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Abstract

Cardiovascular diseases (CVD's) are among the leading cause of deathworldwide as well as a major blockade to sustainable humandevelopment.1 According to the world health organization (WHO), it is among the leading causes of morbidity and mortality in India with an estimated 17.7 million deaths per year.2 Anticoagulants are among the most essential life?saving drugs that are generally used incardiology for the prevention and treatment of many CVD such asischemic heart disease, left ventricular dysfunction, acute coronarysyndrome, valve abnormalities, Atrial fibrillation, deep vein thrombosis, and pulmonary embolism.By slowing the pace of fibrin synthesis, these medications avoid embolic consequences and thrombus extension.drugs given orally (usually for long-term therapy) or parenterally (for the prevention and commencement of treatment of thrombosis as well as other surgical procedures) are the most frequently implicated drugs that cause adverse drug reactions (ADRs) in hospitalized patients. Elderly patients are particularly vulnerable to anticoagulant-associated ADRs, including ecchymosis, epistaxis, hematuria, gastrointestinal (GI) bleeding, thrombocytopenia, osteoporosis, and hypersensitivity reaction. Antiplatelet medications, namely aspirin and P2Y12 receptor antagonists, have considerably decreased the morbidity and mortality linked to arterial thrombosis in recent decades. Numerous clinical trials evaluating their safety and effectiveness in diverse clinical contexts have demonstrated antithrombotic efficacy, and their pharmacological properties, such as pharmacokinetic/pharmacodynamic profiles, have been well investigated.

Keywords

antiplatelets and anticoagulant drugs, Aspirin, Clopidogrel, Prasugrel.

Introduction

Globally, atherothrombotic events continue to be a major cause of death and disability. Antiplatelet medication is essential to the treatment of various ischemic illnesses since platelet activation is a key mediator of these conditions. Numerous intravenous and oral antiplatelet medications have been created in recent years. Their ability to prevent and treat atherothrombotic events, which include peripheral arterial, cardiovascular, and cerebrovascular disorders, has increased. The mainstay of pharmacological treatment for atherothrombotic events, encompassing a range of cardiovascular and cerebrovascular conditions as well as peripheral artery illnesses, are antiplatelet medicines, among which aspirin and P2Y12 receptor antagonists are important essential molecules. Antiplatelet preventative and therapeutic approaches have undergone substantial modifications in recent decades. To ensure that the correct patient receives the right therapy at the right time, the transition from a population-based approach to patient-centered precision medicine necessitates a better understanding of the unique risks and advantages connected to the various antiplatelet methods.

Commonly Used Antiplatelet Drugs :

1. Aspirin: Often used to prevent heart attacks, aspirin was the first antiplatelet drug. In patients with PAD, CAD, and cerebrovascular accidents, it is also utilized for secondary prophylaxis.

 2. Clopidogrel: This inhibitor of the adenosine diphosphate (ADP) receptor reduces the stickiness of platelets.

 3. Ticagrelor: An inhibitor of the ADP receptor.

4. Prasugrel: An inhibitor of the ADP receptor.

5.Cilostazol: An inhibitor of phosphodiesterase that dilates blood arteries and prevents platelets from adhering to one another.

6. Dipyridamole: An adenosine reuptake inhibitor that inhibits clotting-related enzymes.

Pentoxifylline, tirofiban, eptifibatide, and vorapaxar are other antiplatelet medications.

Who Guidelines For The Use Antiplatlet Drugs :

*Risk <10>

It is not recommended that people in this low-risk category use aspirin(1++, A)

*Risk 10 to <20>

*Risk 20 to <30>

Aspirin should probably not be given to Individuals in this risk category. (1++, A)

*Risk ?30%: Low-dose aspirin should be administered to people in this risk group.(1++, A)

Drugs That Are Not Recommended

Hormone replacement, vitamins B, C, E and Folic acid supplements are not recommended for Reduction of cardiovascular risk.In regions where the prevalence of coronary heart disease is higher than that of stroke, take aspirin. Best Practice Points: The least expensive preparation of the aforementioned drug classes should be utilized unless there are strong indications to employ a particular drug. It is advised to use high-quality generic versions of the medications on the WHO Essential Medicines List. Before administering rigorous antihypertensive medication and statins, a cost-effective preventive strategy in settings with limited resources might provide aspirin and beginning antihypertensive treatment to everyone at high risk. In cardiovascular disorders, antiplatelet medications like aspirin and clopidogrel are necessary because they lower the chance of new clot formation and improve survival.

