ATHEROSCLEROSISATHEROSCLEROSISATHEROSCLEROSISATHEROSCLEROSIS

MORPHOLOGY

&

COMPLICATIONS

MORPHOLOGY

&

COMPLICATIONS

-S.SHRINATH

83 Batch.

MORPHOLOGY

FATTY STREAK

ATHEROSCLEROTIC PLAQUE

-:FATTY STREAK:-

•It is the earliest lesions in Atherosclerosis which is composed of foam cells.

•Earlier formed as small flat yellow spots and then to a plaque.

•Does not cause any obstruction to the blood flow.

-:ATHEROSCLEROTIC PLAQUE:-

•Intimal thickening and lipid accumulation.

•Lodged in the lumen of the artery (0.3-1.5 cm in dia).

•Grossly they appear as white to yellow patches.

•Lesions are mostly eccentric but rarely circumferential.

•Local flow disturbances –increased susceptibility to plaque formation.

Most extensively affected vessels are:

•Abdominal aorta

•Coronary arteries

•Popliteal arteries

•Internal carotid arteries

•Circle of willis

Components of Plaque:

Cells

•T-cells

•Smooth muscle cells

•Macrophages.

ECM

•Collagen

•Elastic fibers

•Proteoglycans

Lipids

•Intracellular and extracellular.

-:DESCRIPTION – PLAQUE:-

•Typically composed of superficial composed fibrous cap (smooth muscle cells and collagen).

•Beneath it contains cellular area.

•Deeply containing lipid core, cell debris, foam cells, fibrin, thrombus, plasma proteins.

•Periphery shows neovascularisation.

-:NATURE OF THE PLAQUE:-

Progressively enlarges due to:-

•Cell death and degeneration.

•Synthesis and remodeling of collagen.

•Organization of thrombus.

Often undergo calcification.

CHANGES IN THE ATHEROSCLEROTIC PLAQUE

•Rupture ,erosion ,ulceration.

•Hemorrhage into a plaque.

•Atheroembolism.

•Aneurysm formation.

RUPTURE

HEMORRHAGE INTO PLAQUE

ATHERO EMBOLISM

ANEURYSMS FORMATION

COMPLICATIONSCOMPLICATIONS

-:COMPLICATIONS:-

•Myocardial infarction

•Cerebral infarction (stroke).

•Aneurysm

•Peripheral vascular disease (PVD).

Atherosclerotic stenosis

Small arteries plaques occlude lumen compromising blood flow ischemia.

Critical stenosis

•Chronic occlusion significantly limits flow .

occurs at approx 70% occlusion in coronary circulation.

Consequences of stenosis

•Mesenteric occlusion

and bowel ischemia.

•Chronic IHD.

•Ischemic encephalopathy.

•Intermittent claudication.

ACUTE PLAQUE CHANGE

•Partial or complete vascular thrombosis due to erosion or rupture of plaque resulting in acute tissue infarction.

•Rupture expose high thrombogenic substances.

•Erosion expose thrombogenic sub endothelial basement membrane.

•Hemorrhage expands the volume.

PLAQUE CONFIGURATION

•Composition of plaque is dynamic .

•Based on the plaque configuration it may be of stable or vulnerable.

•Stable plaque•Thick fibrous cap

•Small lipid core

•Vulnerable plaque•Thin fibrous cap

•Dense lipid core

EVENTS TRIGGERING CHANGES IN PLAQUE CONFIGURATION

INTRINSIC FACTORS - plaque structure and composition

Fibrous cap

•Collagen (produced by smooth cells).

•Collagen turnover is regulated by

•Matrix metalloproteinase (macrophages within plaque),

•Tissue inhibitors of metalloproteinase (endothelial cells,smooth muscle cells)

EXTRINSIC FACTORS -BP and platelet activity.

•adrenergic stimulation increase BP increasing physical stress.

ROLE OF FREE RADICALS

(OXIDATIVE STRESS)

LDL Oxidised LDL

Release of free radicals

DAMAGE TO THE ARTERIAL WALL

Into macrophages

THROMBOSIS

•Partial or complete thrombosis associated with disrupted plaque is critical to the pathogenesis of acute stenosis.

•Thrombosis is a potent activator of multiple growth related signals which contribute to the growth of atherosclerotic lesion.

VASOCONSTRICTION

•This compromises lumen size and by increasing the local mechanical forces and can potentiate the plaque disruption.

CLINICAL FEATURES

ON CORONARY ARTERIES:

•Angina

•Hyperhidrosis•Shortness of breath•Palpitations•Tachycardia•Weakness or dizziness•Nausea

ON CAROTID ARTERIES:

•Transient ischemic attacks

•Dizziness ,Confusion ,Fainting , Coma

•Loss of eyesight

•Hemiplegia.

•Claudication is the most common symptom of this condition. 

•Pain

•Coolness, numbness

• Poor healing of wounds  

•Ulcers leading to Gangrene formation

•Black discoloration

ON PERIPHERAL ARTERIES:

DIAGNOSISDIAGNOSIS

DIAGNOSIS

SEROLOGICAL IMAGING

LIPID PROFILE

 HbA1c

CRP-HS

HOMOCYSTEINE

LDL LEVEL

LIPOPROTEIN a

CT SCAN

INTRAVASCULAR ULTRASOUND

ANGIOGRAPHY

DOPPLER STUDY

TREATMENTTREATMENT

TREATMENT

NON-PHARMACEUTICAL PHARMACEUTICAL

NON-FAT DIET

CESSATION OF SMOKING

REGULAR EXERCISE

REDUCE ALCOHOL CONSUMPTION

Use of drug

surgical

PHARMACOTHERAPY

DRUGS FOR REDUCING HYPERCHOLESTROLEMIA

STATINS

ATORVASTATIN

FLUVASTATIN

LOVASTATIN

PRAVASTATIN

SIMVASTATIN

ROSUVASTATIN

USES OF STATINS

•REDUCING PLAQUE SIZE.

•STABILIZING PLAQUES.

•DECREASING BLOOD CLOT FORMATION.

•DECREASING CRP LEVELS.

DRUGS FOR REDUCING CLOT FORMATION

VITAMIN –K ANTAGONIST

WARFARIN ACENOCOUMAROL PHENINDIONE

HEPARIN DERIVATIVES

HEPARIN FONDAPARINUX INDRAPARINUX

DIRECT THROMBIN INHIBITORS

ARGATROBAN LEPIRUDIN BIVALURIDIN

THE DRUGS THAT BREAKSDOWN THE BLOOD CLOT

tissue plasminogen activator t-PA:

alteplase (Activase)reteplase (Retavase)tenecteplase (TNKase)

antistreplase (Eminase)

streptokinase (Kabikinase, Streptase)

urokinase (Abbokinase)

SURGICAL INTERVENTION

•BALOON ANGIOPLASTY AND STENTING

•ATHERECTOMY

•SURGICAL BYPASS

•ENDATERECTOMY

SUMMARY

MORPHOLOGY

MORPHOLOGY

COMPLICATIONS

MYOCARDIAL INFARCTIONSTROKEPERIPHERAL VASCULAR DISEASEANEURYSM FORMATION

COMPLICATIONS

Atherosclerotic stenosis

•Critical stenosis

•Consequences of stenosis

Acute plaque change

•Stable plaque & vulnerable plaque

•Factors that bring about the Change.

THANK YOU