Acute Coronary Syndrome - Ministry of Public Health · • Acute coronary syndrome is defined as ... studentpresentation08-04-03.ppt. ... • Poor surgical technique (post CABG)

Acute Coronary Syndrome

PRESENTED BYALIN SINTURAT

Definitions

• Acute coronary syndrome is defined as myocardial ischemia due to myocardial infarction (NSTEMI or STEMI) or unstable angina

• Unstable angina is defined as angina at rest, new onset exertional angina (<2 months), recent acceleration of angina (<2 months), or post revascularization angina

http://www.cardiology.tulane.edu/presentations/

studentpresentation08-04-03.ppt



Diagnosis

• Dx of acute coronary syndrome is based on history, physical exam, ECG, cardiac enzymes

• Patients can then be divided into several groups– Non-cardiac chest pain (i.e., Gastrointestinal,

musculoskeletal, pulmonary embolus)– Stable angina– Unstable angina– Myocardial infarction (STEMI or NSTEMI)– Other cardiac causes of chest pain (i.e., aortic

dissection, pericarditis)



Pathophysiology of ACS

• Plaque rupture and subsequent formation of thrombus – this can be either occlusive or non-occlusive (STEMI, NSTEMI, USA)

• Vasospasm such as that seen in Prinzmetal’sangina, cocaine use (STEMI, NSTEMI, USA)

• Progression of obstructive coronary atherosclerotic disease (USA)

• In-stent thrombosis (early post PCI)• In-stent restenosis (late post PCI• Poor surgical technique (post CABG)



ACS PATHOPHYSIOLOGY

• Disruption of coronary artery plaque -> platelet activation/aggregation /activation of coagulation cascade -> endothelial vasoconstriction ->intraluminalthrombus/embolisation -> obstruction -> ACS

• Severity of coronary vessel obstruction & extent of myocardium involved determines characteristics of clinical presentation

Treatment of NSTEMI/USA

• ASA• NTG (consider MSO4 if pain not relieved)• Beta Blocker• Heparin/LMWH• ACE-I• +/- Statin• +/- Clopidogrel (don’t give if CABG is a

possibility)• +/- IIBIIIA inhibitors (based on TIMI risk score)



Treatment of STEMI

• ASA• NTG (consider MSO4 if pain not relieved)• Beta Blocker• Heparin/LMWH• ACE-I• +/-Clopidogrel (based on possibility of CABG)• IIBIIIA • +/- Statin• Activate the Cath Lab!!!



Treatment of ACS; Aspirin

• Aspirin is an antiplatelet agent that initiates the irreversible inhibition of cyclooxygenase, thereby preventing platelet production of thromboxane A2 and decreasing platelet aggregation

• Administration of ASA in ACS reduces cardiac endpoints



ACC/AHA Guidelines for Aspirin Therapy

• Aspirin should be given in a dose of 75-325 mg/day to all patients with ACS unless there is a contraindication (in which case, clopidogrel should be given)



Treatment of ACS; Clopidogrel

• Clopidogrel is a potent antiplatelet agent• It should be administered to all patients

who cannot take ASA• The CURE trial suggests a benefit to

adding Clopidogrel to ASA/Heparin in patients going for PCI

• Give 300 mg loading dose followed by 75 mg/day



AHA/ACC Guidelines for Clopidogrel

• Clopidogrel should be administered to patients who cannot take ASA because of hypersensitivity or gastrointestinal intolerance

• In hospitalized patients in whom an early, noninterventional approach is planned, clopidogrel should be added to ASA as soon as possible on admission and administered for at least 1 month and up to 9 months. Do not use clopidogrel if there is any possibility patient may be candidate for CABG



Treatment of ACS; IIBIIIA Inhibitors

• More potent inhibition of platelet aggregation may be of importance in patients with ACS that is associated with unstable coronary lesion and thrombus formation. This can be achieved by the use of GP IIBIIIA inhibitors

• Administration of IIBIIIA inhibitors reduces cardiac endpoints



AHA/ACC Guidelines for use of IIBIIIA inhibitors

• A IIBIIIA inhibitor should be administered to all patients in whom a percutaneousintervention is planned (in addition to heparin/ASA)

• Eptifibatide or Tirofiban should be administered to patients with ACS in whom PCI is not planned if other high risk features are present (TIMI risk score >3)



