Dr.Toba kazemi Associate Professor of Cardiology BUMS-BCRC 24Farvardin 1391 Harisson 2012 1983-1991

Dr.Toba kazemiAssociate Professor of Cardiology

BUMS-BCRC24Farvardin 1391Harisson 2012 1983-1991

IntroductionIntroduction::

Disease of blood vessels – large arteries.Disease of blood vessels – large arteries. Modern life style disease… *Modern life style disease… * Major cause of IHD, MI, Stroke & Aortic Major cause of IHD, MI, Stroke & Aortic

disease - Major cause of death & disability.disease - Major cause of death & disability. Incidence is decreasing since 1995 - WestIncidence is decreasing since 1995 - West Better understanding & Change in life style. Better understanding & Change in life style.

DefinitionDefinition::

““Chronic inflammatory disorder of Chronic inflammatory disorder of intimaintima of of largelarge arteriesarteries characterised characterised

by formation of fibrofatty plaques by formation of fibrofatty plaques called atheromacalled atheroma.”.”

Hardening of arteries - ArteriosclerosisHardening of arteries - Arteriosclerosis

EtiologyEtiology::

Exact cause is unknownExact cause is unknown Variation in severity & distribution.Variation in severity & distribution. Starts with endothelial injury.Starts with endothelial injury. Genetic/Familial Genetic/Familial Risk Factors… Risk Factors…

Age, Htn, DM, Smoking – endothelial damage.Age, Htn, DM, Smoking – endothelial damage. Obesity, lifestyle, economic status, - lipid.Obesity, lifestyle, economic status, - lipid. Activation of Platelet / Coagulation.Activation of Platelet / Coagulation.

Oxidised LDL.Oxidised LDL.

Lipoprotiens - LDL & HDLLipoprotiens - LDL & HDL

• Good and Bad Fats?• Lower LDL, Increase HDL• Mono unsaturated fats• Poly unsaturated fats• Omega-3 fatty acids (Fish)• LDL indicate Positive lipid

balance, HDL – negative.

Risk FactorsRisk Factors::

Non modifiableNon modifiable AgeAge Male Sex, Male Sex, Genetic - Hyperchol. Genetic - Hyperchol. Family historyFamily history

Potentially ModifiablePotentially Modifiable Hyperlipidemia – Hyperlipidemia –

HDL/LDL ratio.HDL/LDL ratio. Hypertension.Hypertension. Smoking.Smoking. Diabetes.Diabetes.

PathogenesisPathogenesis:: intimal injuryintimal injury Inflammation, NecrosisInflammation, Necrosis Lipid – Cholesterol accumulation (soft.a)Lipid – Cholesterol accumulation (soft.a) Fibrosis, smooth muscle proliferation (hard.a)Fibrosis, smooth muscle proliferation (hard.a) Extension of lesion and destruction of vesselExtension of lesion and destruction of vessel Complications - Thrombosis, embolism, Complications - Thrombosis, embolism,

aneurism, dissection & rupture.aneurism, dissection & rupture.

Structure of AtheromaStructure of Atheroma::

Fibrous Cap

Necrotic center

Cholesterol Cry.

Macrophages

Pathogenesis-stagesPathogenesis-stages

Type I – Fatty dots - Foam cellsType I – Fatty dots - Foam cells Type II – Fatty streakType II – Fatty streak Type III – Extracellular lipid poolType III – Extracellular lipid pool Type IV – Atheroma – Core of lipidType IV – Atheroma – Core of lipid Type V – Fibroatheroma – Fibrotic layerType V – Fibroatheroma – Fibrotic layer Type VI – Complicated – Ulcer, Ca+Type VI – Complicated – Ulcer, Ca+

Hemorrhage, thrombus, embolism, aneurysm.Hemorrhage, thrombus, embolism, aneurysm.

Development of Development of Coronary AtherosclerosisCoronary Atherosclerosis::

ComplicationsComplications::

Thrombosis, Thrombo-embolismThrombosis, Thrombo-embolism Rupture – HaemorrhageRupture – Haemorrhage AneurysmAneurysm Fibrosis & CalcificationFibrosis & Calcification Ischemia / Infarction – end organ damage.Ischemia / Infarction – end organ damage. Stroke, Myocardial Infarctions, Renal Stroke, Myocardial Infarctions, Renal

infarction, Mesentric vein thrombosis, infarction, Mesentric vein thrombosis, intermittent claudication, gangrene etc. intermittent claudication, gangrene etc.

