31 Clinical Trials for Various Conditions
The purpose is to conduct a dietary intervention study in which human participants will consume beverages sweetened with erythritol or aspartame, each for 2 weeks, in a randomized crossover design
The goal is to determine whether fentanyl and morphine have similar effects in reducing aspirin's effect upon platelets in emergency department patients with chest discomfort. Morphine has been shown to worsen outcomes in heart attack patients due to reduction of oral anti-platelet agent effectiveness and so many providers have switches to using fentanyl. However, it is largely unknown whether fentanyl has similar effects.
This study is assessing the impact of timing of PD assessments on measures of platelet reactivity in patients undergoing PCI treated with cangrelor.
Investigating Synergistic Effects of Apixaban with Dual Anti-Platelet Therapy (DAPT) in Lowering Platelet Reactivity and Thrombin Generation
This is a multi-center convenience sample prospective study comparing the results of the Verify Now® Aspirin Test and PRUTest® Platelet Reactivity Tests with the Japan investigational reagents to reagents registered in Japan in the expected population receiving aspirin (ASA) and the P2Y12 inhibitor clopidogrel.
The investigators have previously observed a reduced level of platelet aggregation 2 hours after healthy male individuals were asked to drink extra virgin olive oil (EVOO) that provided a higher level of one specific phenolic known as oleocanthal. This study will help the investigators further determine the effects of oleocanthal-rich EVOO intake on platelet function at 2, 4 and 6 hours after intake with food compared to platelet function in the morning after an overnight fast.
Prospective, single center, double-blind, randomized pharmacodynamic experimental study. The study will enroll 150 subjects with ASCVD on optimal statin therapy as per physician and Diabetes Mellitus (DM) undergoing elective Percutaneous Coronary Intervention (PCI). Eligible patients will be randomized for 30 day treatment to either 1) evolocumab 420 mg ; or 2) placebo.
Clopidogrel is the most widely used P2Y12 receptor inhibitor and is the only agent of this class currently recommended in patients with stable coronary artery disease (CAD) undergoing PCI, and for the treatment of stroke or PAD. Pharmacodynamic (PD) studies have shown that approximately 30-40% of patients experience high on-treatment platelet reactivity (HPR) while receiving clopidogrel treatment. Importantly HPR status has been strongly associated with an increased risk of ischemic events. Multiple approaches have been advocated to reduce HPR rates. In a previous study treatment with high-dose atorvastatin in addition to double-dose clopidogrel reduced platelet reactivity significantly more than double-dose clopidogrel alone in statin-naïve patients with stable CAD and HPR. To date, the exact biological mechanisms involved in the statin modulation of platelet function are not fully understood, although likely attributed to both its lipid-lowering and non-lipid-related effects. Evolocumab is a monoclonal antibody targeting proprotein convertase subtilisin/kexin type 9 (PCSK9). The use of evolocumab plus standard therapy, as compared with standard therapy alone, significantly reduced the incidence of cardiovascular events. Whether the reduction in cardiovascular events is simply due to LDL reduction or might be related to other mechanisms is currently subject of investigation. Although LDL reduction with statin therapies has been associated with reduction in platelet reactivity, to date the effects on platelet aggregation of adjunctive lipid lowering with evolocumab has not been explored. The aim of the present study is to investigate the effects of evolocumab in addition to statin therapy on HPR rates and platelet reactivity in patients with atherosclerotic cardiovascular disease (ASCVD) and HPR while on clopidogrel treatment.
With the widespread use of clopidogrel, resistance to clopidogrel has been attracting increasing attention, and emerged as a new challenge adversely affecting patients clinical risk and outcome. Clopidogrel resistance means that blood platelets show little or no response to clopidogrel. It is closely associated with increased risk of serious cardiovascular events, seriously affects the prognosis of patients, and brings difficulties to clinical treatment. Guideline recommendations on the use of dual antiplatelet therapy have been formulated that ticagrelor 90 mg twice daily plus aspirin in preference to clopidogrel 75mg daily plus aspirin for ACS patients. Recent study found that ticagrelor 90mg twice a day orally could significantly reduce the occurrence of clopidogrel resistance and adverse cardiovascular events. The previous studies have reported that half-dose ticagrelor had the similar inhibitory effect on platelet aggregation as the standard-dose ticagrelor, which was significantly stronger than that in the clopidogrel group. But it is still not very clear that the effect of low-dose ticagrelor on platelet function in patients with clopidogrel resistance and coronary heart disease. Therefore, we performed this randomized, single-blind clinical trial to observe the effects of low-dose ticagrelor and double standard-dose clopidogrel on platelet aggregation and prognosis in clopidogrel resistance's patients with coronary heart disease.