TIMI Risk Score

• Age >65 yrs• Daily ASA Therapy (>7 days prior to

event)• Symptoms of Unstable Angina• Documented CAD (stenosis > 50%)• 3 or more traditional cardiac risk factors• Elevated cardiac enzymes• ECG changes



TIMI Risk Score

• Score of 3 or less = low risk• Score of 4-5 = intermediate risk (use

IIBIIIA)• Score of 6-7 = high risk (use IIBIIIA)



Treatment of ACS; Heparin

• Heparin (unfractionated heparin or UFH) has traditionally been the mainstay of therapy in acute coronary syndromes as its efficacy has been documented in several large, randomized trials



Treatment of ACS; LMWH

• More recent studies indicate that low molecular weight heparin is also effective in the reduction of end points such as myocardial infarction or death

• Some studies report that LMWH, when used in combination with ASA, may be superior to continuous infusion of Heparin



ACC/AHA Guidelines for Heparin Therapy

• All patients with acute coronary syndromes should be treated with a combination of ASA (325 mg/day) and heparin (bolus followed by continuous infusion with goal of PTT 1-2.5X control) or ASA and low molecular weight heparin unless one of the drugs is contraindicated



Treatment of ACS; Beta Blockers

• Beta Blockers reduce myocardial oxygen demand by reducing heart rate, contractility, and ventricular wall tension

• Administration of beta blockers in ACS reduces cardiac endpoints



AHA/ACC Guidelines for Beta Blocker Therapy

• Intravenous beta blockers should be used initially in all patients (without contraindication) followed by oral beta blockers with the goal being decrease in heart rate to 60 beats per minute

• A combination of beta blockers and nitrates can be viewed as first line therapy in all patients with ACS



Treatment of ACS; Nitrates

• Nitroglycerin is considered a cornerstone of anti-anginal therapy, despite little objective evidence for its benefit

• Benefit is thought to occur via reduction in myocardial O2 demand secondary to venodilation induced reduction in preload as well as coronary vasodilation and afterload reduction

• Titrate to relief of chest pain; chest pain = death of myocardial cells

• No documented mortality benefit



Treatment of ACS; ACE-I

• The best documented mechanism by which these agents act is to reduce ventricular remodeling over days to weeks after myocardial damage. However, there is data that a mortality benefit exists when these agents are used early in the course of ACS

• Administration of ACE-I in ACS reduces cardiac endpoints



AHA/ACC Guidelines for ACE-I Therapy

• ACE-I should be administered to all patients in the first 24 hours of ACS provided hypotension and other clear cut contraindications are absent



Treatment of ACS; Statins

• Statins may be of benefit in ACS• Possible mechanisms include plaque

stabilization, reversal of endothelial dysfunction, decreased thrombogenicity, and reduction of inflammation



Treatment of ACS; Emergent Revascularization

• In the setting of STEMI primary PCI is associated with better outcomes than thrombolysis

• Emergent PCI is also indicated in the setting of a new LBBB



AHA/ACC Guidelines for Primary PCI

• Primary PCI is indicated as an alternative to thrombolysis when the following criteria are met:– STEMI or new LBBB– Can undergo PCI within 12 hours of the onset of

symptoms– The MD doing the intervention does more than 75

PCI’s/yr– The procedure is done in a center that does more

than 200 PCI’s/yr and has surgical backup



Approach to Chest Discomfort

• Good History and Physical (note time and duration of symptoms)

• Careful evaluation of ECG (compare to previous when possible)

• Check Cardiac Enzymes• Monitor on Telemetry• Oxygen



THANK YOU FOR

YOUR ATTENTION

Concepts in the Evaluation

andTreatment of Dyslipidemia

PRESENTED BYALIN SINTURAT

Lipoproteins and Lipid transport� Lipids are insoluble in plasma and must be

transported� Lipoproteins are distinguished according to

their buoyant density, lipid and protein composition, role in lipid transport and association with apoproteins

� Chylomicrons� Very Low-Density Lipoproteins (VLDL)� Low- Density Lipoproteins (LDL)� High Density Lipoproteins (HDL)

Lipid� Lipids are necessary for human life� Cholesterol

� Essential component of cell membrane� Precursor to the sterol and steroid compounds

� Triglycerides (TG)� Composed of 3 fatty acids and glycerol� Main storage form of fuel, generate high-energy

compound such as ATP, that provides energy for muscle contraction and metabolic reactions

