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"Potential Effect of Acute and Chronic Caffeine Administration on Platelet Reactivity in Patient With Coronary Artery Disease on Dual Antiplatelet Therapy" (CyCLOPS)

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ClinicalTrials.gov Identifier: NCT02054988
Recruitment Status : Unknown
Verified June 2015 by Polacco Marina, University of Roma La Sapienza.
Recruitment status was:  Recruiting
First Posted : February 4, 2014
Last Update Posted : June 9, 2015
Sponsor:
Information provided by (Responsible Party):
Polacco Marina, University of Roma La Sapienza

Brief Summary:

Prasugrel is a potent thienopyridine antiplatelet agent that selectively and irreversibly inhibits ADP-induced platelet aggregation mediated by the P2Y12 receptor. Prasugrel is a prodrug that must first undergo biotransformation to its active metabolite via cytochrome P450-mediated hepatic metabolism (CYP1A2). Clopidogrel is currently administered to several million patients especially after coronary stenting. Clopidogrel has been shown to reduce cardiovascular complications in patients with acute coronary syndromes and patients who have undergone coronary stenting. The mechanism of action of clopidogrel's active metabolite involves inhibition of the purinergic adenosine diphosphate (ADP) receptor P2Y12 on the platelet membrane. Blockade of this receptor prevents uncoupling of the associated Gi2 protein which ultimately leads to increased platelet cyclic AMP (cAMP) formation.3 Cyclic AMP is a key signaling molecule in inhibiting platelet aggregation, but its intracellular levels are affected by several other commonly used compounds. For instance, methylxanthines, such as caffeine, theophylline, and theobromine (an ingredient of chocolate), all cause elevation of intracellular cAMP levels by inhibiting adenosine receptors (types A1 and A2) on the platelet membrane. The effect of caffeine consumption on platelet reactivity depends on the caffeine dose and duration of administration. Chronic caffeine consumption (≥7 days) appears to be associated with inhibition of platelet aggregation, probably through upregulation of adenosine receptors.The aim of this study was to examine the effect of acute caffeine consumption, at a dose equivalent to commercial coffee drinks, on the antiplatelet effect of clopidogrel and prasugrel, in patients with coronary artery disease (CAD).

Platelet function will be evaluated using a validated method: the VerifyNow System (Accumetrics Inc., San Diego, CA), which is a point-of-care turbidimetry-based optical detection system that measures platelet-induced aggregation.


Condition or disease Intervention/treatment Phase
CORONARY ARTERY DISEASE Other: caffeine Other: not caffeine Not Applicable

Detailed Description:

Prasugrel is a potent thienopyridine antiplatelet agent that selectively and irreversibly inhibits ADP-induced platelet aggregation mediated by the P2Y12 receptor. Prasugrel is a prodrug that must first undergo biotransformation to its active metabolite via cytochrome P450-mediated hepatic metabolism (CYP1A2). Clopidogrel is currently administered to several million patients especially after coronary stenting. Clopidogrel has been shown to reduce cardiovascular complications in patients with acute coronary syndromes and patients who have undergone coronary stenting. The mechanism of action of clopidogrel's active metabolite involves inhibition of the purinergic adenosine diphosphate (ADP) receptor P2Y12 on the platelet membrane. Blockade of this receptor prevents uncoupling of the associated Gi2 protein which ultimately leads to increased platelet cyclic AMP (cAMP) formation.3 Cyclic AMP is a key signaling molecule in inhibiting platelet aggregation, but its intracellular levels are affected by several other commonly used compounds. For instance, methylxanthines, such as caffeine, theophylline, and theobromine (an ingredient of chocolate), all cause elevation of intracellular cAMP levels by inhibiting adenosine receptors (types A1 and A2) on the platelet membrane. The effect of caffeine consumption on platelet reactivity depends on the caffeine dose and duration of administration. Chronic caffeine consumption (≥7 days) appears to be associated with inhibition of platelet aggregation, probably through upregulation of adenosine receptors. The effect of acute caffeine administration on platelet function is less clear. Different studies have shown either an increase, decrease, or no change in platelet reactivity after acute caffeine administration. The aim of this study was to examine the effect of acute caffeine consumption, at a dose equivalent to commercial coffee drinks, on the antiplatelet effect of clopidogrel and prasugrel, in patients with coronary artery disease (CAD).