?Antiplatelet medications prescribed, 46.03% were on aspirin, 41.4% were on clopidogrel, 6.01% were on aspirin and clopidogrel combination therapy, 4.04% were on ticagrelor, and 1.02% were on prasugrel.The study population's heparin utilization rate was 43.9%. The second most commonly used anticoagulant among the patients was dateparin (29.3%).


Drugs

No Of Cases

Percentage (%)

Aspirin

93

46.03

Clopidogrel

83

41.4

Aspirin+ Clopidogrel

13

6.01

Ticagrelor

08

4.04

Prasugrel

02

1.02


Drugs

No Of Cases

Percentage

Unfractional heparin

36

44

Enoxaparin

14

17.13

Absciximab

3

3.60

dalteparin

24

26.3

warfarin

1

4.77

Fondaparinuc

82

1.20


Antiplatelet Drugs

Antiplatelet medications are substances that prevent thrombus (clot) formation and reduce platelet aggregation. A number of platelet activation agonists, including as thrombin, thromboxane A2 (TXA2), and adenosine diphosphate (ADP), are produced during the platelet activation process.These agonists stimulate platelet aggregation and raise the platelet response.The following categories apply to oral antiplatelet medications:

1 . COX- 1 inhibitors

An effective antiplatelet that blocks platelet cyclooxygenase (COX), a crucial enzyme in the production of TXA2, which causes platelet activation and aggregation, is known as a COX-1 inhibitor. Aspirin is the primary member of this class.

2.P2Y12 receptor antagonists

a)Thienopyridine:

function by preventing the ADP-dependent platelet activation pathway. Ticlopidine, clopidogrel, and prasugrel are a few examples.

 b) Adenosine triphosphate analog: Prevents ADP-induced platelet aggregation by interacting reversibly with the P2Y12 receptor and inhibiting it.

3.Phosphodiesterase inhibitors: Reduce platelet aggregability by inhibiting cyclic GMP phosphodiesterase activity and adenosine absorption. Phosphodiesterase inhibitors are currently utilized in combination with other medications because they have minimal antiplatelet impact when taken alone.

Example includes dipyridamole.

Antiplatlet Drugs


Sr. No

Drug Class

Outcomes

Common Side Effects

Precautions

1]

COX-1 Inhibitor

Prevented atherothrombosis, venous thromboembolism, colorectal cancer and dementia.

Bronchospasm, gastrointenstinal irritation such as nausea, gastrointestinal haemorrhage, other haemorrhages (eg:subconjuctival)

Use with cautions in patient with renal impairment and during third trimester of pregnancy, asthma, uncontrolled hypertension, previous peptic ulceration, concomitant use of drugs that increase the risk of bleeding G6PD deficiency, dehydration and elderly patient.

2]

P2Y12 Receptor antagonists

(1)Thienopyridine

(2) Adenosine Triphosphate Analogue

(3) Phosphodiesterase Inhibitor

Reduced risks thrombotic events in patients with a recent MI ,CVA or peripheral vascular disease.

Lesser risks of myocardial infarction in future.

Heamorrhage, rashes, GI disturbance such as dyspepsia, abdominal pain , diarrhoea, blood

Dyscrasia

Heamorrhage, bruising,dyspnoea,

Gastrointestinal effect, dizziness, myalgia, HTN, throbbing headache, rashes, increased bleeding during or after suregery.

Use with caution in patients with renal and hepatic impairment , avoid use in those with severe hepatic impairment.

Use with caution in patient at the risk of increased bleeding or with concomitant use of drugs that increase risk of bleeding.

Use with caution in patient at increased the risk of bleeding, asthma, chronic obstructive pulmonary disease.

Use with caution in rapid worsening of angina, aerotic stenosis, recent myocardial infarction, heart failure.


