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Abstract

Cardiovascular diseases (CVD) remain the leading cause of morbidity and mortality globally, necessitating effective therapeutic interventions to mitigate their burden. Among these, antiplatelet therapy has emerged as a cornerstone in the prevention and management of atherosclerotic events, particularly in patients with acute coronary syndromes (ACS), myocardial infarction (MI), and those undergoing percutaneous coronary interventions (PCI). This review synthesizes the current evidence on the efficacy, safety, and outcomes of antiplatelet therapy in CVD management, with a focus on mono- and dual-antiplatelet regimens. Antiplatelet agents, including aspirin, P2Y12 inhibitors (such as clopidogrel, prasugrel, and ticagrelor), and glycoprotein IIb/IIIa inhibitors, play a critical role in reducing thrombotic complications in CVD. Aspirin, a cyclooxygenase-1 inhibitor, has been a mainstay of therapy due to its efficacy in reducing arterial thrombosis. In combination with P2Y12 inhibitors, dual antiplatelet therapy (DAPT) has demonstrated superior outcomes in reducing recurrent ischemic events compared to monotherapy. Numerous large-scale clinical trials have substantiated the benefits of antiplatelet therapy in diverse CVD settings. For instance, the CAPRIE trial highlighted clopidogrel’s efficacy over aspirin in reducing composite cardiovascular events in high-risk patients. Similarly, ticagrelor was found to be superior to clopidogrel in individuals with ACS by the PLATO trial. In post-PCI settings, prolonged DAPT has shown to significantly reduce stent thrombosis and major adverse cardiovascular events (MACE), albeit at an increased risk of bleeding. Future directions include developing novel agents targeting new pathways, personalized therapies based on genetic testing, and optimizing combination regimens to improve safety and efficacy.

Keywords

CVD, Antiplatelet drugs, Indications, Aspirin, Clopidogrel, prasugrel, ticagrelor.

Introduction

Heart disease, or cardiovascular disease, encompasses four  different conditions: peripheral artery disease (PAD), cerebrovascular disease, coronary artery disease (CAD), commonly known as coronary heart disease –(CHD), and aortic atherosclerosis. Decreased myocardial perfusion in CAD leads to ischemia-induced angina, which can cause myocardial infarction (MI) and/or heart failure. Coronary artery disease (CAD): Also known as coronary heart disease (CHD), this condition. It accounts for between one-third and one-half of all cardiovascular disease cases. on is brought on by a reduction in myocardial perfusion, which can lead to heart failure, myocardial infarction (MI), and/or angina. It is responsible for between one-third and half of CVD case.

  • Transient ischemic attack (TIA) and stroke are included in cerebrovascular disease (CVD).
  • Peripheral artery disease (PAD): Particularly arterial disease involving the limbs that may result in claudication.
  • Aortic atherosclerosis: Including thoracic and abdominal aneurysms.

The primary cause of death globally and a significant hindrance to sustainable human development is cardiovascular disease (CVD). It is one of the main reasons for both morbidity and death. Antiplatelet drugs have an established place in the prevention of vascular events in a variety of clinical conditions, such as myocardial infarction, stroke and cardiovascular death. Antiplatelet medications should be used in individuals with established coronary heart disease and other atherosclerotic conditions, according to both European and American guidelines. In order to treat acute ischemic syndromes (both coronary and cerebrovascular) and prevent their recurrence, antiplatelet medications offer first-line antithrombotic therapy because the possible advantages and disadvantages of combining them with other preventative measures are not entirely clear, their role in the primary prevention of atherothrombosis is still debatable. In high-income nations, ischemic events like myocardial infarction (MI) and stroke are the leading cause of morbidity and mortality, accounting for 15 million deaths annually globally. An important factor in the processes that lead to atherothrombosis and consequent end organ damage is undesired intravascular platelet activation at the site of endothelial injury. Antiplatelet therapy thus emerged as a key component in the secondary prevention of unfavorable cardiovascular outcomes.