Platelet function will be evaluated using a validated method: the VerifyNow System (Accumetrics Inc., San Diego, CA), which is a point-of-care turbidimetry-based optical detection system that measures platelet-induced aggregation. Platelet function will be measured with the VerifyNow P2Y12 test at baseline, (after 5 day wash-out period to avoid any carryover effect ) and after 10 days of taking caffeine.

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Study Type : Interventional  (Clinical Trial)
Estimated Enrollment : 240 participants
Allocation: Randomized
Intervention Model: Crossover Assignment
Masking: Quadruple (Participant, Care Provider, Investigator, Outcomes Assessor)
Official Title: "Potential Effect of Acute and Chronic Caffeine Administration on Platelet Reactivity in Patient With Coronary Artery Disease on Dual Antiplatelet Therapy"
Study Start Date : January 2014
Estimated Primary Completion Date : June 2015
Estimated Study Completion Date : June 2015

Resource links provided by the National Library of Medicine


Arm Intervention/treatment
Experimental: caffeine
three cups of coffee will be administered for 10 days (on chronic phase) and two cups of coffee will be consecutively administered for "acute" evaluation.
Other: caffeine

After 5 day coffee wash-out period, patients were randomly assigned to caffeine for 10 days. At baseline: 2 cups of coffee consecutively after 5 hour by clopidogrel or prasugrel intake. Afterwards, 3 cups of coffee daily for 10 days.

Platelet reactivity (expressed as P2Y(12) reaction units (PRU) by the point-of-care VerifyNow assay [Accumetrics, San Diego, California]) was measured at baseline and after 10-days of coffee intake.


Active Comparator: not caffeine
not caffeine will be administered for the duration of the study
Other: not caffeine
evaluate the platelet reactivity after 10 days of no caffeine intake




Primary Outcome Measures :
  1. Assessment of platelet reaction units [ Time Frame: After 10 days of caffeine intake ]
    Absolute changes in platelet reactivity (expressed as P2Y(12) reaction units by the point-of-care VerifyNow assay [Accumetrics, San Diego, California]



Information from the National Library of Medicine

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Ages Eligible for Study:   18 Years to 80 Years   (Adult, Older Adult)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   Yes
Criteria

Inclusion Criteria:

  1. All consecutive patients undergone PTCA
  2. Patients on dual antiplatelet therapy with ASA and clopidogrel or prasugrel or ticagrelor.

Exclusion Criteria:

  1. People unable to understand and willing to sign the informed consent form;
  2. Smokers

Information from the National Library of Medicine

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT02054988


Contacts
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Contact: Marina Polacco MD 3204093510 polamari@libero.it

Locations
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Italy
Sapienza University of Rome Recruiting
Rome, Lazio, Italy, 00166
Contact: marina polacco MD         
Sponsors and Collaborators
University of Roma La Sapienza
Investigators
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Principal Investigator: Marina MD Polacco Sapienza University of Rome

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Responsible Party: Polacco Marina, MD, University of Roma La Sapienza
ClinicalTrials.gov Identifier: NCT02054988    
Other Study ID Numbers: PM3110
First Posted: February 4, 2014    Key Record Dates
Last Update Posted: June 9, 2015
Last Verified: June 2015
Additional relevant MeSH terms:
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Coronary Artery Disease
Myocardial Ischemia
Coronary Disease
Heart Diseases
Cardiovascular Diseases
Arteriosclerosis
Arterial Occlusive Diseases
Vascular Diseases
Caffeine
Central Nervous System Stimulants
Physiological Effects of Drugs
Phosphodiesterase Inhibitors
Enzyme Inhibitors
Molecular Mechanisms of Pharmacological Action
Purinergic P1 Receptor Antagonists
Purinergic Antagonists
Purinergic Agents
Neurotransmitter Agents