Anticoagulant Drugs

Anticoagulants slow down the coagulation process by interfering with certain clotting factors.Oral anticoagulants can be classified as follows:

1.Vitamin K antagonists: Stop the coagulation factors that are dependent on vitamin K from activating. The level of clotting factor depression varies with dosage. Warfarin is the only vitamin K antagonist that is accessible in Hong Kong.

2.Direct thrombin inhibitors (DTIs): Bind with thrombin which is the central effector of coagulation to inactivate thrombin. Example includes dabigatran etexilate.

3.Direct factor Xa inhibitors: selectively bind to coagulation factor Xa to prevent its action.. Examples include apixaban and rivaroxaban.

Anticoagulant Drugs


Sr. No

 

1]

 

              2]

 

 

 

 

 

 

 

3]

 

Drug Class

Vit-K Antagonists

 

 

Direct factor Xa Inhibitor

 

 Direct thrombin     Inhibitor

Outcomes

Reduced risk of stroke, cardio embolism, pulmonary embolism, thromboembolism.Reduced risks of blood clotting, stroke and embolism, future cardiovascular events.

Prevention of death or myocardial infarction in patients with acute coronary syndromes.

Common  Side Effects

Precautions

Heamorrhage ,nausea, vomiting, jaumdice , hepatic dysfunction, pancreatitis, alopecia

Use with cautions in mild , moderate renal impairment,                                    monitor INR impairment , regular blood test to check how long it takes blood to clot and dose may be need to be adjusted.

Apixaban

Heamorrhage , bruising, anaemia

Rivoroxaban

Abdmonial pain , dizziness, constipation,

Use with cautions in patient at risk of bleeding or taking

With severe hepatic or renal impairment

Heamorrhage , nausea, anaemia, abdominal pain

Use with cautions in elderly and in patients with low body weight  use with caution in patients with bleeding disorder, thrombocytopenia, increased risk of bleeding or with severe hepatic impairment.


For a brief period following a small noncardioembolic stroke, dual antiplatelet therapy (DAPT) using aspirin and clopidogrel is advised. Antiplatelet monotherapy (MAPT) is used to treat the majority of noncardioembolic strokes. The American Heart Association/American Stroke Association acute ischemic stroke prevention guidelines, however, take into account the use of dual antiplatelet therapies (DAPTs) for a brief period (21 days) following acute minor noncardioembolic stroke based on the findings of two independent large randomized controlled trials (RCTs): the CHANCE trial (Clopidogrel in High-Risk Patients With Acute Non-disabling Cerebrovascular Events) and the POINT trial (Clopidogrel and Aspirin in Acute Ischemic Stroke and High-Risk TIA).

Combination Antiplatelet Therapy

Aspirin has been used in conjunction with one or two other antiplatelet medications in the majority of trials on antiplatelet therapy in secondary prevention to date, but there is a great desire for research that questions this conventional wisdom. At the moment, DAPT combined with aspirin and an oral P2Y12 antagonist is the most common approach for high-risk individuals. ACS has also investigated the use of vorapaxar in conjunction with DAPT, which consists of aspirin and clopidogrel or SAPT.Aspirin and dipyridamole, on the other hand, have been proven to be effective in secondary prevention following TIA or stroke and have not yet been effectively contested.

Aspirin And Clopidogrel

In order to control ACS, the CURE Clopidogrel in Unstable angina to avoid Recurrent Events) research demonstrated the feasibility of using DAPT in conjunction with aspirin and clopidogrel: While the risk of serious bleeding was higher (3.7% vs. 2.7%; RR: 1.38; 95% CI: 0.72 to 0.90; p < 0>

