Diseases of blood vessels
ARTERIOSCLEROSIS
Atherosclerosis
is characterised by intimal lesions called atheromas or fibrofatty plaques - protrude into and obstruct vascular lumen and weaken the underlying media.
•Since 1900, CVD has been the No. 1 killer in the United States every year but 1918. •Nearly 2,600 Americans die of CVD each day, an average of 1 death every 33 seconds. •CVD claims more lives each year than the next 5 leading causes of death combined, which are cancer, chronic lower respiratory diseases, accidents, diabetes mellitus, influenza and pneumonia.
Global disease Half of all deaths in Western world
Major cause of IHD, MI & Stroke. Incidence is decreasing since 1995 Better understanding & Change in life
style.
RISK FACTORS
MAJOR
NON MODIFIABLE POTENTIALLY CONTROLLABLE Hyperlipidemia Hypertension Cigarette smoking Diabetes
Increasing age Male gender Family History Genetic
Risk Factors
MINOR
Diet Physical Inactivity Obesity Type A personality Alcohol
High blood cholesterol High blood pressure Smoking Obesity Lack of physical activity
Hyperlipidemia:
Hypercholesterolemia – Risk LDL – Increased risk-delivers cholesterol
to peripheral tissues HDL – lowers the risk – Reverse transport
Mobilises the cholesterol from tissues to liver.
CHOLESTEROL AND
SATURATED FAT
Trans unsaturated fat
Good Fats:
Mono unsaturated fats Poly unsaturated fats Omega-3 fatty acids (Fish)
KNOW THE FATS!
THE GOOD
THE BAD THE UGLY
Poly and mono unsaturated fats
Saturated fats
Trans unsaturated fats
Other major risk factors
HYPERTENSION DIABETES
SMOKING
CLASSIFICATION OF ATHEROSCLEROTIC LESIONS
Type I (Fatty dots) Type II (Fatty streak)
Type III (Intermediate lesion) Type IV(Atheroma)
Type V (Fibroatheroma)
Type VI (Complicated lesion)
Fatty streaks are the earliest lesion that can be recognised. –are composed of lipid filled foam cells. -multiple , yellow spots less than 1mm in diameter. Can be seen in seen by the age of 1 year
Common Sites:
Large Blood Vessels
: Aorta, Carotid & Iliac Medium Blood Vessels : Coronary, Cerebral, Limbs. Small Blood Vessels &
Veins: Never affected.
Atherosclerotic plaque
Appear white to whitish yellow ,measuring 0.3-1.5 cm in diameter ,patchy lesions along the vessel wall may coalesce and form diffuse lesions Abdominal aorta is the most involved, followed by coronary arteries
Morphologic types:
Fatty dots
Atheroma -Plaques
Complicated
PLAQUE
Complicated
Coronary Atherosclerosis:
Atherosclerosis Aorta- Aneurysm
Development of Coronary Atherosclerosis:
Atheroma Coronary Artery:
Atheroma Aorta:
MORPHOLOGY
Atheroma or Atheromatous plaque has a central soft yellow core of lipid covered by firm fibrous cap
Morphology
FIBROUS CAP: composed of smooth muscle cells (SMC), extracellular matrix JUST BENEATH THE CAP: macrophages,lymphocytes and SMC NECROTIC CENTRE: Lipid and foam cells (lipid laden macrophages)
ETIOPATHOGENESIS
REACTION TO INJURY HYPOTHESIS
Considers atherosclerosis to be a chronic inflammatory response of the arterial wall to some form of injury to the endothelium
1.Chronic endothelial Injury
2.Endothelial Dysfunction
3.Macrophage activation and smooth muscle emigration
4.Macrophages and smooth muscle cells engulf lipids
5.Fibrofatty plaque
1)Endothelial injury/Endothelial dysfunction leads to increased endothelial permeability and adhesion of leukocytes & macrophages -Migration into the intima With chronic hyperlipidemia ,lipoproteins accumulate within the intima. Oxidation by free radicals released by macrophages or endothelial cells –to Oxidised LDL
- Oxidised LDL is ingested by
macrophages-forming foam cells Macrophages secrete IL-1 and TNF -Release of growth factors –smooth muscle proliferation Smooth muscle cells proliferate and deposit extracellular matrix –collagen,elastin
PRECLINICAL
(
CLINICAL
WALL WEAKENING
PLAQUE RUPTURE
YOUNG AGE
PROGRESSIVE GROWTH
ADULT LIFE
Coronary Narrowing in Atherosclerosis:
MYOCARDIAL INFARCTION
Coronary Thrombosis With Infarction
Cerebral Infarction (Stroke) :
Haemorrhagic Necrosis
Coronary Angioplasty: