The document provides an overview of antiplatelet agents, including their mechanisms of action, pharmacology, and places in therapy. It reviews how hemostasis involves platelet plug formation and coagulation, and how different medications can affect this process. The major classes of antiplatelet agents discussed are aspirin, P2Y12 receptor antagonists like clopidogrel and ticagrelor, glycoprotein IIb/IIIa inhibitors like abciximab, cyclic AMP inhibitors like dipyridamole, and thrombin receptor antagonists like vorapaxar. Each drug's mechanism of action, pharmacokinetics, indications, and safety considerations are outlined.
Ticagrelor in acute myocardial infarctionVasif Mayan
Potential benefits of dual antiplatelet therapy beyond 1 year after an MI has not been studied
Patients with MI are at increased risk of RECURRENT ISCHAEMIC EVENTS
Intensive secondary prevention is theoretically beneficial
Finding an ideal drug with best risk-benefit ratio is a challenge
TICAGRELOR
--- Direct acting
Not a pro-drug; does not require metabolic activation
Rapid onset of inhibitory effect on the P2Y12 receptor
Greater inhibition of platelet aggregation than clopidogrel
--- Reversibly bound
Degree of inhibition reflects plasma concentration
Faster offset of effect than clopidogrel
Functional recovery of circulating platelets within ~48 hours
PLATO trial
PEGASUS TIMI trial
Ticagrelor in acute myocardial infarctionVasif Mayan
Potential benefits of dual antiplatelet therapy beyond 1 year after an MI has not been studied
Patients with MI are at increased risk of RECURRENT ISCHAEMIC EVENTS
Intensive secondary prevention is theoretically beneficial
Finding an ideal drug with best risk-benefit ratio is a challenge
TICAGRELOR
--- Direct acting
Not a pro-drug; does not require metabolic activation
Rapid onset of inhibitory effect on the P2Y12 receptor
Greater inhibition of platelet aggregation than clopidogrel
--- Reversibly bound
Degree of inhibition reflects plasma concentration
Faster offset of effect than clopidogrel
Functional recovery of circulating platelets within ~48 hours
PLATO trial
PEGASUS TIMI trial
Beta Blockers in current cardiovascular practice Praveen Nagula
betablockers are the drug of choice for prevention of progression of heart failure with mortality benefit, after the evolution of neurohormonal regulation as pathogenesis of heart failure
Cardiovascular safety of anti-diabetic drugs.Cardiovascular Outcome Trials ...magdy elmasry
Cardiologists and diabetes.Target organs and action mechanism of antidiabetic drugs.Cardiovascular Outcome Trials
( CVOTs ) in Diabetes.Completed and ongoing CVOTs in type 2 diabetes.Diabetes Medications
and
Cardiovascular Impact.Recommendations for management of diabetes
Cardiovascular safety of anti-diabetic drugs.
Beta Blockers in current cardiovascular practice Praveen Nagula
betablockers are the drug of choice for prevention of progression of heart failure with mortality benefit, after the evolution of neurohormonal regulation as pathogenesis of heart failure
Cardiovascular safety of anti-diabetic drugs.Cardiovascular Outcome Trials ...magdy elmasry
Cardiologists and diabetes.Target organs and action mechanism of antidiabetic drugs.Cardiovascular Outcome Trials
( CVOTs ) in Diabetes.Completed and ongoing CVOTs in type 2 diabetes.Diabetes Medications
and
Cardiovascular Impact.Recommendations for management of diabetes
Cardiovascular safety of anti-diabetic drugs.
Drugs for prophylaxis of Myocardial InfarctionJervinM
Drugs for prophylaxis of Myocardial Infarction
Myocardial Infarction
Drugs for primary prevention of MI
Drugs for secondary prevention of MI
Recent advances
Cardiac rehabilitation
Robert Sinha, M.D., Radiation Oncologist .Western Radiation Oncology - Dorothy Schneider Cancer Center - 2013 Mills-Peninsula Health Services Cancer Symposium
Mills-Peninsula Health Services Cancer Symposium - Kimberly Moore Dalal, MD, FACS
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Mills-Peninsula Health Services 2013 Cancer Symposium presentation - Brad Ekstrand, MD/PhD, California Cancer Care Mills-Peninsula Health Services San Mateo, CA
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CHAPTER 1 SEMESTER V PREVENTIVE-PEDIATRICS.pdfSachin Sharma
This content provides an overview of preventive pediatrics. It defines preventive pediatrics as preventing disease and promoting children's physical, mental, and social well-being to achieve positive health. It discusses antenatal, postnatal, and social preventive pediatrics. It also covers various child health programs like immunization, breastfeeding, ICDS, and the roles of organizations like WHO, UNICEF, and nurses in preventive pediatrics.
The dimensions of healthcare quality refer to various attributes or aspects that define the standard of healthcare services. These dimensions are used to evaluate, measure, and improve the quality of care provided to patients. A comprehensive understanding of these dimensions ensures that healthcare systems can address various aspects of patient care effectively and holistically. Dimensions of Healthcare Quality and Performance of care include the following; Appropriateness, Availability, Competence, Continuity, Effectiveness, Efficiency, Efficacy, Prevention, Respect and Care, Safety as well as Timeliness.
Global launch of the Healthy Ageing and Prevention Index 2nd wave – alongside...ILC- UK
The Healthy Ageing and Prevention Index is an online tool created by ILC that ranks countries on six metrics including, life span, health span, work span, income, environmental performance, and happiness. The Index helps us understand how well countries have adapted to longevity and inform decision makers on what must be done to maximise the economic benefits that comes with living well for longer.
Alongside the 77th World Health Assembly in Geneva on 28 May 2024, we launched the second version of our Index, allowing us to track progress and give new insights into what needs to be done to keep populations healthier for longer.
The speakers included:
Professor Orazio Schillaci, Minister of Health, Italy
Dr Hans Groth, Chairman of the Board, World Demographic & Ageing Forum
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Dr Natasha Azzopardi Muscat, Director, Country Health Policies and Systems Division, World Health Organisation EURO
Dr Marta Lomazzi, Executive Manager, World Federation of Public Health Associations
Dr Shyam Bishen, Head, Centre for Health and Healthcare and Member of the Executive Committee, World Economic Forum
Dr Karin Tegmark Wisell, Director General, Public Health Agency of Sweden
Empowering ACOs: Leveraging Quality Management Tools for MIPS and BeyondHealth Catalyst
Join us as we delve into the crucial realm of quality reporting for MSSP (Medicare Shared Savings Program) Accountable Care Organizations (ACOs).
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Antibiotic Stewardship by Anushri Srivastava.pptxAnushriSrivastav
Stewardship is the act of taking good care of something.
Antimicrobial stewardship is a coordinated program that promotes the appropriate use of antimicrobials (including antibiotics), improves patient outcomes, reduces microbial resistance, and decreases the spread of infections caused by multidrug-resistant organisms.
WHO launched the Global Antimicrobial Resistance and Use Surveillance System (GLASS) in 2015 to fill knowledge gaps and inform strategies at all levels.
ACCORDING TO apic.org,
Antimicrobial stewardship is a coordinated program that promotes the appropriate use of antimicrobials (including antibiotics), improves patient outcomes, reduces microbial resistance, and decreases the spread of infections caused by multidrug-resistant organisms.
ACCORDING TO pewtrusts.org,
Antibiotic stewardship refers to efforts in doctors’ offices, hospitals, long term care facilities, and other health care settings to ensure that antibiotics are used only when necessary and appropriate
According to WHO,
Antimicrobial stewardship is a systematic approach to educate and support health care professionals to follow evidence-based guidelines for prescribing and administering antimicrobials
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Antimicrobial Stewardship(AMS) refers to the optimal selection, dosing, and duration of antimicrobial treatment resulting in the best clinical outcome with minimal side effects to the patients and minimal impact on subsequent resistance.
