Effect of amlodipine on platelet inhibition by clopidogrel in patients with ischaemic heart disease: a randomised, controlled trial

Li, Andrew; Ng, Fook‐Hong; Chan, Francis K.L.; Tunggal, Prabowo; Chan, Kit; Lau, Yuk-Kong

doi:10.1136/heartjnl-2012-302801

Cited by 19 publications

(12 citation statements)

References 41 publications

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“…The result of this study is consistent with previous studies 8,9. Nevertheless, one previous study has suggested that concomitant amlodipine use has no negative impact on clopidogrel mediated platelet inhibition 11. The previous study was designed to compare PRU between amlodipine and placebo treated groups, and PRU was measured at baseline and 4 weeks.…”

Section: Discussionsupporting

confidence: 89%

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Antiplatelet Effect of Clopidogrel Can Be Reduced by Calcium-Channel Blockers

et al. 2014

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PurposeClopidogrel is metabolized by the hepatic cytochrome P450 (CYP) system into its active thiol metabolite. CYP3A4 is involved in the metabolism of both clopidogrel and dihydropyridine calcium channel blockers (CCBs). A few reports have suggested an inhibitory interaction between CCBs and clopidogrel. Accordingly, the aim of this study was to determine the effect of CCBs on the antiplatelet activity of clopidogrel by serial P2Y12 reaction unit (PRU) measurements.Materials and MethodsWe assessed changes in antiplatelet activity in patients receiving both clopidogrel and CCBs for at least 2 months prior to enrollment in the study. The antiplatelet activity of clopidogrel was measured by VerifyNow P2Y12 assay in the same patient while medicated with CCBs and at 8 weeks after discontinuation of CCBs. After discontinuation of the CCBs, angiotensin receptor blockers were newly administered to the patients or dosed up for control of blood pressure.ResultsThirty patients finished this study. PRU significantly decreased after discontinuation of CCBs (238.1±74.1 vs. 215.0±69.3; p=0.001). Of the 11 patients with high post-treatment platelet reactivity to clopidogrel (PRU≥275), PRU decreased in nine patients, decreasing below the cut-off value in seven of these nine patients after 8 weeks. Decrease in PRU was not related to CYP2C19 genotype.ConclusionCCBs inhibit the antiplatelet activity of clopidogrel.

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Section: Discussionsupporting

confidence: 89%

“…A few ex vivo studies have suggested an inhibitory interaction between CCBs and clopidogrel 8,9,10. In contrast, one study showed that concomitant amlodipine did not impact clopidogrel-mediated platelet inhibition 11. However, these previous studies were retrospective studies and simply compared patients under CCB medication or not.…”

Section: Introductionmentioning

confidence: 99%

Antiplatelet Effect of Clopidogrel Can Be Reduced by Calcium-Channel Blockers

et al. 2014

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“…Certainly, there is evidence of inter-action, and in one study of 1258 patients receiving clopidogrel, amlodipine administration was associated with higher on-treatment platelet reactivity only in those patients with a loss-of-function P450 (CYP) genotype (249±83 vs. 228±84 P2Y12 reaction units), and this was associated with a higher incidence of cardiovascular events (4.6% vs. 0.6%) (27). However, in a more recent randomised trial, platelet function in 98 patients with stable coronary artery disease taking clopidogrel was similar regardless of amlodipine therapy (28). At present, therefore, there is no guideline recommendation about concomitant prescription of these drugs in patients taking clopidogrel.…”

Section: Secondary Prevention Of Stable Coronary Diseasementioning

confidence: 92%

Almanac 2013-stable coronary artery disease

Islam

2014

Anadolu Kardiyol Derg

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ALMANAC series 219Coronary heart disease in decline Epidemiological data from Europe, the USA and elsewhere in the developed world show a steep decline in coronary heart disease (CHD) mortality during the last 40 years (1). Concern about levelling of mortality rates in younger adults (2) has been somewhat alleviated by data from The Netherlands showing that in men aged <55 years, rates of decline have again accelerated, increasing from only 16% in 1993-1999 to 46% in 1999-2007 (3). A similar pattern was observed in young women with rates of decline of 5% and 38% during the same time periods. This is encouraging, particularly in the context of data from Denmark and the UK showing declining mortality and also a sharp fall in standardised incidence rates for acute myocardial infarction indicating that coronary prevention, as well as acute treatments, has contributed to recent mortality trends (4, 5). Meanwhile an Australian study reminds us that myocardial infarction is but one of several manifestations of cardiovascular disease by reporting that decreasing incidence and recurrence rates for hospitalised CHD from 2000 to 2007 have also been seen for cerebrovascular and peripheral arterial disease (6).However, the epidemiological news is not all good, and data from the UK show that the pernicious relationship between socioeconomic status (SES) and CHD has shown no tendency to go away in recent years, the gradients between top and bottom SES quintile groups for hospital admissions remaining essentially unchanged across the age range (7). Whether this has contributed to the almost 3-fold risk of myocardial infarction associated with stillbirth and 9-fold risk associated with recurrent miscarriage in a recent German study is unclear because the investigators made no adjustment for SES (8). Nor is it clear if SES has contributed to the persistent ethnic differences in both US and UK studies of CHD mortality although other factors appear also to be important. Thus, African-American men have greater exposure to CHD risk factors than Caucasians and, when adjustment is made for this, their susceptibility to CHD is no greater, although mortality rates are twice as high (9). For African-American women, incidence and mortality rates are higher than their Caucasian counter-parts. These findings suggesting that exposure to risk factors contributes to ethnic differences in the incidence of CHD are to some extent reflected in a recent report from the Health Survey for England in which 13 293 Caucasian and 2120 S Asians consented to mortality followup (10). Physical inactivity increased susceptibility to disease and not by increased case-fatality rates (11). Diagnosis of stable coronary artery diseaseThe recent AHA/ACC guideline update (12) emphasised the importance of individualising the diagnostic workup based on the estimated probability of coronary artery disease. In this respect, it mirrored an earlier National Institute of Clinical Excellence (NICE) guideline on chest pain diagnosis (13), but there were important differences ...

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“…Certainly, there is evidence of interaction, and in one study of 1258 patients receiving clopidogrel, amlodipine administration was associated with higher on-treatment platelet reactivity only in those patients with a loss-of-function P450 (CYP) genotype (249±83 vs 228±84 P2Y12 reaction units), and this was associated with a higher incidence of cardiovascular events (4.6% vs 0.6%) 27. However, in a more recent randomised trial, platelet function in 98 patients with stable coronary artery disease taking clopidogrel was similar regardless of amlodipine therapy 28. At present, therefore, there is no guideline recommendation about concomitant prescription of these drugs in patients taking clopidogrel.…”

Section: Secondary Prevention Of Stable Coronary Diseasementioning

confidence: 95%

Almanac 2013: stable coronary artery disease

Islam

2013

Heart

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Effect of amlodipine on platelet inhibition by clopidogrel in patients with ischaemic heart disease: a randomised, controlled trial

Cited by 19 publications

References 41 publications

Antiplatelet Effect of Clopidogrel Can Be Reduced by Calcium-Channel Blockers

Antiplatelet Effect of Clopidogrel Can Be Reduced by Calcium-Channel Blockers

Almanac 2013-stable coronary artery disease

Almanac 2013: stable coronary artery disease

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