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Antiplatelet response to the 150-mg maintenance dose of clopidogrel in patients with insufficient platelet inhibition after clopidogrel loading for elective coronary stent placement.
Trenk, D, Hochholzer, W, Müller, B, Stratz, C, Valina, CM, Schmiebusch, P, Büttner, HJ, Neumann, FJ
EuroIntervention : journal of EuroPCR in collaboration with the Working Group on Interventional Cardiology of the European Society of Cardiology. 2008;(2):214-21
Abstract
AIMS: Our prospective study sought to investigate whether inadequate platelet responses to clopidogrel can be corrected by increasing the daily maintenance dose from 75 mg to 150 mg. METHODS AND RESULTS In 117 patients with elective PCI after loading with 600 mg clopidogrel, we determined residual platelet aggregation in response to 5 micromol/l ADP (RPA) by optical aggregometry after the first 75 mg maintenance dose (baseline), and at days 14 and 28. In patients with RPA >14% at baseline, we increased the daily dose to 150 mg. Fifty-seven additional patients without dose adjustment served as historic control. In 39 patients with baseline RPA >14%, the increase in maintenance dose to 150 mg reduced median RPA significantly (P<0.001) from 24% [interquartile range: 18-32%] at baseline to 14% [8-20%1 at 14 days without any further significant change. In patients with RPA < or = 14%, who continued on 75 mg clopidogrel, RPA increased during the first 14 days by 4.5% (0-14%; P<0.001). At 14 days, the study group with selective dose adjustment had a significantly lower RPA than the control group without dose adjustment (10.0% [4-20%1 versus 17.0% [9-32%], P<0.001). CONCLUSIONS In patients with a low initial response to clopidogrel, platelet inhibition can be improved by increasing the maintenance dose to 150 mg.
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Simvastatin inhibits lymphocyte function in normal subjects and patients with cardiovascular disease.
Hillyard, DZ, Cameron, AJ, McDonald, KJ, Thomson, J, MacIntyre, A, Shiels, PG, Panarelli, M, Jardine, AG
Atherosclerosis. 2004;(2):305-13
Abstract
HMG-CoA reductase inhibitors (statins) block the mevalonate pathway, preventing biosynthesis of cholesterol and isoprenoids. We investigated the effect of simvastatin on lymphocytes from normal human subjects and cardiovascular disease patients in order to provide a model for the in vivo actions of statins. Thirteen healthy volunteers were treated with 40 mg per day of simvastatin following which mean total cholesterol was reduced by 23% (S.D.+/- 11.7%) and mean LDL-cholesterol by 36% (S.D.+/- 16.3%). Lymphocyte lipid raft levels, represented by Lyn and Fyn, were also reduced by simvastatin. Treatment with simvastatin did not alter ex vivo T-lymphocyte proliferation. However, the in vitro addition of 1 microM simvastatin reduced T-lymphocyte proliferation by 39% (S.D.+/- 18.1%) and a combination of prenyl transferase inhibitors reduced proliferation by 19% (S.D.+/- 22.7%). We also assessed the cytotoxicity of natural killer (NK) cells-a T-lymphocyte subset. NK cell cytotoxicity ex vivo was reduced by 30% (S.D.+/- 33.6%) following oral simvastatin treatment and by 56% (S.D.+/- 24.68%) after the in vitro addition of 1 microM simvastatin. Significant ex vivo reductions in T-cell proliferation and NK cell cytotoxicity were observed in patients with cardiovascular disease on treatment with statins. NK cells have been implicated in the pathogenesis of atherosclerosis, so the effect of statin therapy on NK cell cytotoxicity may contribute to the benefits of statins in cardiovascular disease.
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3.
Scatter and cross-talk correction for one-day acquisition of 123I-BMIPP and 99mtc-tetrofosmin myocardial SPECT.
