| Cardioprotective effect of an L/N-type calcium channel blocker in patients with hypertensive heart disease. | |
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MedLine Citation:
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PMID: 19782264 Owner: NLM Status: In-Process |
Abstract/OtherAbstract:
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BACKGROUND: Left ventricular (LV) diastolic dysfunction is related to increased cardiac sympathetic activity. We investigated the effect of cilnidipine, an L/N-type calcium channel blocker, on LV diastolic function and cardiac sympathetic activity in patients with hypertensive heart disease (HHD) using radionuclide myocardial imaging. METHODS AND RESULTS: Thirty-two frame electrocardiography (ECG) -gated (99m)Tc-sestamibi (MIBI) myocardial single photon emission computed tomography (SPECT), and (123)I-metaiodobenzylguanidine (MIBG) imaging were performed before and 6 months after drug administration in 32 outpatients with HHD. Sixteen of the patients were treated with cilnidipine and the other 16 were treated with nifedipine retard. The parameters for assessing LV diastolic function evaluated using ECG-gated (99m)Tc-MIBI SPECT were peak filling rate (PFR), first-third filling rate (1/3FR), and time to peak filling (TPF). Cardiac sympathetic activity was assessed as early and delayed heart to mediastinum (H/M) ratios and a washout rate (WR), using (123)I-MIBG imaging. The PFR and 1/3FR significantly increased after 6 months of treatment with cilnidipine (p<0.05 for both), but did not with nifedipine retard. The H/M ratios significantly increased (p<0.05 for both) in conjunction with a decreased WR (p<0.05) in the cilnidipine group. Moreover, a significant positive correlation was seen between the rate of change in PFR and the rate of change in early and delayed H/M ratios in the cilnidipine group (p<0.05 for both). The same results were obtained for the relationship between the rate of change in 1/3FR and the rate of change in H/M ratios (p<0.05 for both). However, no such relationship was seen in the nifedipine group. CONCLUSION: These data indicate that cilnidipine seems to suppress cardiac sympathetic overactivity via blockade of N-type calcium channels and improves LV diastolic function in patients with HHD. |
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Authors:
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Toshimitsu Kosaka; Masayasu Nakagawa; Masaru Ishida; Kenji Iino; Hiroyuki Watanabe; Hitoshi Hasegawa; Hiroshi Ito |
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Publication Detail:
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Type: Journal Article Date: 2009-07-05 |
Journal Detail:
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Title: Journal of cardiology Volume: 54 ISSN: 1876-4738 ISO Abbreviation: J Cardiol Publication Date: 2009 Oct |
Date Detail:
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Created Date: 2009-09-28 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8804703 Medline TA: J Cardiol Country: Japan |
Other Details:
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Languages: eng Pagination: 262-72 Citation Subset: IM |
Affiliation:
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Department of Internal Medicine, Division of Cardiovascular and Respiratory Medicine, Akita University School of Medicine, 1-1-1 Hondo, Akita 010-8543, Japan. kosaka@doc.med.akita-u.ac.jp |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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