Aspirin And Prasugrel

The pharmacokinetic and pharmacodynamic advantages of prasugrel explain its higher antithrombotic efficacy compared with clopidogrel, particularly with regard to prevention of stent thrombosis in patients with ACS undergoing PCI . Consequently, DAPT with aspirin and prasugrel is recommended as a first-line option in patients with ACS planned for PCI, in preference to aspirin and clopidogrel .DAPT with prasugrel, compared with clopidogrel, was also associated with higher rates of CABG-related bleeding and, in another study, did not significantly reduce ischemic events in patients with ACS who were medically managed .Consequently, prasugrel is not recommended in patients with ACS who are not planned for PCI. Pre-treatment of ACS patients with a prasugrel loading dose before coronary angiography was not found to be more effective than treatment at the time of PCI  and is therefore also not recommended . Prasugrel is contraindicated in individuals with a history of cerebrovascular disease due to concerns about potential risk, and those over 75 are advised not to use it due to the lack of net benefit seen in these patients . Prasugrel is also not recommended in patients who require OAC. In patients who need continuous treatment with potent CYP2C19 or CYP3A inhibitors, DAPT should be chosen since, unlike clopidogrel, prasugrel’s pharmacokinetics are not substantially impacted by these CYP pathway inhibitors . After PCI, longer-term (>12 months) aspirin and clopidogrel or prasugrel medication is linked to a lower incidence of stent thrombosis and MI but a higher risk of severe hemorrhage .After a thorough evaluation of the patient’s ischemia and bleeding risks, P2Y12 inhibitor medication in addition to aspirin after more than a year following ACS may be taken into consideration .A treatment algorithm for duration of P2Y12 inhibitor therapy in patients with recent ACS (non–ST-segment elevation ACS or ST-segment elevation MI) has been proposed by the 2016 ACC/AHA guideline focused update .

Aspirin And Ticagrelor

In the first year following ACS, DAPT with aspirin and ticagrelor compared to DAPT with aspirin and clopidogrel lowers major vascular events, including cardiovascular death (9.8% vs. 11.7%; HR: 0.84; 95% CI: 0.77 to 0.92; p < 0 xss=removed>

In patients with no prior history of cerebrovascular disease, longer-term treatment with ticagrelor-based DAPT longer than one year after MI has also been demonstrated to reduce serious vascular events when compared to aspirin alone (ticagrelor 60 mg b.i.d. vs. placebo: 7.8% vs. 9.0%; HR: 0.84; 95% CI: 0.74 to 0.95; p = 0.004), albeit at the expense of an increased risk of nonfatal bleeding (Thrombolysis In Myocardial Infarction [TIMI] major bleeding, 2.3% vs. 1.1%; HR: 2.32; 95% P < 0>

Combination Therapy With Vorapaxar

In patients with a history of atherosclerotic disease, vorapaxar added to standard-of-care treatment (usually aspirin and/or clopidogrel) was found to lower the rates of serious vascular events. However, it also significantly increased the risk of ICH and other major bleeding, especially in those who had previously experienced an ischemic stroke. As a result, the benefits seemed to be limited to subgroups with MI or PAD who had no history of stroke. Vorapaxar, when used in conjunction with standard-of-care treatment (primarily clopidogrel-based DAPT) for non-ST-segment elevation ACS patients, failed to significantly reduce the primary endpoint and was linked to an increased risk of ICH and other major bleeding, especially in patients with a history of ischemic cerebrovascular disease. Patients with stable atherosclerotic disease, especially PAD, who do not have a history of cerebrovascular disease or other factors that may increase their risk of ICH may find that adding vorapaxar to aspirin or clopidogrel is an option. However, the lack of a prospective trial in this particular population limits the recommendation. The overall therapeutic benefit of vorapaxar in addition to current antiplatelet treatment in patients with symptomatic PAD is unclear, per the 2016 AHA/ACC guideline Aspirin And Dipyridamole:-

For secondary prophylaxis, low-dose aspirin and dipyridamole continue to be the best choice for people with a history of TIA or noncardioembolic ischemic stroke . For other indications, there is no evidence to recommend this combination.