Kaneta, T, Kurihara, H, Hakamatsuka, T, Ito, H, Maruoka, S, Fukuda, H, Takahashi, S, Yamada, S
Annals of nuclear medicine. 2004;(8):647-52
Abstract
OBJECTIVE 123I-15-(p-iodophenyl)-3-(R,S)-methylpentadecanoic acid (BMIPP) and 99mTc-tetrofosmin (TET) are widely used for evaluation of myocardial fatty acid metabolism and perfusion, respectively. ECG-gated TET SPECT is also used for evaluation of myocardial wall motion. These tests are often performed on the same day to minimize both the time required and inconvenience to patients and medical staff. However, as 123I and 99mTc have similar emission energies (159 keV and 140 keV, respectively), it is necessary to consider not only scattered photons, but also primary photons of each radionuclide detected in the wrong window (cross-talk). In this study, we developed and evaluated the effectiveness of a new scatter and cross-talk correction imaging protocol. METHODS Fourteen patients with ischemic heart disease or heart failure (8 men and 6 women with a mean age of 69.4 yr, ranging from 45 to 94 yr) were enrolled in this study. In the routine one-day acquisition protocol, BMIPP SPECT was performed in the morning, with TET SPECT performed 4 h later. An additional SPECT was performed just before injection of TET with the energy window for 99mTc. These data correspond to the scatter and cross-talk factor of the next TET SPECT. The correction was performed by subtraction of the scatter and cross-talk factor from TET SPECT. Data are presented as means +/- S.E. Statistical analyses were performed using Wilcoxon's matched-pairs signed-ranks test, and p < 0.05 was considered significant. RESULTS The percentage of scatter and cross-talk relative to the corrected total count was 26.0 +/- 5.3%. EDV and ESV after correction were significantly greater than those before correction (p = 0.019 and 0.016, respectively). After correction, EF was smaller than that before correction, but the difference was not significant. Perfusion scores (17 segments per heart) were significantly lower after as compared with those before correction (p < 0.001). CONCLUSIONS Scatter and cross-talk correction revealed significant differences in EDV, ESV, and perfusion scores. These observations indicate that scatter and cross-talk correction is required for one-day acquisition of 123I-BMIPP and 99mTc-tetrofosmin SPECT.
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Prolonged postischemic regional left ventricular delayed relaxation or diastolic asynchrony detected by color kinesis following coronary vasospasm.
Ishii, K, Miwa, K, Makita, T, Okuda, N
The American journal of cardiology. 2003;(11):1366-9
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Nicorandil enhances myocardial tolerance to ischemia without progressive collateral recruitment during coronary angioplasty.
Sakai, K, Yamagata, T, Teragawa, H, Matsuura, H, Chayama, K
Circulation journal : official journal of the Japanese Circulation Society. 2002;(4):317-22
Abstract
Nicorandil, a hybrid nitrate and ATP-sensitive potassium channel opener, has had a preconditioning effect in some coronary angioplasty studies. The present study investigated whether the cardioprotective effects of nicorandil involve coronary collateral function. Thirty-two patients with stable angina pectoris were randomized to receive a 1-min intravenous infusion of nicorandil (100 microg/kg) or normal saline. Five minutes later they underwent three 2-min balloon inflations 5-min apart. The maximum ST-segment elevation (deltaSTmax), the sum of ST-segment elevations in all leads (sigmaST), and the chest pain score were determined at the end of each balloon inflation. The collateral flow index (CFI) was derived from simultaneous measurement of the mean aortic pressure and the coronary wedge pressure obtained from a pressure guidewire during balloon inflation. The deltaSTmax, sigmaST, and chest pain score decreased progressively during the 3 sequential balloon inflations in both groups, and the deltaSTmax and sigmaST were less in the nicorandil group than in the control group during each inflation. The CFI did not change during the 3 inflations in either group and was similar in the 2 groups during each inflation. In conclusion, pretreatment with intravenous nicorandil enhances myocardial tolerance to ischemia without progressive collateral recruitment during coronary angioplasty.
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6.
[Study on homocysteine metabolism related enzymes gene mutations in Chinese patients with ischemic cardiovascular and cerebrovascular diseases].
Dai, C, Zhang, G
Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi. 2001;(9):484-7
Abstract
OBJECTIVE To explore the significance of gene mutations of cystathionine beta-synthase (CBS844ins68), methionine synthase (MS A2756G) and methylenetetrahydrofolate reductase (MTHFR C677T) in ischemic cardiovascular and cerebrovascular diseases. METHODS The genotypes of CBS 844ins68, MS A2756G and MTHFR C677T were determined by PCR-based assay in 102 patients with brain infarction, 73 with myocardial infarction and 100 healthy controls. RESULTS The prevalences of CBS 844ins68 and MS A2756G in the cohort studied were somewhat lower than that in western Caucasian populations. There were no significant differences in the frequencies of CBS 844ins 68, MS A2756G and MTHFR C677T mutations between the patient the and control groups. However, the heterozygous form of CBS 844ins 68 tended to be more prevalent in the controls than in the patients. CONCLUSION Gene mutations as CBS 844ins 68, MS A2756G and MTHFR C677T may not be independent risk factors for ischemic cardiovascular and cerebrovascular disease in Southern Chinese Han population. The prevalences of CBS 844ins 68 and MS A2756G may vary with different ethnic groups or geographic regions.
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[Intensification in vivo of free radical oxidation of low density lipoproteins in plasma from patients with myocardial ischemia treated by HMG-CoA-reductase pravastatin and suppression of lipid peroxidation by ubiquinone Q10].
Lankin, VZ, Tikhaze, AK, Kaminnaia, VI, Kaminnyĭ, AI, Konovalova, GG, Kukharchuk, VV
Biulleten' eksperimental'noi biologii i meditsiny. 2000;(2):176-9