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VISION
Being proactive
Supporting optimal animal and human health
Exploring ways to reduce overall use of antimicrobials
Using the drugs that prevent and treat disease by killing microscopic organisms in a responsible way
GOAL
to prevent the generation and spread of antimicrobial resistance (AMR). Doing so will preserve the effectiveness of these drugs in animals and humans for years to come.
being to preserve human and animal health and the effectiveness of antimicrobial medications.
to implement a multidisciplinary approach in assembling a stewardship team to include an infectious disease physician, a clinical pharmacist with infectious diseases training, infection preventionist, and a close collaboration with the staff in the clinical microbiology laboratory
to prevent antimicrobial overuse, misuse and abuse.
to minimize the developme
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Defecation
Normal defecation begins with movement in the left colon, moving stool toward the anus. When stool reaches the rectum, the distention causes relaxation of the internal sphincter and an awareness of the need to defecate. At the time of defecation, the external sphincter relaxes, and abdominal muscles contract, increasing intrarectal pressure and forcing the stool out
The Valsalva maneuver exerts pressure to expel faeces through a voluntary contraction of the abdominal muscles while maintaining forced expiration against a closed airway. Patients with cardiovascular disease, glaucoma, increased intracranial pressure, or a new surgical wound are at greater risk for cardiac dysrhythmias and elevated blood pressure with the Valsalva maneuver and need to avoid straining to pass the stool.
Normal defecation is painless, resulting in passage of soft, formed stool
CONSTIPATION
Constipation is a symptom, not a disease. Improper diet, reduced fluid intake, lack of exercise, and certain medications can cause constipation. For example, patients receiving opiates for pain after surgery often require a stool softener or laxative to prevent constipation. The signs of constipation include infrequent bowel movements (less than every 3 days), difficulty passing stools, excessive straining, inability to defecate at will, and hard feaces
IMPACTION
Fecal impaction results from unrelieved constipation. It is a collection of hardened feces wedged in the rectum that a person cannot expel. In cases of severe impaction the mass extends up into the sigmoid colon.
DIARRHEA
Diarrhea is an increase in the number of stools and the passage of liquid, unformed feces. It is associated with disorders affecting digestion, absorption, and secretion in the GI tract. Intestinal contents pass through the small and large intestine too quickly to allow for the usual absorption of fluid and nutrients. Irritation within the colon results in increased mucus secretion. As a result, feces become watery, and the patient is unable to control the urge to defecate. Normally an anal bag is safe and effective in long-term treatment of patients with fecal incontinence at home, in hospice, or in the hospital. Fecal incontinence is expensive and a potentially dangerous condition in terms of contamination and risk of skin ulceration
HEMORRHOIDS
Hemorrhoids are dilated, engorged veins in the lining of the rectum. They are either external or internal.
FLATULENCE
As gas accumulates in the lumen of the intestines, the bowel wall stretches and distends (flatulence). It is a common cause of abdominal fullness, pain, and cramping. Normally intestinal gas escapes through the mouth (belching) or the anus (passing of flatus)
FECAL INCONTINENCE
Fecal incontinence is the inability to control passage of feces and gas from the anus. Incontinence harms a patient’s body image
PREPARATION AND GIVING OF LAXATIVESACCORDING TO POTTER AND PERRY,
An enema is the instillation of a solution into the rectum and sig
Explore our infographic on 'Essential Metrics for Palliative Care Management' which highlights key performance indicators crucial for enhancing the quality and efficiency of palliative care services.
This visual guide breaks down important metrics across four categories: Patient-Centered Metrics, Care Efficiency Metrics, Quality of Life Metrics, and Staff Metrics. Each section is designed to help healthcare professionals monitor and improve care delivery for patients facing serious illnesses. Understand how to implement these metrics in your palliative care practices for better outcomes and higher satisfaction levels.
2. Course Outline
• Review hemostatic mechanisms
• Review mechanisms of action of each class of
antiplatelet agent
• Compare and contrast pharmacology of
antiplatelet agents
• Identify unique places in therapy for each
antiplatelet agent
3. Hemostasis
• Normal physiological
response that prevents
significant blood loss after
vascular injury
• Clot formation involves
multiple system responses:
– Vasoconstriction
– Platelet plug formation
– Coagulation
• Once the vessel heals,
primary fibrinolysis is
triggered and clot formation
processes are inhibited
Image source: http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/hematology-oncology/hypercoagulable-states/
5. Medications That Affect Hemostasis
• Antithrombotics prevent or interfere with the formation and
growth of blood clots.
•Antiplatelet agents—decrease platelet activation and
aggregation release of granule contents, and platelet-
mediated vascular constriction.