       
            Platelet Functions and Molecular Targets.png
       

Figure 01: Platelet Functions and Molecular Targets.

Antiplatelet drugs’ molecular targets and platelet function. Von Willebrand factor (VWF) binds to the platelet surface GPIb?IX?V complex, and exposed collagen binds to platelet surface glycoprotein (GP) VI and integrin ?2?1 to initiate platelet adherence to injured vascular walls. Additionally, this complex is a receptor for leukocyte integrin ?M?2, procoagulant factors (thrombin, kininogen, factor XI, and factor XII), and additional platelet ligands (thrombospondin, collagen, and P-selectin). Protease-activated receptors (PAR) 1 and 4 on the platelet surface allow thrombin, which is produced by the coagulation cascade, to strongly activate human platelets. Important positive feedback loops for platelet activation are provided by three types of platelet surface receptors:

Clinical Pharmacology Of Antiplatelet Drugs:

Platelet activation and aggregation are influenced  by a number of pathways, and while pharmaceutical interference with these processes lowers the risk of atherothrombotic consequences, it also raises the risk of bleeding.

It is important to emphasize that the thromboxane (TX) A2-, adenosine diphosphate (ADP)-, and thrombin-activated pathways transduce independent signals of platelet activation and represent nonredundant targets for its pharmacological modulation. The additive character of the combination antiplatelet therapy’s effects reflects this.

Types Of Antiplatelet Drugs:

Antiplatelet drugs can be broadly categorized into the following types based on their mechanisms of action:

  1. Cyclooxygenase (COX) Inhibitors:

Example: Aspirin (Acetylsalicylic Acid)

Mechanism: Irreversibly inhibits COX-1, preventing thromboxane A2 production, a    potent stimulator of platelet aggregation.

Usage: First-line therapy in secondary prevention of CVD, including post-MI, stable angina, and stroke prevention.

  1. P2Y12 Receptor Inhibitors:

Examples: Clopidogrel, Prasugrel, Ticagrelor

Mechanism: Block the P2Y12 receptor on platelets, inhibiting ADP-mediated platelet activation and aggregation.

Usage: Often used in combination with aspirin in dual antiplatelet therapy (DAPT) for acute coronary syndrome (ACS), post-percutaneous coronary intervention (PCI), and stent placement.

Preferences: Clopidogrel is widely used due to cost and accessibility; newer agents like Prasugrel and Ticagrelor are preferred in high-risk patients due to enhanced efficacy.

  1. Protease-Activated Receptor-1 (PAR-1) Antagonists:

Example: Vorapaxar

Mechanism: Blocks platelet activation brought on by thrombin through the the PAR-1 receptor

Usage: Added in select cases with history of MI or peripheral arterial disease.

  1. Glycoprotein IIb/IIIa Inhibitors:

Examples: Abciximab, Eptifibatide, Tirofiban

Mechanism: Block the final common pathway of platelet aggregation by inhibiting the glycoprotein IIb/IIIa receptor.

Usage: Primarily in high-risk ACS or during PCI in hospital settings. In cardiovascular disorders, antiplatelet medications like aspirin and clopidogrel are necessary because they lower the chance of new clot formation and improve survival. Aspirin accounted for 46.03% of the antiplatelet medications administered, clopidogrel for 41.4%, aspirin and clopidogrel for 6.01%, ticagrelor for 4.04%, and prasugrel for 1.02%.


Table 1: Details of antiplatelet drugs administered to the patients

Drugs

Peercentage

Aspirin

46.03

Clopidogrel

41.4

Aspirin+ Clopidogrel

6.01

Ticagrelor

4.04

Prasugrel

1.01


Overview Of Antiplatelet Indications:

The possible indications for dual antiplatelet therapy reviewed here include coronary artery disease(CAD),atherosclerotic ischemic stroke, and atrial fibrillation within the broad category of CAD, one must look at primary and secondary prevention of events in patients with stable CAD, non–ST-segment elevation myocardial infarction (MI) and/or unstable angina, and ST-segment elevation MI acute coronary syndrome (ACS), as well as in patients with percutaneous coronary intervention (PCI). Unless otherwise noted, all trials described here were randomized, double-blind, and placebo-controlled, with no significant differences in baseline patient characteristics or concomitant medications.