CONCLUSION:

In conclusion, for cardiovascular diseases (CVDs) to be effectively managed, antiplatelet and anticoagulant medication prescribing patterns are essential. Anticoagulants treat venous thromboembolic problems, such as those observed in atrial fibrillation or deep vein thrombosis, while antiplatelets generally target arterial thrombosis. Both medication classes have different roles in preventing and treating thromboembolic events. Patients with coronary artery disease, ischemic stroke, or those having percutaneous coronary procedures are frequently offered antiplatelet therapy, which includes medications like aspirin and P2Y12 inhibitors. However, in order to lower the risk of clot formation in the veins or heart chambers, anticoagulants like warfarin and direct oral anticoagulants (DOACs) are more frequently prescribed in disorders like atrial fibrillation and venous thromboembolism. Comorbidities, the underlying cardiovascular illness being treated, and the patient's risk of bleeding all influence the choice between these drugs. Prescription practices have recently shifted toward personalized medicine, combining clinical monitoring and pharmacogenetic testing to maximize medication selection and dosage. For example, compared to more conventional drugs like warfarin, gains in reducing bleeding risks and streamlining treatment are reflected in the increased desire for newer, more convenient DOACs. Although these drugs are essential for lowering harmful cardiovascular events, using them necessitates carefully weighing the therapeutic advantages against any possible hazards, especially those related to bleeding. For the management of cardiovascular illnesses to be as successful as possible, adherence to clinical guidelines, continuous patient monitoring, and customized treatment plans are necessary. Future prescription trends and patient care in cardiovascular medicine will be shaped by further study on the long-term effects, safety, and efficacy of medications.