»Examples: Aspirin, thienopyridines, glycoprotein IIb/IIIa
Inhibitors, P2Y12 platelet receptor inhibitors, Protease-Activated
Receptor-1 (PAR-1) Antagonist
•Anticoagulants—interfere with clotting factors
»Examples: heparin, low molecular weight heparins (LMWH),
warfarin, factor Xa inhibitors, direct thrombin inhibitors
• Antifibrinolytics inhibit clot dissolution
»Example: Aminocaproic Acid, tranexamic acid
• Thrombolytics dissolve existing clots
»Example: Alteplase (tPA)
6. Platelet Activation and Aggregation
Front. Pharmacol., 24 October 2011 | http://dx.doi.org/10.3389/fphar.2011.00061
7. Aspirin
• Aspirin
– Possible use of salycilates (willow bark) as early as 3000 BC
– Developed into a pharmaceutical agent throughout the 1800s
– OTC ASA available by the early 1900s and widely available
• Common Indications:
– Broad number of indications due to antithrombotic,
analgesic, antipyretic, and anti-inflammatory effects
• Primary and secondary prevention of cardiovascular disease
• Part of acute treatment for ischemic stroke/TIA, and Acute
Coronary Syndrome
• Analgesia
• Anti-inflammatory
8. Aspirin—Mechanism of Action
• Acetylates COX-1 and COX-
2, blocking the conversion
of arachidonic acid to
prostaglandins and
thromboxane A2 (Tx A2)
– Blocks Platelet aggregation
– Irreversible, lasts life of
platelet (7-10 days)
• Low doses inhibit COX-1
• Higher doses inhibit COX-2,
which also leads to
analgesia and reduction in
inflammation
9. Aspirin
• Bioavailability: 50% to 75%
• Cmax: 30-60 min (IR)
• Half life:
– Parent drug: 15-20 min; Salycylates: 3 to 10 hours
– Normal hemostasis returns in ~4-7 days
• Optimal dose is >75mg or ≤325mg
• Bleeding :
– GI bleeds are most common
– Several meta-analyses show ~1-2X increase risk of major bleeding over
placebo
• Aspirin resistance
– Leads to treatment failures, higher rates of death, MI, stroke
– Incidence between 5-40% at doses of 325mg daily
• Aspirin sensitivity/allergy
10. P2Y12 Receptor Antagonists
• Common Indications:
– Secondary prevention of
cardiovascular disease
– Acute Coronary Syndrome
• Percutaneous coronary
intervention (PCI)
• Medical management
– Prevention of stent
thrombosis
– ASA substitute for patients
with ASA sensitivity
Thienopyridine Route Approval
Ticlopidine (Ticlid®) Oral 1991
Clopidogrel (Plavix®) Oral 1997
Prasugrel (Effient®) Oral 2009
Non-thienopyridine Route Approval
Ticagrelor (Brilinta®) PO 2011
Cangrelor (Kengreal®) IV 2015
11. P2Y12 Receptor Antagonists
• The P2Y12 receptor
antagonists block the
binding of adenosine
diphosphate (ADP) to the
platelet receptor P2Y12,
inhibiting activation of the
(GP) IIb/IIIa complex
– Binding to the receptors
– Changing conformation of
the receptor
• Blocks platelet activation
and aggregation
12. P2Y12 Receptor Antagonists
Clopidogrel Prasugrel Ticagrelor Cangrelor
Prodrug Yes Yes No No
Route Oral Oral Oral Intravenous
Binding Irreversible Irreversible Reversible Reversible
Onset of
Action
Loading dose:
<2hours
Maintenance: Day
2 of tx
Loading dose:
<0.5 hours
Loading dose:
<0.5 hours
Within 2
minutes of
infusion
Duration of
Action
After d/c, Gradual
decline over 5-10
days
After d/c,
Gradual decline
over 5-10 days
After d/c,
Gradual
decline over 2-
5 days
Return of
platelet
function within
1 hour after d/c
of infusion
Dosing
Frequency
Daily Daily BID Continuous
infusion
Dual ASA
therapy
75-100 mg/day 81 mg/day, up
to 325 mg/day
81 mg/day, up
to 100mg/day
N/A
13. • Bleeding Events
– Newer, more potent agents associated with increased bleeding risks
compared to clopidogrel
– Prasugrel 10 mg daily contraindicated if patient is ≥75 years or weight
<60 kg.