  • Primary Prevention of CAD and Secondary
  • Prevention in Stable CAD:-

Primary prevention of CAD with aspirin and clopidogrel currently lacks data assessing efficacy as a primary outcome in patients without a prior event. Dual antiplatelet therapy for secondary prevention in patients with stable CAD was investigated in CHARISMA (Clopidogrel for High Atherothrombotic Risk and Ischemic Stabilization, Management, and Avoidance). This trial assessed the safety and efficacy of clopidogrel in addition to aspirin in15,603 patients at high risk for cardiovascular events. Randomization to clopidogrel 75 mg/day or placebo was in addition to 75–162 mg/day of aspirin and investigator-driven appropriate standard therapy. The first instance of MI, stroke, or cardiovascular mortality in the whole study population served as the main outcome. A variety of secondary end points were also assessed, including a number of subgroup analyses of the primary endpoint, as well as bleeding. More than 75% of patients were included because they had a history of cardiovascular disease (secondary prevention), and the remaining patients were included because they had several risk indicators for an atherothrombotic event (primary prevention). A median of 28 months was spent following the patients. Clopidogrel treatment was beneficial for secondary prevention patients, according to subgroup analysis, with a 12% RRR (relative risk reduction) in the primary endpoint (p = 0.046). The rate of death from all causes increased by 31% (p = 0.04) and the rate of cardiovascular death increased by 44% (p = 0.01) in primary prevention patients, while the primary endpoint increased by an insignificant 20% (p = 0.20) RR (relative risk) with combination therapy. No significant differences were found in any other subgroups. In addition to increasing the risk of moderate and moderate-to-severe bleeding, the authors found that adding clopidogrel to aspirin did not lower the incidence of the primary endpoint. They also found that, although there was evidence of benefit in patients with documented disease, primary prevention patients had worse outcomes.

Factors In Fluencing Prescription Pattern Of CVDs

Factors that can influence prescription patterns for cardiovascular disease (CVD) include:

Patient characteristics Age, gender, smoking status, alcohol consumption, body mass index (BMI), blood pressure (BP), total cholesterol (TC), and comorbidities  Disease-related factors The long-term nature of CVD, its often asymptomatic nature, comorbidities, and the need for lifelong treatment Medication-related factorsThe burden of the illness and the use of medicines, and the occurrence of side effects Healthcare team and system-related factors Poor patient-HCP relationships and insufficient communication

Other factors Medication potency, patient circumstances, prescriber traits, medical facilities, mode of payment, and pharmaceutical advertising.

Benefits And Risks of Antiplatlet Therapy:

Benefits:

Though they are mainly used to stop blood clots from recurring after a heart attack or stroke, antiplatelet medications can also be used to prevent blood clots, heart attacks, and strokes. Symptoms including shortness of breath, poor circulation, and chest pain can also be alleviated by them.

Risks:        

Excessive bleeding is the primary danger associated with antiplatelet medications. All clots, including ones your body might require, are prevented by the medications. A wound on your skin or internal bleeding, for instance, could bleed so much that it becomes dangerous.

Despite their benefits, antiplatelet drugs come with significant challenges. The major limitation is the risk of bleeding, particularly gastrointestinal and intracranial hemorrhage. Balancing the antithrombotic benefits with the bleeding risk is a constant challenge in clinical practice. Moreover, variability in patient response to these drugs due to genetic differences (such as CYP2C19 polymorphisms affecting clopidogrel metabolism) can lead to suboptimal outcomes.

Antiplatelets stop platelets from clumping together and causing blood clots. For those who are at risk of having a heart attack or stroke, they are a popular treatment. Prolonged bleeding is the main danger associated with antiplatelet treatment.