REFERENCES

  1. Patrono C., Andreotti F., Arnesen H.et al. : "Antiplatelet agents for the treatment and prevention of atherothrombosis". Eur Heart J 2011; 32: 2922. CrossrefMedlineGoogle Scholar
  2. Coxib and traditional NSAID Trialists' (CNT) Collaboration : "Vascular and upper gastrointestinal effects of non-steroidal anti-inflammatory drugs: meta-analyses of individual participant data from randomised trials". Lancet 2013; 382: 769. CrossrefMedlineGoogle Scholar
  3. Wiviott S.D., Braunwald E., McCabe C.H., et al. and for the TRITON–TIMI 38 Investigators : "Prasugrel versus clopidogrel in patients with acute coronary syndromes". N Engl J Med 2007; 357: 2001. CrossrefMedlineGoogle Scholar
  4. Wallentin L., Becker R.C., Budaj A., et al. and for the PLATO Investigators : "Ticagrelor versus clopidogrel in patients with acute coronary syndromes". N Engl J Med 2009; 361: 1045. CrossrefMedlineGoogle Scholar
  5. Tricoci P., Huang Z., Held C., et al. and for the TRACER Investigators : "Thrombin-receptor antagonist vorapaxar in acute coronary syndromes". N Engl J Med 2012; 366: 20. CrossrefMedlineGoogle Scholar
  6. Rocca B. and Patrono C. : "Determinants of the interindividual variability in response to antiplatelet drugs". J Thromb Haemost 2005; 3: 1597. CrossrefMedlineGoogle Scholar
  7. Mega J.L., Close S.L., Wiviott S.D.et al. : "Genetic variants in ABCB1 and CYP2C19 and cardiovascular outcomes after treatment with clopidogrel and prasugrel in the TRITON-TIMI 38 trial: a pharmacogenetic analysis". Lancet 2010; 376: 1312. CrossrefMedlineGoogle Schola
  8. Simon T., Verstuyft C., Mary-Krause M., et al. and for the French Registry of Acute ST-Elevation and Non–ST-Elevation Myocardial Infarction (FAST-MI) Investigators : "Genetic determinants of response to clopidogrel and cardiovascular events". N Engl J Med 2009; 360: 363. CrossrefMedlineGoogle Scholar
  9. Mega J.L., Close S.L., Wiviott S.D.et al. : "Cytochrome P-450 polymorphisms and response to clopidogrel". N Engl J Med 2009; 360: 354. CrossrefMedlineGoogle Scholar
  10. Roberts J.D., Wells G.A., Le May M.R.et al. : "Point-of-care genetic testing for personalisation of antiplatelet treatment (RAPID GENE): a prospective, randomised, proof-of-concept trial". Lancet 2012; 379: 1705. CrossrefMedlineGoogle Scholar
  11. Hiatt W.R., Fowkes F.G.R., Heizer G., et al. and for the EUCLID Trial Steering Committee and Investigators : "Ticagrelor versus clopidogrel in symptomatic peripheral artery disease". N Engl J Med 2017; 376: 32. CrossrefMedlineGoogle Scholar
  12. Hulot J.S., Collet J.P. and Montalescot G. : "Thienopyridine-associated drug-drug interactions: pharmacologic mechanisms and clinical relevance". Curr Cardiol Rep 2011; 13: 451. CrossrefMedlineGoogle Scholar
  13. Wallentin L., James S., Storey R.F., et al. and for the PLATO Investigators : "Effect of CYP2C19 and ABCB1 single nucleotide polymorphisms on outcomes of treatment with ticagrelor versus clopidogrel for acute coronary syndromes: a genetic substudy of the PLATO trial". Lancet 2010; 376: 1320. CrossrefMedlineGoogle Scholar
  14. Hawes B.E., Zhai Y., Hesk D.et al. : "In vitro pharmacological characterization of vorapaxar, a novel platelet thrombin receptor antagonist". Eur J Pharmacol 2015; 762: 221. CrossrefMedlineGoogle Scholar
  15. Li X., Fries S., Li R.et al. : "Differential impairment of aspirin-dependent platelet cyclooxygenase acetylation by nonsteroidal antiinflammatory drugs". Proc Natl Acad Sci U S A 2014; 111: 16830. CrossrefMedlineGoogle Schola
  16. Patrono C. : "Aspirin as an antiplatelet drug". N Engl J Med 1994; 330: 1287. CrossrefMedlineGoogle Scholar
  17. Aradi D., Storey R.F., Komócsi A., et al. and for the Working Group on Thrombosis of the European Society of Cardiology : "Expert position paper on the role of platelet function testing in patients undergoing percutaneous coronary intervention". Eur Heart J 2014; 35: 209. CrossrefMedlineGoogle Scholar
  18. Collet J.P., Cuisset T., Rangé G., et al. and for the ARCTIC Investigators : "Bedside monitoring to adjust antiplatelet therapy for coronary stenting". N Engl J Med 2012; 367: 2100. CrossrefMedlineGoogle Scholar
  19. Price M.J., Berger P.B., Teirstein P.S., et al. and for the GRAVITAS Investigators : "Standard- vs high-dose clopidogrel based on platelet function testing after percutaneous coronary intervention: the GRAVITAS randomized trial". JAMA 2011; 305: 1097. CrossrefMedlineGoogle Scholar
  20. Trenk D., Stone G.W., Gawaz M.et al. : "A randomized trial of prasugrel versus clopidogrel in patients with high platelet reactivity on clopidogrel after elective percutaneous coronary intervention with implantation of drug-eluting stents: results of the TRIGGER-PCI (Testing Platelet Reactivity In Patients Undergoing Elective Stent Placement on Clopidogrel to Guide Alternative Therapy With Prasugrel) Study". J Am Coll Cardiol 2012; 59: 2159. View ArticleGoogle Scholar
  21. Cayla G., Cuisset T., Silvain J., et al. and for the ANTARCTIC Investigators : "Platelet function monitoring to adjust antiplatelet therapy in elderly patients stented for an acute coronary syndrome (ANTARCTIC): an open-label, blinded-endpoint, randomised controlled superiority trial". Lancet 2016; 388: 2015. CrossrefMedlineGoogle Scholar
  22. Sibbing D., Aradi D., Jacobshagen C., et al. and for the TROPICAL-ACS Investigators : "A randomised trial on platelet function-guided de-escalation of antiplatelet treatment in ACS patients undergoing PCI. Rationale and design of the Testing Responsiveness to Platelet Inhibition on Chronic Antiplatelet Treatment for Acute Coronary Syndromes (TROPICAL-ACS) Trial". Thromb Haemost 2017; 117: 188. CrossrefMedlineGoogle Scholar
  23. Roffi M., Patrono C., Collet J.P.et al. : "2015 ESC guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC)". Eur Heart J 2016; 37: 267. CrossrefMedlineGoogle Scholar
  24. Malm C.J., Hansson E.C., Åkesson J.et al. : "Preoperative platelet function predicts perioperative bleeding complications in ticagrelor-treated cardiac surgery patients: a prospective observational study". Br J Anaesth 2016; 117: 309. Cross ref Medline Google Scholar