This study investigates the potential protective effects of fatty acid supplementation through inhibition of platelet activation. fatty acids (omega-3 and omega-6) will be evaluated for protection from agonist-mediated platelet activation in platelets from type 2 diabetics and healthy controls. Post-menopausal women with type 2 diabetes mellitus and healthy post-menopausal women will be treated with omega-3 and omega-6 fatty acid supplements to determine protection from platelet activation and thrombosis in this high risk population.
The primary objective is to determine the pharmacodynamic effect of ticagrelor dosing (180mg LD/ 90mg BID) at 2, 4 hours and 14 days in stable Coronary artery disease (CAD) patients who exhibit high-on prasugrel platelet reactivity defined as Vasodilator Stimulated Phosphoprotein-Phosphorylation (VASP-P) \>50%.
This is a prospective, randomized study from pre-surgery to 6 weeks post-surgery designed to detect changes in coagulability following elective total knee and hip arthroplasty. Patients will be randomized to one of the two standard prophylaxis treatments used at Sinai Hospital: 1. Arixtra (2.5 mg SQ/QD) subcutaneous injection daily for 2 weeks followed by aspirin 325 mg for 5 weeks, or 2. Pneumatic compression stockings (MCS, Active Care, medical compression systems Inc., Israel) for 2 weeks with concomitant Aspirin 325 mg daily for 5 weeks.
Plavix (clopidogrel) is a drug that is approved by the FDA (Food and Drug Administration) to reduce the risk of having another heart attack by preventing platelets (blood cells that are important in forming blood clots) from sticking together and forming another clot. Platelet activity can be measured by a machine called VerifyNow. The purpose of this study is to see whether Hispanic women and White non-Hispanic women have the same platelet response to a commonly used drug, Plavix (clopidogrel). Recent studies have shown that platelets may be more active in Hispanics, making it more difficult to prevent clots from forming, even when using Plavix. In addition, studies have shown that women may also have more active platelets than men. There have been no studies of Hispanic women and the effect of Plavix on platelet activity.
Patients who have a heart attack are regularly treated with either clopidogrel or ticagrelor. In a large clinical trial, treatment with ticagrelor before coronary bypass surgery (CABG) was associated with a lower risk of death than treatment with clopidogrel. The reason for this difference cannot be explained on the basis of the study. One possible explanation is that the reversible binding of ticagrelor is advantageous because when new platelets are released, they are inhibited by the drug. Because clopidogrel binds irreversibly it cannot redistribute. The investigators will recruit patients who are scheduled for surgery after an acute coronary syndrome who have been treated with either ticagrelor or clopidogrel. After the patient provides informed consent, the investigators will review their medical record,record information and on the day after surgery the investigators will take one sample of blood. That blood will be analyzed for evidence of platelet activation (platelet microparticles, and platelet-leukocyte aggregates), the reactivity of young platelets, and the concentration of inflammatory cytokines. The investigators hypothesize that the evidence of platelet activation (platelet microparticles and platelet-leukocyte aggregates) and the reactivity of young platelets will be less in patients who have been treated previously with ticagrelor.
The objective is to describe and quantify levels of platelet reactivity in three different cohorts of patients taking thienopyridine: patients who report nuisance bleeding, patients who report alarming bleeding, and patients who report no nuisance or alarming bleeding. The investigators hypothesize that patients with nuisance or alarming bleeding events on maintenance thienopyridine therapy will have lower levels of platelet reactivity than patients without nuisance or alarming bleeding on thienopyridine therapy.
To determine the efficacy of prasugrel versus clopidogrel for the reduction of adverse cardiovascular outcomes in patients with high platelet reactivity on clopidogrel after successful implantation of coronary drug-eluting stents. To determine the adverse event profile of prasugrel in patients with high platelet reactivity on clopidogrel after implantation of coronary drug-eluting stents. To determine the effect of prasugrel on inhibition of platelet activation in patients with high platelet reactivity on clopidogrel.
Single center randomized parallel group study to determine if: 1. there is a temporary increase in platelet reactivity after abrupt discontinuation of clopidogrel due to a potential rebound phenomenon. 2. the effect of sudden discontinuation of clopidogrel 6 months post coronary angioplasty with adjunct drug eluting stent implantation compared to 12 month continuation of clopidogrel on platelet reactivity. And the association with MACE up to 12 months post coronary angioplasty.