LipoproteinsWater-soluble way to transport hydrophobic lipids

� Envelope of phospholipids and free cholesterol

� Triglyceride and cholesteryl ester-rich core

� Vary in size and density

From: Braunwald et al, Heart Disease: A Textbook of Cardiovascular Medicine 6th ed., 2001

1.20

1.100

1.063

1.019

1.006

0.95

5 10 20 40 60 80 1000

ChylomicronRemnants

VLDL

LDL-R

HDL2

HDL3DL3

Particle Size (nm)

Den

sity

(g/

ml)

Chylomicron

VLDLRemnants

Lipoprotein Particles

Lp(a)

IDL

Only these lipoprotein particles found in plaque at biopsy.

1.050

Chylomicrons - transport dietary lipids from the gut to the adipose tissue and liverChylomicron remnants-produced from Chylomicronsby lipoprotein lipases in endothelial cells and transport cholesterol to the liverVLDL -made in the liver and secreted in to plasma deliver triglycerides to adipose tissue in the process get converted to IDL and LDLLDL- (bad cholesterol)delivers cholesterol to peripheral tissues via receptors and is phagocytosed by macrophages thus delivering cholesterol to the plaques (atheromas)HDL- (good cholesterol) produced in gut and liver cells, HDL transports cholesterol from atheromasto the liver (reverse cholesterol transport )

DYSLIPIDEMIA� Increases concentrations of lipids and

lipoproteins� Hypercholesterolemia; high concentration

of cholesterol � Atherosclerosis and coronary artery disease

� Hypertriglyceridemia; high concentration of triglyceride� Pancreatitis

� Development of atherosclerosis and heart disease

Coronary Heart Disease (CHD)� The main cause of premature death in

industrialized countries

� Modifiable risk factors� Hypertension

� Cigarette smoking � Low high density lipoprotein (HDL) <40 mg/dl

� Unmodifiable risk factors

� Male gender� Family history of premature CHD; CHD in

first-degree male relative <55, female <65� Advance age; Men>45, Women >55

Progression of CHD Damage to endothelium and invasion of macrophages

Smooth muscle migration

Cholesterol accumulates around macrophage and muscle cells

Collagen and elastic fibers form a matrix around the cholesterol, macrophages and muscle cells

Accumulation of Other Risk Factors Compound Effects of Dyslipidemia on Risk of CHD

0

5

10

15

20

25

30

35

40

185 210 235 260 285 310 335

Low HDL

Smoking

Hyperglycemia

Hypertension

No Other Risk Factors

Schaefer EJ, adapted from the Framingham Heart Study

CH

D R

isk

Per

100

0 (i

n 6

yea

rs)

Serum Cholesterol (mg/dL)

Causes of Dyslipidemia

� Genetics and environmental factors� Increase the formation or reduce the

clearance of LP from circulation� Factors

� Biochemical defects in LP metabolism� Excessive dietary intake of lipids

� Endocrine abnormality � Use of drugs that perturb LP formation or

catabolism

NCEP ATP III: Evaluation -Major Risk Factors for CAD

Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. JAMA. 2001;285:2486.

� Age (men ≥45 y; women ≥55 y)� Cigarette smoking

� Hypertension (BP ≥140/90 mm Hg or antihypertensive medication)

� HDL-C <40 mg/dL� Family history of premature CAD

� <55 y in first-degree male relative

� <65 y in first-degree female relative

NCEP ATP III: Evaluation -CAD Risk Equivalents


� Diabetes

� Atherosclerotic disease

� Peripheral artery disease� Abdominal aortic aneurysm� Symptomatic carotid artery disease

� CAD 10-year risk >20%

NCEP ATP III: Evaluation -Need for Framingham Calculation


No>20%CAD or CAD risk equivalent

Yes0%-10%≥2 RF

No<10%≤1 RF

Need for Framingham Calculation

10-Year Risk for CADRisk Profile

Yes10%-20%

Note: Risk estimates were derived from the experience of the Framingham Heart Study, a predominantly Caucasian population in Massachusetts, USA.

Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. JAMA. 2001;285:2486-2497.