Reference

  1. Patrono C., Andreotti F., Arnesen H.et al. : "Antiplatelet agents for the treatment and prevention of atherothrombosis". Eur Heart J 2011; 32: 2922. CrossrefMedlineGoogle Scholar
  2. Coxib and traditional NSAID Trialists' (CNT) Collaboration : "Vascular and upper gastrointestinal effects of non-steroidal anti-inflammatory drugs: meta-analyses of individual participant data from randomised trials". Lancet 2013; 382: 769. CrossrefMedlineGoogle Scholar
  3. Wiviott S.D., Braunwald E., McCabe C.H., et al. and for the TRITON–TIMI 38 Investigators : "Prasugrel versus clopidogrel in patients with acute coronary syndromes". N Engl J Med 2007; 357: 2001. CrossrefMedlineGoogle Scholar
  4. Wallentin L., Becker R.C., Budaj A., et al. and for the PLATO Investigators : "Ticagrelor versus clopidogrel in patients with acute coronary syndromes". N Engl J Med 2009; 361: 1045. CrossrefMedlineGoogle Scholar
  5. Tricoci P., Huang Z., Held C., et al. and for the TRACER Investigators : "Thrombin-receptor antagonist vorapaxar in acute coronary syndromes". N Engl J Med 2012; 366: 20. CrossrefMedlineGoogle Scholar
  6. Rocca B. and Patrono C. : "Determinants of the interindividual variability in response to antiplatelet drugs". J Thromb Haemost 2005; 3: 1597. CrossrefMedlineGoogle Scholar
  7. Mega J.L., Close S.L., Wiviott S.D.et al. : "Genetic variants in ABCB1 and CYP2C19 and cardiovascular outcomes after treatment with clopidogrel and prasugrel in the TRITON-TIMI 38 trial: a pharmacogenetic analysis". Lancet 2010; 376: 1312. CrossrefMedlineGoogle Schola
  8. Simon T., Verstuyft C., Mary-Krause M., et al. and for the French Registry of Acute ST-Elevation and Non–ST-Elevation Myocardial Infarction (FAST-MI) Investigators : "Genetic determinants of response to clopidogrel and cardiovascular events". N Engl J Med 2009; 360: 363. CrossrefMedlineGoogle Scholar
  9. Mega J.L., Close S.L., Wiviott S.D.et al. : "Cytochrome P-450 polymorphisms and response to clopidogrel". N Engl J Med 2009; 360: 354. CrossrefMedlineGoogle Scholar
  10. Roberts J.D., Wells G.A., Le May M.R.et al. : "Point-of-care genetic testing for personalisation of antiplatelet treatment (RAPID GENE): a prospective, randomised, proof-of-concept trial". Lancet 2012; 379: 1705. CrossrefMedlineGoogle Scholar
  11. Hiatt W.R., Fowkes F.G.R., Heizer G., et al. and for the EUCLID Trial Steering Committee and Investigators : "Ticagrelor versus clopidogrel in symptomatic peripheral artery disease". N Engl J Med 2017; 376: 32. CrossrefMedlineGoogle Scholar
  12. Hulot J.S., Collet J.P. and Montalescot G. : "Thienopyridine-associated drug-drug interactions: pharmacologic mechanisms and clinical relevance". Curr Cardiol Rep 2011; 13: 451. CrossrefMedlineGoogle Scholar
  13. Wallentin L., James S., Storey R.F., et al. and for the PLATO Investigators : "Effect of CYP2C19 and ABCB1 single nucleotide polymorphisms on outcomes of treatment with ticagrelor versus clopidogrel for acute coronary syndromes: a genetic substudy of the PLATO trial". Lancet 2010; 376: 1320. CrossrefMedlineGoogle Scholar
  14. Hawes B.E., Zhai Y., Hesk D.et al. : "In vitro pharmacological characterization of vorapaxar, a novel platelet thrombin receptor antagonist". Eur J Pharmacol 2015; 762: 221. CrossrefMedlineGoogle Scholar
  15. Li X., Fries S., Li R.et al. : "Differential impairment of aspirin-dependent platelet cyclooxygenase acetylation by nonsteroidal antiinflammatory drugs". Proc Natl Acad Sci U S A 2014; 111: 16830. CrossrefMedlineGoogle Schola