– Hx of stroke or TIA:
• Clopidogrel preferred
• Ticagrelor not contraindicated, but experience is limited
• Prasugrel contraindicated
• Clopidogrel Resistance and Treatment Failures
• Genetic polymorphisms (CYP2C19 and ABCB1), drug interactions,
disease states, compliance, obesity and diabetes,
hyporesponsiveness to clopidogrel
P2Y12 Receptor Antagonists
14. Cangrelor (Kangreal®)
• New IV P2Y12 agent with rapid onset and offset
• Approved as an adjunct to PCI for reducing the risk
of periprocedural myocardial infarction (MI), repeat
coronary revascularization, and stent thrombosis in
patients who have not previously been treated with
an oral P2Y12 inhibitor and who are not being given
a GP IIb/IIIa inhibitor.
• Compared to clopidgrel or placebo
– Slightly higher bleeding, hypersensitivity reactions,
worsening renal function, and dyspnea in cangrelor
patients.
15. Glycoprotein IIb/IIIa Inhibitors
• Indications:
– Acute Coronary Syndrome
• Percutaneous coronary intervention (PCI)
• Medical Management
Agents Route Type of medication Approval
Abciximab (ReoPro®) IV Humanized chimeric fragment of the
mouse antibody 7E3
1998
Tirofiban
(Aggrastat®)
IV Small molecule 1998
Eptifibatide
(Integrilin®)
IV Small molecule 1998
16. Glycoprotein IIb/IIIa Inhibitors
• The platelet integrin receptor GPIIb/IIIa mediates interactions
between platelets and several ligands, primarily fibrinogen, leading
to platelet aggregation
• GPIIb/IIIa antibodies and receptor antagonists inhibit this binding by
antagonizing or binding to the receptor.
Abciximab (ReoPro®)
Noncompetitive
irreversible inhibitor of
intact GPIIb/IIIa receptor
Tirofiban (Aggrastat®)
Eptifabatide (Integrilin)
Competitive and
reversible antagonists that
act specifically on the αIIb-
subunit of GPIIb/IIIa
17. Glycoprotein IIb/IIIa Inhibitors
Tirofiban Eptifibatide Abciximab
Onset 10 min 5 min 30 min
Half Life 2 hours
Normal hemostasis:
4-8 hours
2.5 hours
Normal hemostasis:
4-8 hours
30 min
Normal hemostasis:
72 hours
Clearance Renal
(Dose adjust for
moderate-severe
renal dysfunction)
Renal
(Dose adjust for
moderate-severe renal
dysfunction; CI for HD)
Metabolized via
proteolytic cleavage
Bleeding Major: 1.4%
Minor: 10.5%
Major: 1.3-10.8%
Minor: 3-13.1%
Major: 0.8-3.8%
Minor: 3.2-7.6%
Contra-
indications
History of
thrombocytopenia
Uncontrolled HTN; hx of
stroke (within 30 days),
dialysis paitents
Hypersensitivity to
murine proteins, 6
week hx of major
bleeding, hx of CVA
within 2 years, use in a
patient taking an OAC
18. Glycoprotein IIb/IIIa Inhibitors
• Common adverse events
– Bleeding: GI and arterial access sites most common sites
– Thrombocytopenia
• Within minutes to hours
• Abciximab > tirofiban, eptifibatide
• Cross-reactivity may exist between agents
– Abciximab associated with infusion-related reactions,
headache, hypotension, chest pain, nausea/vomiting
– Abciximab re-exposure associated with higher risk of
hypersensitivity reaction
• Monitoring: Platelets, Hgb/Hct, SCr, PT/aPTT prior to treatment,
then within 6 hours following load, then daily, then once prior to
discharge. ACT during PCI.
19. Cyclic AMP Inhibitors
Common Indications:
• Prevention of stroke
(Aggrenox®)
• Intermittent claudication
(Cilostazol)
• Evaluation of coronary
artery disease
(Dipyridmadole)
Agent Route
Dipyridamole
(Persantine®)
PO, IV
Dipyridamole +
Aspirin (Aggrenox®)
PO
Cilostazol (Pletal®) PO
20. Cyclic AMP Inhibitors
• Mechanism of Action:
– Both dipyridamole and cilostasol:
• Inhibit the phosphodiesterase enzymes that break down cAMP,
thereby increasing cAMP levels that block the platelet response to
ADP and prevent platelet activation
– Dipyridamole:
• Blocks thromboxane synthase and the thromboxane receptor
preventing thromboxane A2 formation, which inhibits platelet
aggregation.
