparently caused by an increase of the tPA antigen level (SMD 0.16 (95% CI −0.05 to 0.37)) and a decrease of the plasminogen activator inhibitor-1 antigen antigen (SMD −0.36 (95% CI −0.74 to 0.02)). A sensitivity analysis showed that dihydropyridines, but not phenylalkylamines, exert a fibrinolytic effect. This fibrinolytic effect is not only seen in patients with subarachnoid hemorrhage but also in hypertensive patients. In conclusions, calcium antagonists increase fibrinolytic activity. This may add to the beneficial pharmacological effect of calcium antagonists to prevent ischemic events in patients with hypertension and subarachnoid hemorrhage. |
| doi_str_mv | 10.1038/sj.jcbfm.9600431 |
| format | Article |
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Because this cannot be fully attributed to blood pressure lowering effects, other mechanisms seem to play a role. Previously we found in patients with subarachnoid hemorrhage that nimodipine enhances fibrinolytic activity. The purpose of this systematic review was to investigate the fibrinolytic effect of calcium antagonists in general, especially in patients with hypertension. We systematically studied the entire PUBMED and EMBASE database with the search terms ‘calcium antagonist’ combined with ‘fibrinolysis’, ‘(euglobulin) clot lysis time’ (ECLT), ‘tissue plasminogen activator’ (tPA), or ‘plasminogen activator inhibitor’ (PAI). Twenty-six prospective studies were identified and 22 manuscripts were included (802 investigated individuals). The results show that calcium antagonists significantly increase fibrinolysis as shown by a reduction of the ECLT standardized mean differences (SMD) −0.58 (95% confidence interval (CI) −1.05 to −0.11)) and an increase of tPA activity (SMD 0.73 (95% CI 0.25 to 1.21)). This increase of fibrinolysis is apparently caused by an increase of the tPA antigen level (SMD 0.16 (95% CI −0.05 to 0.37)) and a decrease of the plasminogen activator inhibitor-1 antigen antigen (SMD −0.36 (95% CI −0.74 to 0.02)). A sensitivity analysis showed that dihydropyridines, but not phenylalkylamines, exert a fibrinolytic effect. This fibrinolytic effect is not only seen in patients with subarachnoid hemorrhage but also in hypertensive patients. In conclusions, calcium antagonists increase fibrinolytic activity. This may add to the beneficial pharmacological effect of calcium antagonists to prevent ischemic events in patients with hypertension and subarachnoid hemorrhage.</description><identifier>ISSN: 0271-678X</identifier><identifier>EISSN: 1559-7016</identifier><identifier>DOI: 10.1038/sj.jcbfm.9600431</identifier><identifier>PMID: 17191079</identifier><identifier>CODEN: JCBMDN</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Biological and medical sciences ; Biotechnology ; Calcium Channel Blockers - pharmacology ; Dihydropyridines - pharmacology ; Fibrinolysis - drug effects ; Fundamental and applied biological sciences. Psychology ; Gene therapy ; Health. Pharmaceutical industry ; Humans ; Hypertension - complications ; Hypertension - drug therapy ; Industrial applications and implications. Economical aspects ; Ischemia - etiology ; Ischemia - prevention & control ; Medical sciences ; Neurology ; Neuropharmacology ; Neuroprotective agent ; Pharmacology. Drug treatments ; Subarachnoid Hemorrhage - complications ; Subarachnoid Hemorrhage - drug therapy ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Journal of Cerebral Blood Flow & Metabolism, 2007-07, Vol.27 (7), p.1293-1308</ispartof><rights>2007 ISCBFM</rights><rights>2008 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jul 2007</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c488t-94f3ef70f2a60227ca6d9091d9c243a2ea5ac3b2e8b4fd36b3a58a26ec67e9d73</citedby><cites>FETCH-LOGICAL-c488t-94f3ef70f2a60227ca6d9091d9c243a2ea5ac3b2e8b4fd36b3a58a26ec67e9d73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1038/sj.jcbfm.9600431$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1038/sj.jcbfm.9600431$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,315,782,786,794,21828,27931,27933,27934,43630,43631</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19893774$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17191079$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Di Vergouwen, Mervyn</creatorcontrib><creatorcontrib>Vermeulen, Marinus</creatorcontrib><creatorcontrib>de Haan, Rob J</creatorcontrib><creatorcontrib>Levi, Marcel</creatorcontrib><creatorcontrib>Roos, Yvo BWEM</creatorcontrib><title>Dihydropyridine calcium antagonists increase fibrinolytic activity: a systematic review</title><title>Journal of Cerebral Blood Flow & Metabolism</title><addtitle>J Cereb Blood Flow Metab</addtitle><description>Calcium antagonists have been shown to be superior over other antihypertensive drugs to prevent stroke. Because this cannot be fully attributed to blood pressure lowering