Pharmacogenomics of Antiplatelet Response - II (PARes-II) (PARes-II)
This study has been completed.
Information provided by (Responsible Party):
Rehan Qayyum, Johns Hopkins University
First received: July 3, 2013
Last updated: November 10, 2016
Last verified: November 2016
This clinical trial is examining the effect of 4-week aspirin therapy on platelet transcriptome in persons at high-risk for myocardial infarction or stroke due to family history of early-onset coronary artery disease.
||Intervention Model: Single Group Assignment
Masking: None (Open Label)
Primary Purpose: Basic Science
||Pharmacogenomics of Antiplatelet Response - II
Primary Outcome Measures:
- Changes in Platelet Transcriptome [ Time Frame: 4 weeks ]
Comparison of platelet transcriptome before aspirin therapy with platelet transcriptome after aspirin therapy.
The expression levels of genes before aspirin therapy was compared with the expression level of the genes after aspirin therapy. The expression levels were measured using the FPKM unit (Fragments Per Kilobase of transcript per Million mapped reads). The gene with the highest difference (pre vs. post) in FPKM is being reported with name in the units area and the actual difference in the number area
| Study Start Date:
| Study Completion Date:
| Primary Completion Date:
||August 2014 (Final data collection date for primary outcome measure)
Participants treated with aspirin - there is no control group. Participant's baseline will act as their control.
81 mg daily for 4 weeks
Platelet aggregation can initiate thrombosis on ulcerated arterial plaques resulting in acute coronary syndrome (ACS). There is large variation in platelet aggregation between individuals. As the genetic message to the cell machinery is conveyed through its transcriptome, we hypothesize that much of the variability in platelet function can be explained by transcriptome changes including differences in gene or isoform expression, altered splicing events, or allele-specific expression. Moreover, aspirin modifies gene expression in several cells, but whether it also affects platelet transcriptome has not yet been studied. Our goal is to characterize the platelet transcriptome and identify genes that are up- or down-regulated after 4-week aspirin therapy. A major strength of our study is that it enrolls individuals from European Americans and African Americans and thus will have the ability to study similarities and differences between the two. The study will produce innovative comparative genomic/platelet phenotype data and will provide a potential pharmacogenomic and diagnostic template for the future discovery of novel antiplatelet regimens to prevent thrombosis-related cardiovascular disease events.
|Ages Eligible for Study:
||45 Years to 75 Years (Adult, Senior)
|Sexes Eligible for Study:
|Accepts Healthy Volunteers:
- Participants from the GeneSTAR cohort
- Unaffected with no overt coronary artery disease or serious vascular event (stroke or peripheral vascular disease diagnosis
- Women who are postmenopausal.
- Women who use a reliable contraceptive method; a reliable contraceptive method will be defined as personal history of tubal ligation, ongoing use of intra-uterine device, or ongoing use of oral contraceptive pills.
- Presence of any CAD or stroke, transient ischemic attacks, peripheral arterial disease
- Persons taking aspirin, NSAIDS, or any anti-coagulants who are medically unable to stop them for a two week pre-trial
- A history of allergy to aspirin or clopidogrel
- Weight < 60kg
- Age < 45 and > 75 years of age
- A history of recent or any active bleeding
- Serious or current co-morbidity (AIDS, cancer)
- Pregnant women as determined by urine dipstick pregnancy test
- Any aneurysms on cranial magnetic resonance imaging/magnetic resonance angiography (obtained recently in the GeneSTAR participants)
- Blood pressure above >=159/95mmHg
- History of a gastric or duodenal ulcer, or significant gastrointestinal disease, like regional enteritis
- Mental incompetence to make a decision to participate (developmentally disabled, and persons with diagnosed psychiatric disorders—documented in primary care records).
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Please refer to this study by its ClinicalTrials.gov identifier: NCT01894555
|Johns Hopkins University School of Medicine
|Baltimore, Maryland, United States, 21287 |
Johns Hopkins University
||Rehan Qayyum, MD
||Johns Hopkins School of Medicine
||Rehan Qayyum, Assistant Professor of Medicine, Johns Hopkins University
History of Changes
|Other Study ID Numbers:
K23HL105897 ( U.S. NIH Grant/Contract )
|Study First Received:
||July 3, 2013
|Results First Received:
||August 1, 2016
||November 10, 2016
Keywords provided by Rehan Qayyum, Johns Hopkins University:
Coronary Artery Disease
Arterial Occlusive Diseases
Additional relevant MeSH terms:
ClinicalTrials.gov processed this record on August 17, 2017
Anti-Inflammatory Agents, Non-Steroidal
Sensory System Agents
Peripheral Nervous System Agents
Physiological Effects of Drugs
Fibrin Modulating Agents
Molecular Mechanisms of Pharmacological Action
Platelet Aggregation Inhibitors