Assessing CHD Risk in MenStep 1: Age

Years Points

20-34 -935-39 -440-44 045-49 350-54 655-59 860-64 1065-69 1170-74 1275-79 13

Step 2: Total Cholesterol

TC Points at Points at Points at Points at Points at

(mg/dL) Age 20-39 Age 40-49 Age 50-59 Age 60-69 Age 70-79

<160 0 0 0 0 0160-199 4 3 2 1 0200-239 7 5 3 1 0240-279 9 6 4 2 1≥≥≥≥280 11 8 5 3 1

HDL-C

(mg/dL) Points

≥≥≥≥60 -1

50-59 0

40-49 1

<40 2

Step 3: HDL-Cholesterol

Systolic BP Points Points

(mm Hg) if Untreated if Treated

<120 0 0120-129 0 1130-139 1 2140-159 1 2≥≥≥≥160 2 3

Step 4: Systolic Blood Pressure

Step 5: Smoking Status

Points at Points at Points at Points at Points at

Age 20-39 Age 40-49 Age 50-59 Age 60-69 Age 70-79

Nonsmoker 0 0 0 0 0Smoker 8 5 3 1 1

AgeTotal cholesterolHDL-cholesterolSystolic blood pressureSmoking statusPoint total

Step 6: Adding Up the Points

Point Total 10-Year Risk Point Total 10-Year Risk

<0 <1% 11 8%0 1% 12 10%1 1% 13 12%2 1% 14 16%3 1% 15 20%4 1% 16 25%5 2% ≥≥≥≥17 ≥≥≥≥30%6 2%7 3%8 4%9 5%10 6%

Step 7: CHD Risk

ATP III Framingham Risk Scoring

© 2001, Professional Postgraduate Services ®

www.lipidhealth.org

Point Total 10-Year Risk Point Total10-Year

Risk

<9 <1% 20 11%9 1% 21 14%10 1% 22 17%11 1% 23 22%12 1% 24 27%13 2% ≥≥≥≥25 ≥≥≥≥30%14 2%15 3%16 4%17 5%18 6%19 8%

Assessing CHD Risk in Women

Note: Risk estimates were derived from the experience of the Framingham Heart Study, a predominantly Caucasian population in Massachusetts, USA.

Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. JAMA. 2001;285:2486-2497.

Step 1: Age

Years Points

20-34 -735-39 -340-44 045-49 350-54 655-59 860-64 1065-69 1270-74 1475-79 16

TC Points at Points at Points at Points

at Points at

(mg/dL) Age 20-39 Age 40-49 Age 50-59 Age 60-69Age

70-79

<160 0 0 0 0 0160-199 4 3 2 1 1200-239 8 6 4 2 1240-279 11 8 5 3 2≥≥≥≥280 13 10 7 4 2

HDL-C

(mg/dL) Points

≥≥≥≥60 -1

50-59 0

40-49 1

<40 2

Step 3: HDL-Cholesterol

Systolic BP Points Points

(mm Hg) if Untreated if Treated

<120 0 0120-129 1 3130-139 2 4140-159 3 5≥≥≥≥160 4 6

Step 4: Systolic Blood Pressure

Step 5: Smoking Status

Points at Points at Points at Points

at Points at

Age 20-39 Age 40-49 Age 50-59 Age 60-69Age

70-79

Nonsmoker 0 0 0 0 0Smoker 9 7 4 2 1

AgeTotal cholesterolHDL-cholesterolSystolic blood pressureSmoking statusPoint total

Step 6: Adding Up the Points

Step 7: CHD Risk

Step 2: Total Cholesterol

ATP III Framingham Risk Scoring

© 2001, Professional Postgraduate Services ®

www.lipidhealth.org

Framingham Ten Year Risk

Men Women


0


0

3 Non-Smoker

0


0

3

0 HDL = 43

1


0

3

01

SBP = 119, untreated

0

4


0

3

010

4

Guidelines for Management of Hypercholesterolemia;

The Adult Treatment Panel III (ATPIII)

� Therapeutic lifestyle changes (TLC) and drug therapy for persons in different risk categories

≥190 mg/dL(optional: 160-190 mg/dL)

≥160 mg/dL<160 mg/dLLower risk:

0-1 risk factor

≥160 mg/dL≥130 mg/dL<130 mg/dLModerate risk:2+ risk factors

(10-year risk <10%)

≥130 mg/dL(optional: 100-129 mg/dL)

≥130 mg/dL<130 mg/dL

(optional: <100 mg/dL)