• Increases plasma adenosine levels and potentiates nitric oxide
signaling through cyclic GMP, which inhibits platelet aggregation.
21. Cyclic AMP Inhibitors
• Dipyridamole/Aspirin (Aggrenox)
– Extended release form of dipyridamole with low dose of
aspirin (25mg)
– Mainly used for secondary prevention of stroke
– Common side effect is headache
• Dipyridamole (IV, immediate release oral)
– IV formulation dilates coronary arteries for stress testing
– Immediate release PO form rarely used
• Cilostazol (Pletal)
– Mostly used for Peripheral Artery Disease and claudication
– May be alternative agent to ASA or Clopidogrel if allergies or
intolerances exist and dual antiplatelet therapy is necessary
22. Thrombin Receptor (PAR-1) Antagonists
Indication:
• Reduction of thrombotic
cardiovascular
events(cardiovascular
death, myocardial infarction
[MI], stroke, urgent
coronary revascularization)
in patients with a history of
MI or with peripheral
arterial disease.
Agent Route Approval
Vorapaxar
(Zontivity®)
Oral May 2014
Atopaxar Oral Not FDA
approved
23. Thrombin Receptor (PAR-1) Antagonists
• Platelet activation by
thrombin is mediated via two
Protease-Activated Receptors
(PARs):
– (PAR-1) is the major human
platelet receptor, exhibiting 10–
100-times higher affinity for
thrombin when compared with
the PAR-4
• Voraxapar and atopaxar
selectively and competitively
antagonize the PAR-1 receptor.
24. Vorapaxar (Zontivity®)
Bioavailability 100%. Oral administration only.
Time to peak 1 to 2 hours
Metabolism Hepatic via CYP3A4 and CYP2J2
Excretion Primarily through feces (58%); urine (25%)
Half-life
elimination
Effective half-life: 3 to 4 days
terminal elimination half-life (vorapaxar and active metabolite):
approximately 8 days (range, 5 to 13 days)
Onset ≥80% inhibition of thrombin receptor-activating peptide (TRAP)-
induced platelet aggregation within 1 week
Duration Dose and concentration dependent; inhibition of TRAP-induced
platelet aggregation at a level of 50% can be expected 4 weeks after
discontinuation.
Bleeding
Concerns
Any: 26%; Major: 13%; Use is contraindicated in patients with history
of stroke, TIA, or ICH; or active pathological bleeding.
Special
Considerations
There is no experience with use of vorapaxar as monotherapy or with
other antiplatelet agents other than aspirin and clopidogrel
26. Conclusion
• Several mechanisms may be targeted to inhibit
platelet activation and aggragation.
• Several agents have an established place in treating
acute cardiovasular events as well as primary and
secondary prevention of cardiovascular events.
• Clinical data, pharmacology, bleed risk, and patient
specific factors must all be considered for safe use
of anti-platelet agents
27. Refrences
• Zontivity (vorapaxar). Prescribing information. Merck & Co, Inc; April 2015.
• Abciximab (Reopro). Prescribing information. Eli Lilly and Company. December 2013.
• Eftifibatide (Integrilin). Prescribing information. Merck Sharp & Dohme Corp.. April
2014.
• Aggrenox Prescribing information. Boehringer Ingelheim Pharmaceuticals, Inc.
December 2013.
• Clopidogrel Prescribing information. Bristol-Myers Squibb/Sanofi Pharmaceuticals
Partnership. July 2015.
• Brilinta Prescribing Information. AstraZeneca. September 2015.
• Effient .Prescribing information. Eli Lilly and Company July 2015.
• Kengreal. Prescribing information. The Medicines Company. June 2015.
• McQuaid KR, et al. Systematic review and meta-analysis of adverse events of low-
dose aspirin and clopidogrel in randomized controlled trials. Am J Med.
2006;119(8):624
• LexiComp Database. Accessed September 2015.
• Facts and Comparisons Database. Accessed September 2015.