Coronary AtheorsclerosisCoronary Atheorsclerosis

•Left Coronary Artery.•Anterior Descending (LAD)•Left Circumflex (LCx)

•Right Coronary Artery.

LCx

LAD

Coronary Coronary Thrombosis Thrombosis

With InfarctionWith Infarction

Coronary AngioplastyCoronary Angioplasty::

Atheroma - Objectives 1Atheroma - Objectives 1

Definition of atheromaDefinition of atheromaMacroscopic appearancesMacroscopic appearancesMicroscopic appearancesMicroscopic appearancesEffectsEffects

AtheromaAtheroma

DefinitionDefinition

Atheroma is the accumulation of Atheroma is the accumulation of intracellular and extracellular lipid in the intracellular and extracellular lipid in the intima of large and medium sized arteriesintima of large and medium sized arteries

AtherosclerosisAtherosclerosis

DefinitionDefinition

The thickening and hardening of arterial The thickening and hardening of arterial walls as a consequence of atheromawalls as a consequence of atheroma

The thickening of the walls of arteries and The thickening of the walls of arteries and arterioles usually as a result of arterioles usually as a result of hypertension or diabetes mellitushypertension or diabetes mellitus

Atheroma - Macroscopic Atheroma - Macroscopic FeaturesFeatures

Fatty streakFatty streak Simple plaqueSimple plaque Complicated plaqueComplicated plaque

Atheroma - The Fatty StreakAtheroma - The Fatty Streak

Lipid deposits in Lipid deposits in intimaintima

Yellow, slightly Yellow, slightly raisedraised

Atheroma - The Simple Atheroma - The Simple PlaquePlaque

Raised yellow/whiteRaised yellow/white Irregular outlineIrregular outline Widely distributedWidely distributed Enlarge and Enlarge and

coalescecoalesce

Atheroma - The Complicated Atheroma - The Complicated PlaquePlaque

ThrombosisThrombosis Haemorrhage into Haemorrhage into

plaqueplaque CalcificationCalcification Aneurysm formationAneurysm formation

Atheroma - Common SitesAtheroma - Common Sites

Aorta - especially abdominalAorta - especially abdominal Coronary arteriesCoronary arteries Carotid arteriesCarotid arteries Cerebral arteriesCerebral arteries Leg arteriesLeg arteries

Normal Arterial StructureNormal Arterial Structure

EndotheliumEndothelium Sub-endothelial c.t.Sub-endothelial c.t. Internal elastic Internal elastic

laminalamina Muscular mediaMuscular media External elastic External elastic

laminalamina AdventitiaAdventitia

Atheroma - Microscopic Atheroma - Microscopic FeaturesFeatures

Early changesEarly changes proliferation of smooth muscle cellsproliferation of smooth muscle cells accumulation of foam cellsaccumulation of foam cells extracellular lipidextracellular lipid

EndotheliumEndothelium

Smooth muscle cellSmooth muscle cell

LipidLipid

MatrixMatrix


Later changesLater changes fibrosisfibrosis necrosisnecrosis cholesterol cleftscholesterol clefts +/- inflammatory cells+/- inflammatory cells


Later changesLater changes disruption of internal elastic laminadisruption of internal elastic lamina damage extends into mediadamage extends into media ingrowth of blood vesselsingrowth of blood vessels plaque fissuringplaque fissuring

Atheroma - Coronary ArteryAtheroma - Coronary Artery

Atheroma - Clinical EffectsAtheroma - Clinical Effects

Ischaemic heart diseaseIschaemic heart disease sudden deathsudden death myocardial infarctionmyocardial infarction angina pectorisangina pectoris arrhythmiasarrhythmias cardiac failurecardiac failure

Atheroma – cerebral infarctionAtheroma – cerebral infarction

Atheroma – Abdominal Aortic Atheroma – Abdominal Aortic AneurysmAneurysm

Atheroma - PathogenesisAtheroma - Pathogenesis

AgeAge GenderGender HyperlipidaemiaHyperlipidaemia Cigarette smokingCigarette smoking HypertensionHypertension Diabetes mellitusDiabetes mellitus InfectionInfection

AtheromaAtheroma

AgeAge slowly progressive throughout adult lifeslowly progressive throughout adult life risk factors operate over yearsrisk factors operate over years