Moderately high risk:2+ risk factors

5

(10-year risk 10-20%)

≥100 mg/dL(optional goal: <100 mg/dL)

≥100 mg/dL<100 mg/dL(optional: <70 mg/dL)

High risk: CHD or CHD equivalents

3

(10-year risk4

>20%)

Consider Drug Therapy 2Initiate TLC 2LDL-C goalRisk Category

Risk factors: cigarette smoking, hypertension, low HDL-C, family history of premature CHD, and age


≤≤1 RF

≥≥ 2 RFs

equivalent

CAD or CAD risk

Risk Category

<160

<130

<100

<130

LDL-C Goal

(mg/dL)

≥≥160

≥≥ 130

≥≥ 100

≥≥ 130

LDL-C Level to Initiate

TLC (mg/dL)

LDL-C Level to Initiate

Drug Therapy(mg/dL)

≥≥ 190

≥160

≥≥ 130

≥130

(10-year risk0%-10%)

(10-year risk10%-20%)

NCEP ATP III Guidelines: Treatment

NCEP ATP III: Setting Goals-Secondary-Non-HDL-C


≤1 RF <190

≥2 RFs(CAD risk ≤20%) <160

CAD or CAD risk equivalent <130

(CAD risk >20%)

Risk Category Non–HDL-C Goal (mg/dL)

(Patients With TG ≥200)

NCEP ATP III Guidelines: Treatment

TherapeuticLifestyle Change (TLC)

Improve diet

Weight reduction

Physical activity


PharmacologicTreatment

Statins (HMG-CoAreductase inhibitors)Fibrates

Niacin

Bile acid sequestrants

Updated ATP-III Guidelines

>190mg/dl>160mg/dl<160mg/dlLOW

>160mg/dl>130mg/dl<130mg/dlModerate<10% 10yr

>130mg/dl or 100-130

>130mg/dl<100mg/dlOptional

Mod. High10-20%

>100mg/dl or <100mg

>100mg/dl<70mg/dlOptional

HIGH>20% 10yr

DRUGSTLCLDLRISK

� Drugs for hypercholesterolemia� 3-hydroxy-3- methyglutaryl Co A (HMG-CoA)

reductase inhibitor� Bile acid-binding resin

� Ezetimibe

� Drugs for reducing elevated TG and to raise HDL-C levels� Fibric acid derivatives

� niacin

DRUGS FOR DYSLIPIDEMIA

DRUGS FOR DYSLIPIDEMIADrug class Effect(s) Other

considerationsBile acid sequestrants Lower LDL-C Tend to raise TG

Cholesterol absorptioninhibitor

Lower LDL-C Use as monotherapy orwith a statin

Fibrates Lower TGRaise HDL-CLower TC:HDL-CShift LDL-C from smallerto larger particles

May paradoxically raiseLDL-C in 10-15% ofpatients

Nicotinic acid Lowers TG, LDL-C, apo BRaises HDL-C

May cause insulinresistance and worsenglycemic control

Statins (HMG-CoAreductase inhibitors)

Lower LDL-C and apo BImprove TC:HDL-C

Modest TG lowering andHDL-C raising at highdoses

DRUGS FOR DYSLIPIDEMIADRUGS FOR DYSLIPIDEMIADrug class Generic Name Trade name

Bile acid sequestrants cholestyraminecolestipol

Questran, Questran light,Colestid

Cholesterol absorptioninhibitor

ezetimibe Ezetrol

Fibrates bezafibratefenofibrategemfibrozil

BezalipLipidil Micro, Lipidil SupraLopid

Niacin derivatives nicotinic acid

Statins (HMG-CoAreductase inhibitors)

atorvastatinfluvastatinlovastatinpravastatinrosuvastatinsimvastatin

LipitorLescolMevacorPravacholCrestorZocor

Questran® Prescribing Information, Colestid ® Prescribing Information, WelChol ® Prescribing information, Niaspan ® Prescribing Information, Lopid ® Prescribing Information, TriCor ® Prescribing Information, Lipitor ® Prescribing Information, Zocor ® Prescribing

Information, Mevaco ® r Prescribing Information, Lescol ® Prescribing Information, Pravacol ® Prescribing Information; Zetia ®Prescribing Information.

Effect of Lipid-modifying Therapies

TC–total cholesterol, LDL–low density lipoprotein, HDL–high density lipoprotein, TG–triglyceride. * Daily dose of 40mg of each drug, excluding rosuvastatin.

Good↓↓↓↓ 9%↑↑↑↑ 1%↓↓↓↓ 18%↓↓↓↓ 13%Ezetimibe

Good↓↓↓↓ 14-29%↑↑↑↑ 4-12%↓↓↓↓ 25-50%↓↓↓↓ 19-37%Statins*

Good↓↓↓↓ 30%↑↑↑↑ 11-13%↓↓↓↓ 4-21%↓↓↓↓ 19%Fibrates

(gemfibrozil)

Poor to reasonable↓↓↓↓ 30-70%↑↑↑↑ 14-35%↓↓↓↓ 10-20%↓↓↓↓ 10-20%

Nicotinic acid

PoorNeutral or

↑↑↑↑↑↑↑↑ 3%↓↓↓↓ 10-18%↓↓↓↓ 7-10%

Bile acid sequestrants

Patient tolerability

TGHDLLDLTCTherapy

Pharmacologic Therapy: StatinsHMG CoA Reductase Inhibitors (Statins)

� Reduce LDL-C 18–55% & TG 7–30%

� Raise HDL-C 5–15%

� Major side effects

� Myopathy

� Increased liver enzymes

� Contraindications

� Absolute: liver disease

� Relative: use with certain drugs

Grundy et al. Circulation. 2004;110:227-239.

Doses of Statins Required to Attain 30-40% Reduction of LDL-C

3910Atorvastatin

39-455-10Rosuvastatin

25-3540-80Fluvastatin

35-4120-40Simvastatin

3440Pravastatin

3140Lovastatin

LDL Reduction, %Dose, mg/d

Pharmacologic Therapy: Fibrates� Inhibit hepatic TG production and increase HDL

production

� Used to treat elevated TG (20%-50% ↓) and low HDL-C (10%-20% ↑)

� Variable effect on LDL-C

� Side effects� Dyspepsia, gallstones, myopathy� Increased with statins

� Contraindicated in patients with severe renal or hepatic disease


Pharmacologic Therapy: Niacin

� Reduces HDL catabolism and VLDL production

� Primarily used to treat low HDL-C (15%-35%↑)and elevated TG (20%-50% ↓)

� LDL-C ↓ 5%-25%� Side effects

� Hepatotoxicity, hyperglycemia, hyperuricemia,upper GI distress, flushing, itching

� Contraindicated in patients with liver disease,gout, peptic ulcer


Why combination therapy?

� Few patients achieve LDL-C goal on monotherapy

� Uptitration of dosage is rare

� LDL-C goals are getting more aggressive

� High-dose statins increase risk of side effects

� Can address mixed dyslipidemia (e.g., few pts achieve adequate control of HDL-C and triglycerides on monotherapy)

Options for Patients who Fail to Reach LDL-C Goal on Statin Monotherapy

� Niacin

� Bile acid sequestrant

� Cholesterol absorption inhibitor

Addition of:Addition of:

Bile Acid Sequestrants

� Major actions� Reduce LDL-C 15%-30%� Raise HDL-C 3%-5%� May increase TG

� Side effects� GI distress/constipation� Decreased absorption of other drugs (1st generation)

� Contraindications� Dysbetalipoproteinemia� Elevated TG (especially >400 mg/dL)

Ezetimibe - Localizes at Brush Border of Small Intestine

� Ezetimibe, a selective cholesterol absorption inhibitor, localizes and appears to act at the brush border of the small intestine and inhibits cholesterol absorption

� This results in� A decrease in the delivery of intestinal cholesterol to

the liver� A reduction of hepatic cholesterol stores and an

increase in clearance of cholesterol from the blood

Ezetimibe and StatinsComplementary Mechanisms

� Ezetimibe reduces the delivery of cholesterol to the liver

� Statins reduce cholesterol synthesis in the liver

� The distinct mechanism of ezetimibe is complementary to that of statins

� The effects of ezetimibe, either alone or in addition to a statin, on cardiovascular morbidity or mortality have not been established

Knopp RH. N Engl J Med. 1999;341:498–511.

THANK YOU FOR

YOUR ATTENTION

Documents

Acute Coronary Syndrome - Ministry of Public Health · • Acute coronary syndrome is defined as ... studentpresentation08-04-03.ppt. ... • Poor surgical technique (post CABG)