Common Side Effects of Antiplatlet Therapy Include:

  • Aspirin-induced asthma.
  • Bradicardia.
  • Bleeding more heavily or for a longer time during periods or cuts.
  • Bruises.
  • Hemorrhage.
  • Epistaxis.
  • Upset stomach.
  • Haematuria, which could seem brown, pink, or red.
  • Hematochezia, which could seem black or red.
  • Chest pain.
  • Vomiting or coughing up blood
  • Hematoma (a large, raised bruise).
  • Tinnitus.
  • Stomach pain.

Future Targets Of Antiplatlet Agents:

Protease?activated receptors

Vorapaxar, an authorized PAR-1 antagonist, has a slow off-rate and a lengthy half-life.70 The PAR-1 antagonist atopaxar’s development was stopped in spite of encouraging Phase II evidence.71, 72 A novel cell-penetrating peptide-based PAR-1 inhibitor called PZ-128 may be able to get around these restrictions.73 PZ?128 targets the receptor?G?protein interface on the inside surface of platelets thereby blocking downstream G protein signaling. Recent studies in animal models and humans with CAD or several risk factors for CAD have demonstrated that PZ-128 inhibits platelet activation quickly and reversibly73,74. It may also be beneficial for short-term inhibition of platelet aggregation.

Glycoprotien VI:

Glycoprotein In thrombosis and other platelet-mediated activities, Glycoprotein VI is the primary collagen signaling receptor on human platelets. Inhibitory anti-GPVI antibodies and the soluble GPVI-Fc fusion protein Revacept are two GPVI inhibitors that have been previously explored as possible antiplatelet medications. Targeting the immunoglobulin-like domains of GPVI with Tro?6 and Tro?10 may result in the antiplatelet action. People with cardiovascular disease may benefit from these small-mass hexa-/deca-peptide GPVI antagonists.Targeting the immunoglobulin-like domains of GPVI with Tro?6 and Tro?10 may result in the antiplatelet action. For patients with cardiovascular disease, these small-mass hexa-/deca-peptide GPVI antagonists may be therapeutically useful.

Syk inhibitors have also been studied as potential antiplatelet drugs since spleen tyrosine kinase (Syk) activation downstream of GPVI is essential for platelet activation. 24 hours following transient middle cerebral artery closure in a mouse model, Van Eeuwijk et al. found that the oral selective Syk inhibitor BI1002494 avoided arterial thrombosis, led to reduced infarct sizes, and produced a markedly improved neurological outcome.

Platelet Oxidases:

Lipoxygenases (LOXs) are enzymes catalyzing the oxygenation of polyunsaturated fatty acids which leads to the synthesis of various signaling molecules.70 12?LOX is expressed in megakaryocytes and platelets, and oxidizes arachidonic acid at carbon 12.82 Growing evidence suggests that 12?LOX is involved in platelet activation.83, 84, 85, 86 Recently,. studied the impact of the selective 12?LOX inhibitor ML355 on thrombosis and hemostasis.87 They found a dose?dependent decrease of human platelet aggregation by ML355, an effect that was reversed following in vitro exposure to elevated thrombin concentrations. Moreover, oral administration of ML355 in mice reduced thrombus formation and vessel occlusion in FeCl3?induced mesenteric and laser?induced cremaster arteriole thrombosis models with only minimal effects on hemostasis.

Future Challenges:

There is an intermediate area of cardiovascular risk (10% to 20% at 10 years) where data from aspirin trials are lacking, but the benefits may outweigh the risks.  On this particular subject, there are four key preventative trials currently underway that could impact the guidelines. As repeatedly indicated by multiple lines of data, the apparent long-term benefits of aspirin therapy to lower the incidence of GI cancer and cancer-related mortality represent another intriguing finding. Although several theories have been put forth, the main mechanism of action of low-dose aspirin may be the inhibition of platelet activation at the locations of GI mucosal ulcers. Numerous adjuvant studies comparing low-dose aspirin to a placebo in cancer patients are presently in progress.