effects, other mechanisms seem to play a role. Previously we found in patients with subarachnoid hemorrhage that nimodipine enhances fibrinolytic activity. The purpose of this systematic review was to investigate the fibrinolytic effect of calcium antagonists in general, especially in patients with hypertension. We systematically studied the entire PUBMED and EMBASE database with the search terms ‘calcium antagonist’ combined with ‘fibrinolysis’, ‘(euglobulin) clot lysis time’ (ECLT), ‘tissue plasminogen activator’ (tPA), or ‘plasminogen activator inhibitor’ (PAI). Twenty-six prospective studies were identified and 22 manuscripts were included (802 investigated individuals). The results show that calcium antagonists significantly increase fibrinolysis as shown by a reduction of the ECLT standardized mean differences (SMD) −0.58 (95% confidence interval (CI) −1.05 to −0.11)) and an increase of tPA activity (SMD 0.73 (95% CI 0.25 to 1.21)). This increase of fibrinolysis is apparently caused by an increase of the tPA antigen level (SMD 0.16 (95% CI −0.05 to 0.37)) and a decrease of the plasminogen activator inhibitor-1 antigen antigen (SMD −0.36 (95% CI −0.74 to 0.02)). A sensitivity analysis showed that dihydropyridines, but not phenylalkylamines, exert a fibrinolytic effect. This fibrinolytic effect is not only seen in patients with subarachnoid hemorrhage but also in hypertensive patients. In conclusions, calcium antagonists increase fibrinolytic activity. This may add to the beneficial pharmacological effect of calcium antagonists to prevent ischemic events in patients with hypertension and subarachnoid hemorrhage.</description><subject>Biological and medical sciences</subject><subject>Biotechnology</subject><subject>Calcium Channel Blockers - pharmacology</subject><subject>Dihydropyridines - pharmacology</subject><subject>Fibrinolysis - drug effects</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene therapy</subject><subject>Health. Pharmaceutical industry</subject><subject>Humans</subject><subject>Hypertension - complications</subject><subject>Hypertension - drug therapy</subject><subject>Industrial applications and implications. 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Because this cannot be fully attributed to blood pressure lowering effects, other mechanisms seem to play a role. Previously we found in patients with subarachnoid hemorrhage that nimodipine enhances fibrinolytic activity. The purpose of this systematic review was to investigate the fibrinolytic effect of calcium antagonists in general, especially in patients with hypertension. We systematically studied the entire PUBMED and EMBASE database with the search terms ‘calcium antagonist’ combined with ‘fibrinolysis’, ‘(euglobulin) clot lysis time’ (ECLT), ‘tissue plasminogen activator’ (tPA), or ‘plasminogen activator inhibitor’ (PAI). Twenty-six prospective studies were identified and 22 manuscripts were included (802 investigated individuals). The results show that calcium antagonists significantly increase fibrinolysis as shown by a reduction of the ECLT standardized mean differences (SMD) −0.58 (95% confidence interval (CI) −1.05 to −0.11)) and an increase of tPA activity (SMD 0.73 (95% CI 0.25 to 1.21)). This increase of fibrinolysis is apparently caused by an increase of the tPA antigen level (SMD 0.16 (95% CI −0.05 to 0.37)) and a decrease of the plasminogen activator inhibitor-1 antigen antigen (SMD −0.36 (95% CI −0.74 to 0.02)). A sensitivity analysis showed that dihydropyridines, but not phenylalkylamines, exert a fibrinolytic effect. This fibrinolytic effect is not only seen in patients with subarachnoid hemorrhage but also in hypertensive patients. In conclusions, calcium antagonists increase fibrinolytic activity. This may add to the beneficial pharmacological effect of calcium antagonists to prevent ischemic events in patients with hypertension and subarachnoid hemorrhage.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>17191079</pmid><doi>10.1038/sj.jcbfm.9600431</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Biological and medical sciences Biotechnology Calcium Channel Blockers - pharmacology Dihydropyridines - pharmacology Fibrinolysis - drug effects Fundamental and applied biological sciences. Psychology Gene therapy Health. Pharmaceutical industry Humans Hypertension - complications Hypertension - drug therapy Industrial applications and implications. Economical aspects Ischemia - etiology Ischemia - prevention & control Medical sciences Neurology Neuropharmacology Neuroprotective agent Pharmacology. Drug treatments Subarachnoid Hemorrhage - complications Subarachnoid Hemorrhage - drug therapy Vascular diseases and vascular malformations of the nervous system |
| title | Dihydropyridine calcium antagonists increase fibrinolytic activity: a systematic review |
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