Atherosclerosis 3

this includes morpho,clinical features,complications,diagnosis,treatment....

1. ATHEROSCLEROSISATHEROSCLEROSIS
MORPHOLOGY
&
COMPLICATIONS
-S.SHRINATH
83 Batch.

3. MORPHOLOGY
FATTY STREAK
ATHEROSCLEROTIC PLAQUE

4. -: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.

7. -: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.

8. Most extensively affected vessels
are:
•Abdominal aorta
•Coronary arteries
•Popliteal arteries
•Internal carotid arteries
•Circle of willis

9. Components of Plaque:
Cells
•T-cells
•Smooth muscle cells
•Macrophages.
ECM
•Collagen
•Elastic fibers
•Proteoglycans
Lipids
•Intracellular and extracellular.

10. -: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.

12. -:NATURE OF THE PLAQUE:-
Progressively enlarges due to:-
•Cell death and degeneration.
•Synthesis and remodeling of collagen.
•Organization of thrombus.
Often undergo calcification.

16. CHANGES IN THE ATHEROSCLEROTIC PLAQUE
•Rupture ,erosion ,ulceration.
•Hemorrhage into a plaque.
•Atheroembolism.
•Aneurysm formation.

17. RUPTURE

18. HEMORRHAGE INTO PLAQUE

19. ATHERO EMBOLISM

20. ANEURYSMS FORMATION

21. COMPLICATIONS

22. -:COMPLICATIONS:-
•Myocardial infarction
•Cerebral infarction (stroke).
•Aneurysm
•Peripheral vascular disease (PVD).

23. 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.

24. 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.

25. 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

26. 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.

27. ROLE OF FREE RADICALS
(OXIDATIVE STRESS)
LDL Oxidised LDL
Release of free radicals
DAMAGE TO THE ARTERIAL WALL
Into macrophages

29. 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.

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

31. 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.

32. •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:

33. DIAGNOSIS

34. DIAGNOSIS
SEROLOGICAL IMAGING
LIPID PROFILE
HbA1c
CRP-HS
HOMOCYSTEINE
LDL LEVEL
LIPOPROTEIN a
CT SCAN
INTRAVASCULAR ULTRASOUND
ANGIOGRAPHY
DOPPLER STUDY

35. TREATMENT

36. TREATMENT
NON-PHARMACEUTICAL PHARMACEUTICAL
NON-FAT DIET
CESSATION OF SMOKING
REGULAR EXERCISE
REDUCE ALCOHOL CONSUMPTION
Use of drug
surgical

37. PHARMACOTHERAPY
DRUGS FOR REDUCING HYPERCHOLESTROLEMIA
STATINS
ATORVASTATIN
FLUVASTATIN
LOVASTATIN
PRAVASTATIN
SIMVASTATIN
ROSUVASTATIN

38. USES OF STATINS
•REDUCING PLAQUE SIZE.
•STABILIZING PLAQUES.
•DECREASING BLOOD CLOT FORMATION.
•DECREASING CRP LEVELS.

39. DRUGS FOR REDUCING CLOT FORMATION
VITAMIN –K ANTAGONIST
WARFARIN ACENOCOUMAROL PHENINDIONE
HEPARIN DERIVATIVES
HEPARIN FONDAPARINUX INDRAPARINUX
DIRECT THROMBIN INHIBITORS
ARGATROBAN LEPIRUDIN BIVALURIDIN

40. 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)

41. SURGICAL INTERVENTION
•BALOON ANGIOPLASTY AND STENTING
•ATHERECTOMY
•SURGICAL BYPASS
•ENDATERECTOMY

42. SUMMARY

43. MORPHOLOGY

44. MORPHOLOGY

45. COMPLICATIONS
MYOCARDIAL INFARCTIONSTROKE
PERIPHERAL VASCULAR DISEASE
ANEURYSM FORMATION

46. COMPLICATIONS
Atherosclerotic stenosis
•Critical stenosis
•Consequences of stenosis
Acute plaque change
•Stable plaque & vulnerable plaque
•Factors that bring about the Change.

48. THANK YOU