Combination Of Aspirin And Rivaroxaban In Stable Atherosclerosis:

In 27 395 patients with stable coronary artery disease (CAD) and/or PAD, the recently released COMPASS (Cardiovascular Outcomes for People Using Anticoagulation Strategies) trial compared standard antiplatelet therapy with low-dose aspirin (100 mg/day) vs. rivaroxaban 2.5 mg twice daily plus aspirin or rivaroxaban 5 mg twice daily.34 In addition, atherosclerosis involving at least two vascular beds or at least two additional risk factors (smoking, diabetes, chronic kidney disease with an estimated glomerular filtration rate <60>

CONCLUSION:

The study underscores the critical role of antiplatelet drugs in the management of cardiovascular diseases (CVD). These agents significantly reduce the risk of major adverse cardiovascular events, including myocardial infarction and stroke, by inhibiting platelet aggregation. The findings highlight the efficacy of commonly used antiplatelets like aspirin and P2Y12 inhibitors, particularly in secondary prevention. However, the study also emphasizes the need for individualized therapy to balance the benefits of thrombotic event prevention with the risk of bleeding. Continued research is warranted to optimize dosing strategies, explore novel agents, and address gaps in evidence for diverse patient populations and clinical scenarios.

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Reference

  1. Frazier SC. Health outcomes and polypharmacy in elderly individuals: an integrated literature review. J Gerontol Nurs 2005;31:4-11.
  2.  Nguyen JK, Fouts MM, Kotabe SE, Lo E. Polypharmacy as a risk factor for adverse drug reactions in geriatric nursing home residents. Am J Geriatr Pharmacother 2006;4:36-41.
  3. Aparasu RR, Mort JR. Inappropriate prescribing for the elderly: Beers criteria-based review. Ann Pharmacother 2000;34:338-46. DOI 10.1345/aph.19006
  4. Farley A, McLafferty E, Hendry C. The cardiovascular system. 2012 Oct 31-Nov 6Nurs Stand. 27(9):35-9. [PubMed]
  5. Benjamin EJ, Virani SS, Callaway CW, Chamberlain AM, Chang AR, Cheng S, Chiuve SE, Cushman M, Delling FN, Deo R, de Ferranti SD, Ferguson JF, Fornage M, Gillespie C, Isasi CR, Jiménez MC, Jordan LC, Judd SE, Lackland D, Lichtman JH, Lisabeth L, Liu S, Longenecker CT, Lutsey PL, Mackey JS, Matchar DB, Matsushita K, Mussolino ME, Nasir K, O'Flaherty M, Palaniappan LP, Pandey A, Pandey DK, Reeves MJ, Ritchey MD, Rodriguez CJ, Roth GA, Rosamond WD, Sampson UKA, Satou GM, Shah SH, Spartano NL, Tirschwell DL, Tsao CW, Voeks JH, Willey JZ, Wilkins JT, Wu JH, Alger HM, Wong SS, Muntner P., American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee. Heart Disease and Stroke Statistics-2018 Update: A Report From the American Heart Association. Circulation. 2018 Mar 20;137(12):e67-e492. [PubMed]
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  7. Fox CS, Coady S, Sorlie PD, Levy D, Meigs JB, D'Agostino RB, Wilson PW, Savage PJ. Trends in cardiovascular complications of diabetes. JAMA. 2004 Nov 24;292(20):2495-9. [PubMed]
  8. Vasan RS, Sullivan LM, Wilson PW, Sempos CT, Sundström J, Kannel WB, Levy D, D'Agostino RB. Relative importance of borderline and elevated levels of coronary heart disease risk factors. Ann Intern Med. 2005 Mar 15;142(6):393-402. [PubMed]
  9.  Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, McQueen M, Budaj A, Pais P, Varigos J, Lisheng L., INTERHEART Study Investigators. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet. 2004 Sep 11-17;364(9438):937-52. [PubMed]