GenderGender women protected relatively before women protected relatively before

menopausemenopause presumed hormonal basispresumed hormonal basis

AtheromaAtheroma

HyperlipidaemiaHyperlipidaemia high plasma cholesterol associated with high plasma cholesterol associated with

atheromaatheroma LDL most significantLDL most significant HDL protectiveHDL protective

Atheroma-InfectionAtheroma-Infection

Chlamydia pneumoniaeChlamydia pneumoniae Helicobacter pyloriHelicobacter pylori CytomegalovirusCytomegalovirus

Atheroma - Other Risk FactorsAtheroma - Other Risk Factors

Lack of exerciseLack of exercise ObesityObesity StressStress Familial predisposition well knownFamilial predisposition well known

Atheroma - PathogenesisAtheroma - Pathogenesis

Thrombogenic theoryThrombogenic theory Insudation theoryInsudation theory Monoclonal hypothesisMonoclonal hypothesis Reaction to injury hypothesisReaction to injury hypothesis

Atheroma - Thrombogenic Atheroma - Thrombogenic TheoryTheory

1852 Karl Rokitansky1852 Karl Rokitansky plaques formed by plaques formed by

repeated thrombirepeated thrombi lipid derived from lipid derived from

thrombithrombi overlying fibrous capoverlying fibrous cap

Atheroma - Insudation TheoryAtheroma - Insudation Theory

1856 Rudolf 1856 Rudolf VirchowVirchow endothelial injuryendothelial injury inflammationinflammation increased increased

permeability to permeability to lipid from plasmalipid from plasma

Atheroma - Reaction to Injury Atheroma - Reaction to Injury HypothesisHypothesis

1972 Ross and Glomset1972 Ross and Glomset plaques form in response to endothelial injuryplaques form in response to endothelial injury hypercholesterolaemia leads to endothelial hypercholesterolaemia leads to endothelial

damage in experimental animalsdamage in experimental animals injury increases permeability and allows injury increases permeability and allows

platelet adhesionplatelet adhesion monocytes penetrate endotheliummonocytes penetrate endothelium smooth muscle cells proliferate and migratesmooth muscle cells proliferate and migrate

Atheroma - Reaction to Injury Atheroma - Reaction to Injury HypothesisHypothesis

1986 Ross1986 Ross endothelial injury may be very subtle and endothelial injury may be very subtle and

be undetectable visuallybe undetectable visually LDL, especially oxidised, may damage LDL, especially oxidised, may damage

endotheliumendothelium

Atheroma - The Monoclonal Atheroma - The Monoclonal HypothesisHypothesis

Benditt and BendittBenditt and Benditt crucial role for smooth muscle proliferationcrucial role for smooth muscle proliferation each plaque is monoclonaleach plaque is monoclonal might represent abnormal growth controlmight represent abnormal growth control is each plaque a benign tumour?is each plaque a benign tumour? could atheroma have a viral aetiology?could atheroma have a viral aetiology?

Atheroma - The Processes Atheroma - The Processes InvolvedInvolved

ThrombosisThrombosis Lipid accumulationLipid accumulation Production of intercellular matrixProduction of intercellular matrix Interactions between cell typesInteractions between cell types

Atheroma - The Cells InvolvedAtheroma - The Cells Involved

Endothelial cellsEndothelial cells PlateletsPlatelets Smooth muscle cellsSmooth muscle cells MacrophagesMacrophages LymphocytesLymphocytes NeutrophilsNeutrophils

Atheroma - A Unifying Atheroma - A Unifying Hypothesis 1Hypothesis 1

Endothelial injury due toEndothelial injury due to raised LDLraised LDL ‘‘toxins’ eg cigarette smoketoxins’ eg cigarette smoke hypertensionhypertension haemodynamic stresshaemodynamic stress

Endothelial injury causesEndothelial injury causes platelet adhesion, PDGF release, SMC proliferation platelet adhesion, PDGF release, SMC proliferation

and migrationand migration insudation of lipid, LDL oxidation, uptake of lipid by insudation of lipid, LDL oxidation, uptake of lipid by

SMC and macrophagesSMC and macrophages migration of monocytes into intimamigration of monocytes into intima

Atheroma - A Unifying Atheroma - A Unifying Hypothesis 3Hypothesis 3

Stimulated SMC produce matrix materialStimulated SMC produce matrix material Foam cells secrete cytokines causingFoam cells secrete cytokines causing

further SMC stimulationfurther SMC stimulation recruitment of other inflammatory cellsrecruitment of other inflammatory cells

Atheroma - PreventionAtheroma - Prevention

No smokingNo smoking Reduce fat intake Reduce fat intake Treat hypertensionTreat hypertension Not too much alcoholNot too much alcohol Regular exercise/weight controlRegular exercise/weight control

BUT some people will still develop BUT some people will still develop atheroma!atheroma!

Atheroma - InterventionAtheroma - Intervention

Stop smokingStop smoking Modify dietModify diet Treat hypertensionTreat hypertension Treat diabetesTreat diabetes Lipid lowering drugsLipid lowering drugs

pathogenesispathogenesis

Atherosclerosis: major cause of death & Atherosclerosis: major cause of death & premature disability in developed societypremature disability in developed society

By 2020 :CVD is the leading global cause By 2020 :CVD is the leading global cause of total disease burdenof total disease burden

Atherosclerosis affect various region of Atherosclerosis affect various region of circulation: although its risk factors are circulation: although its risk factors are systemic or generalizedsystemic or generalized

pathogenesispathogenesis

Atherosclerosis of coronary A. :MI, angina Atherosclerosis of coronary A. :MI, angina pectorispectoris

Atherosclerosis of CNS:TIA , strokeAtherosclerosis of CNS:TIA , stroke Atherosclerosis of peripheral A : intermittent Atherosclerosis of peripheral A : intermittent

claudication ,gangreneclaudication ,gangrene Atherosclerosis of splanchnic circulation;. Atherosclerosis of splanchnic circulation;.

Mesentric ischemiaMesentric ischemia Atherosclerosis of kidney:renal art. Atherosclerosis of kidney:renal art.

Stenosis, emboli to Renal A.Stenosis, emboli to Renal A.

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THROMBOSIS ORTHROMBOSIS OR EMBOLISM ON ULCERED PLAQUEEMBOLISM ON ULCERED PLAQUE

ISCHEMIC INFARCTIONISCHEMIC INFARCTION

CEREBRAL FORM OF ATHEROSCLEROSISCEREBRAL FORM OF ATHEROSCLEROSIS

HemorrhageHemorrhage within withinThe brainThe brain

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RENAL FORM OF RENAL FORM OF ATHEROSCLEROSISATHEROSCLEROSIS

Acute form may be as Acute form may be as infarctioninfarction

Chronic form is calledChronic form is calledAtheroscleroticAtheroscleroticNephrosclerosis orNephrosclerosis orPrimary contractedPrimary contractedkidneykidney

5555

Intestinal form of atherosclerosisIntestinal form of atherosclerosis

Acute form may be as Acute form may be as gangrenous necrosis gangrenous necrosis of the intestineof the intestine

Chronic form may be Chronic form may be as ischemic as ischemic enterocolitisenterocolitis

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Extremity form of atherosclerosisExtremity form of atherosclerosis

Acute form may be as gangrenous Acute form may be as gangrenous necrosis.necrosis.

atherosclerosis in arterial bedatherosclerosis in arterial bed Occur focallyOccur focally At branching point: disturbed blood flowAt branching point: disturbed blood flow coronary A. :proximal of LADcoronary A. :proximal of LAD Atherosclerosis renal artery: proximal portionAtherosclerosis renal artery: proximal portion Extra cranial circulation: carotid bifurcationExtra cranial circulation: carotid bifurcation Not always stenotic: ectasia, aneurysmNot always stenotic: ectasia, aneurysm Nonocclosive diffuse intimal irregularity :IVUS , Nonocclosive diffuse intimal irregularity :IVUS ,

postmortempostmortem

Atherosclerosis in human: occure over a Atherosclerosis in human: occure over a period( years / decades)period( years / decades)

Growth of Atherosclerosis:not smooth or Growth of Atherosclerosis:not smooth or linear / but quiesencelinear / but quiesence

rapid evolutionrapid evolution

chronic:chronic:

clinically expression of AT acute: AMI clinically expression of AT acute: AMI ,SCD,stroke,SCD,stroke

never experience never experience clinical manifestation clinical manifestation

6060

Pathogenesis ofPathogenesis of AtherosclerosisAtherosclerosis

According to injury hypothesis According to injury hypothesis considers atherosclerosis to be a considers atherosclerosis to be a chronic inflammatory Response of chronic inflammatory Response of the arterial wall initiated by injury:the arterial wall initiated by injury:

6161


1 1 chronic endothelial injurychronic endothelial injury2 insudation of lipoproteins [LDL]2 insudation of lipoproteins [LDL]3 modification of lipoproteins by 3 modification of lipoproteins by

oxidationoxidation4 adhesion of blood monocytes4 adhesion of blood monocytes5 adhesion of platelets5 adhesion of platelets

6262


6 migration of smooth muscle cells6 migration of smooth muscle cells

from the media into the intimafrom the media into the intima

7 proliferation of smooth muscle cells7 proliferation of smooth muscle cells

in the intimain the intima

8 enhanced accumulation of intra and8 enhanced accumulation of intra and

extra cellular lipids extra cellular lipids

6363

atherosclerotic plaqueatherosclerotic plaque

It has three principle components:It has three principle components: 1 cells –smooth muscle cells, macrophages1 cells –smooth muscle cells, macrophages

other leukocytesother leukocytes

2 Extra cellular matrix- collagen, elastic fibers,2 Extra cellular matrix- collagen, elastic fibers,

proteoglycansproteoglycans

3 Intra cellular and extra cellular lipids3 Intra cellular and extra cellular lipids

6464

There are two types of atherosclerotic There are two types of atherosclerotic plaque plaque

1 vulnerable 1 vulnerable 2 stable2 stable


6565


1 vulnerable 2 STABLE1 vulnerable 2 STABLE

THERE ARETHERE ARE A LOT OF LIPIDSA LOT OF LIPIDS

PathogenesisPathogenesis

Fatty streak: initial lesionFatty streak: initial lesion Mechanism: lipoprotein in intima (not simply Mechanism: lipoprotein in intima (not simply

from permeability or leakiness )from permeability or leakiness ) Lipoprotein bind to extracellular matrix Lipoprotein bind to extracellular matrix

(glycoseaminoglycans ) residence time (glycoseaminoglycans ) residence time of lipid rich particle= slow regress of this particleof lipid rich particle= slow regress of this particle

Oxidative modification of lipoproteinsOxidative modification of lipoproteins

Chronic Chronic inflammatoryinflammatory response of the vascular response of the vascular wall to endothelial injury or dysfunctionwall to endothelial injury or dysfunction

Elevated plasma LDL levels causing the deposit Elevated plasma LDL levels causing the deposit of LDL in the subendothelium of blood vesselsof LDL in the subendothelium of blood vessels

Oxidation of transmigrated LDLOxidation of transmigrated LDL Activation of endothelial cellsActivation of endothelial cells Recruitment of monocytes/macrophages which Recruitment of monocytes/macrophages which

ingest oxLDL through scavenger receptorsingest oxLDL through scavenger receptors Formation of foam cells – fatty streaksFormation of foam cells – fatty streaks Proliferation of smooth muscle cellsProliferation of smooth muscle cells Deposition of extracellular matrix proteinsDeposition of extracellular matrix proteins

Monocyte RecruitmentMonocyte Recruitment

intima

lumen LDL

Lipid Core

lumen

neointima

Formation of Atherosclerotic PlaquesFormation of Atherosclerotic Plaques

Plaque Rupture and ThrombosisPlaque Rupture and Thrombosis

Lipid Core

Tissue Factor Platelet Aggregation

Atherosclerosis is the buildup of plaque on Atherosclerosis is the buildup of plaque on the inside walls of arteries. Plaque is made the inside walls of arteries. Plaque is made up of low density lipoprotein (up of low density lipoprotein (LDLLDL), ), macrophagesmacrophages, , smooth muscle cellssmooth muscle cells, platelets, , platelets, and other substances. It may narrow the and other substances. It may narrow the lumen of a blood vessel and restrict blood lumen of a blood vessel and restrict blood flow. Plaque rupture can induce the formation flow. Plaque rupture can induce the formation of thrombus (blood clot) and block blood flow. of thrombus (blood clot) and block blood flow. This will result in ischemic stroke or heart This will result in ischemic stroke or heart attack. attack.

Formation of foam cellsFormation of foam cells

The first stage in the development of The first stage in the development of atherosclerosis is the formation of atherosclerosis is the formation of foam cellsfoam cells (macrophages with ingested oxidized LDL). The (macrophages with ingested oxidized LDL). The process begins with trap of LDL in the process begins with trap of LDL in the intimaintima, , which lies just below the endothelium (the which lies just below the endothelium (the monolayer of cells lining the arterial wall). monolayer of cells lining the arterial wall). Trapped LDL could be oxidized, triggering Trapped LDL could be oxidized, triggering recruitment of monocytes into the intima. recruitment of monocytes into the intima. Several adhesion molecules are involved, Several adhesion molecules are involved, including vascular-cell adhesion molecule including vascular-cell adhesion molecule (VCAM), integrin, selectin, and others. After (VCAM), integrin, selectin, and others. After entering the intima, monocytes differentiate into entering the intima, monocytes differentiate into macrophages and ingest oxidized LDL. macrophages and ingest oxidized LDL.

Formation of plaqueFormation of plaque

As atherosclerosis progresses, T As atherosclerosis progresses, T lymphocytes, platelets and smooth muscle lymphocytes, platelets and smooth muscle cells also join foam cells, expanding the cells also join foam cells, expanding the plaque size. This involves cytokines to plaque size. This involves cytokines to activate T lymphocytes and growth factors to activate T lymphocytes and growth factors to promote proliferation of smooth muscle cells. promote proliferation of smooth muscle cells. Platelets can also release cytokines and Platelets can also release cytokines and growth factors to enhance migration and growth factors to enhance migration and proliferation of smooth muscle cells. During proliferation of smooth muscle cells. During this stage, a fibrous cap is formed to this stage, a fibrous cap is formed to separate the plaque from the lumenseparate the plaque from the lumen

ThrombosisThrombosis

Thrombosis (formation of thrombus) arises Thrombosis (formation of thrombus) arises from plaque rupture. Macrophages may from plaque rupture. Macrophages may release metalloproteinases and other release metalloproteinases and other proteolytic enzymes to degrade fibrous proteolytic enzymes to degrade fibrous cap, making it susceptible to rupture. cap, making it susceptible to rupture. Plaque rupture activates platelets, leading Plaque rupture activates platelets, leading to formation of blood clots at the site of to formation of blood clots at the site of lesionlesion

NONO((

Molecular mechanisms for the production Molecular mechanisms for the production of nitric oxide (NO) by exercise leading to of nitric oxide (NO) by exercise leading to the protection of atherosclerosis.the protection of atherosclerosis.

Emerging anti-inflammatory therapies in clinical atherosclerosis.

Klingenberg R , Hansson G K Eur Heart J 2009;30:2838-2844

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: [email protected]

Leukocyte diversity in atherosclerosis.

Klingenberg R , Hansson G K Eur Heart J 2009;30:2838-2844


Prognostic role of clinical risk scores and biomarkers of cardiovascular risk.

Kaski J C Eur Heart J 2010;31:274-277


Risk modifiers influence atherogenesis through effects on inflammation as reflected by biomarkers of the acute phase response.

Libby P , Crea F Eur Heart J 2010;31:777-783

Framingham Framingham TenTen Year Risk Year Risk

Men Women

Framingham Ten Year RiskFramingham Ten Year Risk

0


0

3 Non-Smoker

0


0

3

0HDL = 43

1


0

3

0

1SBP = 119, untreated

0

4


0

3

0

1

0

4

ال ايده ال سطح ايده افراد Non HDLNon HDLووLDLLDLسطح افراد در درمختلفمختلف

میزان ریسکوضعیت بیمارLDL هدف

)mg/dl(شروع رژیم

غذایی و فعالیت

شروع دارو

HDL non-

هدف) mg/dl)

وبيماري عروق كرونر ديابت يا چند ريسك

فاكتور قلبي

Very High كمتراز 70

كمتر از ≥70 ≥70 100

بيماري عروق معادالت ياكرونر

آن

High كمتر از100

كمتر از ≥ 100 ≥ 100 130

ريسك فاكتور قلبي 2 ≥و احتمال بيماري كرونر

سال آینده 10در %10-20بين

Moderately High

كمتر از 100

كمتر از ≥ 130 ≥ 130 130

ريسك فاكتور 2 ≥قلبي و احتمال

بيماري كرونر در سال آینده کمتر 10

%10از

Moderate كمتر از130

كمتر از ≥ 160 ≥ 130 160

190كمتر از ≥ 190 ≥ 160 160كمتر از lowيك ريسك فاكتور ويا كمتر

TREATMENTTREATMENT

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Documents

Dr.Toba kazemi Associate Professor of Cardiology BUMS-BCRC 24Farvardin 1391 Harisson 2012 1983-1991