The purpose of this study is to compare levels of clot formation (platelet aggregation), markers of heart muscle damage, and inflammation in two groups undergoing percutaneous coronary stent implantation. The first group will be on a regimen of high-dose clopidogrel used in combination with bivalirudin plus eptifibatide, and the second group will be on a regimen of high-dose clopidogrel with bivalirudin alone. Clinical outcomes will be determined up to one year after enrollment.
The proposed study aims to assess the antiplatelet effects of more potent oral P2Y12 inhibition with low-dose ticagrelor (60 mg bid) compared with standard of care clopidogrel in patients with a high ABCD-GENE score (≥10). We hypothesize that ticagrelor is associated with better pharmacodynamic effects (i.e., lower platelet reactivity and high platelet reactivity rates) compared with clopidogrel in stable coronary artery disease patients undergoing percutaneous coronary intervention with a high ABCD-GENE score.
Despite the relative safety of PCI with new generation stents, peri-PCI thrombotic complications, including myocardial infarction and myocardial injury, are common in elective PCI, occurring in up to 30% of patients. Importantly, these events are associated with poor prognosis. The risk of peri-PCI myocardial infarction/myocardial injury has been in part attributed to HPR. The aim of this study is to prospectively validate the accuracy of the ABCD-GENE score in identifying stable CAD patients undergoing elective PCI treated with standard of care clopidogrel who are at risk of peri-PCI myocardial infarction/myocardial injury. This investigation will be a prospective cohort study conducted in a population of patients (n=500) with stable CAD undergoing elective PCI treated with standard of care clopidogrel. By integrating genetic data with clinical variables, patients will be stratified into 2 cohorts based on their ABCD-GENE score (using a cut-off of 10). Assessments to define HPR status and myocardial infarction/myocardial injury will be performed post-PCI.
Treatment of patients who have had a heart attack with drugs that prevent formation of blood clots has been shown to reduce the patient's risk of subsequent cardiovascular events such as heart attack, stroke, and death. Because new drugs have increased treatment options, the development of tests that can guide treatment should improve treatment selection and further reduce the risk of cardiovascular events as well as bleeding. This study is designed to assess the value of new tests. It is a prospective study that will enroll patients who have had a heart attack. Blood will be taken during hospitalization for a heart attack (1 day after their heart attack) and a second time 6 months later during an ambulatory clinical visit. Investigators will perform biochemical tests on the blood that assess the likelihood of making blood clots. One tablespoon of blood will be taken at each time. Taking this amount of blood poses no risk to the participant. Investigators will ask the participant whether they have had bleeding or cardiovascular events during the initial evaluation, the ambulatory follow-up at 6 months, and during a telephone interview 1 year after enrollment. During their 1 year of participation, investigators will review medical records and record information in a manner that protects the identity of all participants. We hypothesize that the biochemical test results will be similar at baseline and 6 month follow-up and that these biochemical tests will identify patients at greater risk of cardiovascular events and bleeding. Treatment of participants will not be altered by their participation in this study.
Ticagrelor is an oral, reversibly-binding, direct-acting P2Y12 receptor antagonist used clinically for the prevention of atherothrombotic events in patients with acute coronary syndromes (ACS). Guideline recommendations on the use of dual antiplatelet therapy (DAPT) have been formulated that ticagrelor 90 mg twice daily plus aspirin in preference to clopidogrel 75mg daily plus aspirin for patients who have an ACS with or without ST-segment elevation. These recommendations are primarily based on large, randomized, Phase III clinical trials. However, few East Asian patients (or those of East Asian descent) have been included in these trials to assess the use of these drugs. In addition, a growing body of data supported that East Asian might have different adverse event profiles (thrombophilia and bleeding) and "therapeutic window" compared with white subjects. Furthermore, "East Asian paradox" phenomenon has been described that East Asian patients have a higher prevalence of platelet reactivity during DAPT, but an ischaemic event rate following PCI or ACS is similar or even lower than white patients. Therefore, the antiplatelet treatment strategy that is most appropriate for East Asian patients is increasingly urgent. Therefore, we performed the current study to observe the different effects of low-dose ticagrelor (45 mg twice daily), conventional-dose ticagrelor (90 mg twice daily) and clopidogrel (75mg once daily) on high platelet reactivity (HPR) and IPA, and investigated the safety and efficacy of low-dose ticagrelor further in Chinese patients with non-ST-elevation ACS (NSTE-ACS).
Recently, two new oral P2Y12 antagonists have been approved for clinical use: prasugrel, a third generation thienopyridine, and ticagrelor, a first in class cyclopentyltriazolopyrimidine (CPTP). These agents have been shown to be associated with more potent platelet inhibitory effects compared with clopidogrel. In addition, both agents have shown to be superior to clopidogrel in preventing recurrent ischemic events in the setting of acute coronary syndromes (ACS). Understanding how to switch patients from prasugrel to ticagrelor is an unmet need of clinical interest. The proposed PD investigation will have a prospective, randomized, parallel design aimed to show that switching patients from prasugrel to ticagrelor provides similar levels of platelet inhibition.
The primary objective of this prospective clinical registry is to determine the prevalence and level of thienopyridine resistance seen in a population undergoing contemporary percutaneous coronary intervention (PCI) or coronary artery bypass surgery (CABG).
This is a genetic and platelet reactivity study of African-American versus Caucasian patients undergoing percutaneous coronary intervention and receiving clopidogrel or prasugrel. The investigators aim is twofold: to describe differences in allele frequencies between African-Americans and Caucasians, and to explore associations of platelet reactivity and genetic polymorphisms in these two groups.
This study is being done to learn more about platelet reactivity (how well the small cells in the bloodstream work) in people who undergo Percutaneous coronary intervention (PCI) for stable and unstable (acute myocardial infarction) indications. Stable means you have not demonstrated any acute injury to your heart prior to your PCI; unstable means you have demonstrated some acute injury to your heart prior to your PCI. The investigators intend to determine if there is a change in platelet reactivity from the time of PCI to 30days post-PCI and does this change differ depending upon the conduction in which you present for PCI. This is going to be done with a variety of platelet reactivity assays.
* The purpose of this study is to determine the level of inhibition of platelet activation of an approved thienopyridine(clopidogrel or prasugrel) and aspirin regimen in the setting of drug eluting coronary stent implantation. * In subjects with high residual levels of platelet reactivity after receiving either a maintenance or loading dose of either clopidogrel or prasugrel, a cross over of thienopyridine treatment to the alternate medication will occur. * The study tests the hypothesis that adequate platelet inhibition will occur in subjects who have high levels of platelet reactivity and are subsequently switched from clopidogrel to prasugrel(loading or maintenance dose) without increased episodes of bleeding or MACE events at discharge and 30 days post Percutaneous Coronary Intervention (PCI).
The purpose of this study is to compare the effect of dark chocolate with green tea in healthy subjects on clot formation (platelet activity) cholesterol profile and markers of inflammation in two groups. The first group will be on a regimen of dark chocolate, and the second group will be on a regimen of green tea. Clinical outcomes will be determined after seven days of each treatment and both groups will undergo both treatments subsequently and serve as their own control. The hypothesis is that both green tea and dark chocolate will reduce platelet activity and reduce LDL, hsCRP and increase HDL.
Metabolic syndrome is a group of risk factors that increase a patient's likelihood for heart attack, stroke and diabetes. Our research is aimed at understanding whether a drug, resveratrol, commonly found in grapes and red wine, would have any benefit in reducing risk factors in patients that have metabolic syndrome. Despite the use of aspirin and cholesterol reducing medications, patients with metabolic syndrome still often have sticky platelets and dysfunctional lipid profile. This is likely due to inflammation and high oxidative state. In animal studies, this drug has reduced platelet stickiness and reduced oxidative stress. However, the effects of this drug have not been researched in patients with metabolic syndrome. We are interested in studying whether the benefits of resveratrol described in animal models can be translated to patients with metabolic syndrome who display high markers of oxidative stress. We plan to give a short intervention of drug to patients and then determine if the drug successfully: 1. Decreases the stickiness of platelets. This is important because sticky platelets are more likely to form clot and contribute to plaque formation. 2. Reduce the circulating dysfunctional HDL. HDL and its protein and lipid constituents help to inhibit oxidation, inflammation, activation of the blood vessel wall, coagulation, and platelet aggregation. Dysfunctional HDL, as occurs in metabolic syndrome patients, cannot properly protect against atherosclerosis.
This study will identify the potential benefits of regulating platelet activation with sotagliflozin compared to other FDA-approved drugs known to limit platelet activation.