  10. Fox CS, Pencina MJ, Wilson PW, Paynter NP, Vasan RS, D'Agostino RB. Lifetime risk of cardiovascular disease among individuals with and without diabetes stratified by obesity status in the Framingham heart study. Diabetes Care. 2008 Aug;31(8):1582-4. [PMC free article] [PubMed]
  11. Lloyd-Jones DM, Hong Y, Labarthe D, Mozaffarian D, Appel LJ, Van Horn L, Greenlund K, Daniels S, Nichol G, Tomaselli GF, Arnett DK, Fonarow GC, Ho PM, Lauer MS, Masoudi FA, Robertson RM, Roger V, Schwamm LH, Sorlie P, Yancy CW, Rosamond WD., American Heart Association Strategic Planning Task Force and Statistics Committee. Defining and setting national goals for cardiovascular health promotion and disease reduction: the American Heart Association's strategic Impact Goal through 2020 and beyond. Circulation. 2010 Feb 02;121(4):586-613. [PubMed]
  12. Davi G, Patrono C. Platelet activation and atherothrombosis. N Engl J Med. 2007;357:2482–94. [DOI] [PubMed] [Google Scholar
  13. Gremmel T, Frelinger AL 3rd, Michelson AD. Platelet physiology. Semin Thromb Hemost. 2016;42:191–204. [DOI] [PubMed] [Google Scholar]
  14. Ruggeri ZM. Platelets in atherothrombosis. Nat Med. 2002;8:1227–34. [DOI] [PubMed] [Google Scholar]
  15. Michelson AD. Antiplatelet therapies for the treatment of cardiovascular disease. Nat Rev Drug Discov. 2010;9:154–69. [DOI] [PubMed] [Google Scholar]
  16. Patrono C, Rocca B. Aspirin, 110 years later. J Thromb Haemost. 2009;7(Suppl 1):258–61. [DOI] [PubMed] [Google Scholar]
  17. Antithrombotic Trialists’ Collabtoration . Collaborative meta?analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ. 2002;324:71–86. [DOI] [PMC free article] [PubMed] [Google Scholar]
  18.  Baigent C, Blackwell L, Collins R, et al. Aspirin in the primary and secondary prevention of vascular disease: collaborative meta?analysis of individual participant data from randomised trials. Lancet. 2009;373:1849–60. [DOI] [PMC free article] [PubMed] [Google Scholar]
  19. Cattaneo M. New P2Y12 blockers. J Thromb Haemost. 2009;7(Suppl 1):262–5. [DOI] [PubMed] [Google Scholar]
  20. Floyd CN, Passacquale G, Ferro A. Comparative pharmacokinetics and pharmacodynamics of platelet adenosine diphosphate receptor antagonists and their clinical implications. Clin Pharmacokinet. 2012;51:429–42. [DOI] [PubMed] [Google Scholar
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Shweta Nilamwar
Corresponding author

Pharmacy Practice Department Shivlingeshwar College of Pharmacy, Almala. Tq. Ausa, Dist. Latur

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Pranjali Mane
Co-author

Pharmacy Practice Department Shivlingeshwar College of Pharmacy, Almala. Tq. Ausa, Dist. Latur

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Rohan Boralkar
Co-author

Pharmacy Practice Department Shivlingeshwar College of Pharmacy, Almala. Tq. Ausa, Dist. Latur

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Dr. Ashok Giri
Co-author

Pharmacy Practice Department Shivlingeshwar College of Pharmacy, Almala. Tq. Ausa, Dist. Latur

Shweta Nilamwar*, Pranjali Mane, Rohan Boralkar, Dr. Ashok Giri, Study Of Outcomes of Antiplatelet Drugs Used in The Management of Cardiovascular Diseases:, Int. J. of Pharm. Sci., 2024, Vol 2, Issue 12, 2427-2435. https://doi.org/10.5281/zenodo.14514018

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