  16. Patrono C. : "Aspirin as an antiplatelet drug". N Engl J Med 1994; 330: 1287. CrossrefMedlineGoogle Scholar
  17. Aradi D., Storey R.F., Komócsi A., et al. and for the Working Group on Thrombosis of the European Society of Cardiology : "Expert position paper on the role of platelet function testing in patients undergoing percutaneous coronary intervention". Eur Heart J 2014; 35: 209. CrossrefMedlineGoogle Scholar
  18. Collet J.P., Cuisset T., Rangé G., et al. and for the ARCTIC Investigators : "Bedside monitoring to adjust antiplatelet therapy for coronary stenting". N Engl J Med 2012; 367: 2100. CrossrefMedlineGoogle Scholar
  19. Price M.J., Berger P.B., Teirstein P.S., et al. and for the GRAVITAS Investigators : "Standard- vs high-dose clopidogrel based on platelet function testing after percutaneous coronary intervention: the GRAVITAS randomized trial". JAMA 2011; 305: 1097. CrossrefMedlineGoogle Scholar
  20. Trenk D., Stone G.W., Gawaz M.et al. : "A randomized trial of prasugrel versus clopidogrel in patients with high platelet reactivity on clopidogrel after elective percutaneous coronary intervention with implantation of drug-eluting stents: results of the TRIGGER-PCI (Testing Platelet Reactivity In Patients Undergoing Elective Stent Placement on Clopidogrel to Guide Alternative Therapy With Prasugrel) Study". J Am Coll Cardiol 2012; 59: 2159. View ArticleGoogle Scholar
  21. Cayla G., Cuisset T., Silvain J., et al. and for the ANTARCTIC Investigators : "Platelet function monitoring to adjust antiplatelet therapy in elderly patients stented for an acute coronary syndrome (ANTARCTIC): an open-label, blinded-endpoint, randomised controlled superiority trial". Lancet 2016; 388: 2015. CrossrefMedlineGoogle Scholar
  22. Sibbing D., Aradi D., Jacobshagen C., et al. and for the TROPICAL-ACS Investigators : "A randomised trial on platelet function-guided de-escalation of antiplatelet treatment in ACS patients undergoing PCI. Rationale and design of the Testing Responsiveness to Platelet Inhibition on Chronic Antiplatelet Treatment for Acute Coronary Syndromes (TROPICAL-ACS) Trial". Thromb Haemost 2017; 117: 188. CrossrefMedlineGoogle Scholar
  23. Roffi M., Patrono C., Collet J.P.et al. : "2015 ESC guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC)". Eur Heart J 2016; 37: 267. CrossrefMedlineGoogle Scholar
  24. Malm C.J., Hansson E.C., Åkesson J.et al. : "Preoperative platelet function predicts perioperative bleeding complications in ticagrelor-treated cardiac surgery patients: a prospective observational study". Br J Anaesth 2016; 117: 309. Cross ref Medline Google Scholar

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Mane Pandurang
Corresponding author

Shivlingeshwar collage of Pharmacy Almala ta ausa dist latur

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Shweta Nilmawar
Co-author

Shivlingeshwar collage of Pharmacy Almala, ta ausa dist latur

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Rohan Boralkar
Co-author

Shivlingeshwar collage of Pharmacy Almala, ta ausa dist latur

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Dr. Ashok Giri
Co-author

Shivlingeshwar collage of Pharmacy Almala, ta ausa dist latur

Mane Pranjali*, Nilamwar Shweta, Boralkar Rohan, Dr. Ashok Giri, Common Prescription Pattern of Antiplatelet and Anticoagulant Drugs in The Management of Cardiovascular Diseases, Int. J. of Pharm. Sci., 2024, Vol 2, Issue 12, 2468-2476. https://doi.org/10.5281/zenodo.14524300

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