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CORONARY
ARTERY DISEASECORONARY ARTERY DISEASE
GLOBAL BURDEN OF
CVD
• A century ago, Cardio vascular disease (CVD) mortality <10%
• Currently, approximately 30% of mortality worldwide
- 40% in high income countries
- 28% in low and middle income countries
-Braunwald’s Heart Disease( 2008)
VITAL STATISTICS - WHO
• 2 million people die of CVD in India every year
• 32 % are in the age group 35-44
• Four Indians die of a heart ailment every minute
Atherosclerosis
The word atherosclerosis is of Greek origin and literally
means focal accumulation of lipid (ie, athere [gruel]) and
thickening of arterial intima (ie, sclerosis [hardening])
which is an abnormal accumulation of lipid, or fatty,
substances and fibrous tissue in the vessel wall.
Definition
Atherosclerosis is a disease of large and medium-sized
arteries and is characterized by
• Endothelial dysfunction
• Vascular inflammation
• Buildup of lipids, cholesterol, calcium, and cellular debris
within the intima of the vessel wall
CORONARY ARTERY DISEASE IS ALSO KNOWN
AS;
ATHEROSCLEROTIC HEART DISEASE
CORONARYATHEROSCLEROSIS
CORONARYARTERIOSCLEROSIS
CORONARY HEART DISEASE
Blood vessel
DEVELOPMENTAL STAGES
• It is progressive disease that develop over many
years, when it become symptomatic the disease
process usually well advanced
• STAGES
Formation of fatty streak
Formation of fibrous plaque
Development of complicated lesion
Fatty streak
• Earliest lesions of atherosclerosis characterized by
lipid filled smooth muscle
• As streak develop within smooth muscle cells a
yellow tinge appears
• Can be seen by the age of 15 and increase surface
area when age advances
• Reduced LDL cholesterol reverse this process
Fibrous plaque
• Beginning of progressive changes in the endothelium
• Changes can appear in coronary arteries by age of 30
• Normally endothelium repairs normally , but this not
happen with a person with CAD
• LDL and growth factors from platelets stimulate smooth
muscle proliferation and thickening of arterial wall
• Once injury take place lipoproteins deposits cholesterol in
arterial intima forms fibrous plaque
• This results narrowing of vessel lumen decreases blood
flow
Complicated lesion
• Dangerous stage
• As fibrous plaque grows, continued inflammation
can result in plaque instability, ulceration and
rupture
• Once the integrity of the artery’s inner wall is
compromised platelet accumulation leading to a
thrombus formation
• This leading to further narrowing or total occlusion
of artery
Risk factors
Nonmodifiable Risk Factors
• Family history of coronary heart disease
• Increasing age
• Gender (heart disease occurs three times
more often in men than in premenopausal
women)
• Race (higher incidence of heart disease in
African Americans than in Caucasians)
Modifiable Risk Factors
• High blood cholesterol level
• Cigarette smoking, tobacco use
• Hypertension
• Diabetes mellitus
• Lack of estrogen in women
• Physical inactivity
• Obesity
Age, Gender and Ethinicity
• Highest among middle aged men
• After 65 men and women equalizes
• Family history is a risk factor for CAD
• 40-60% Genetic contribution
Non modifiable risk factors
• Elevated serum lipids
• One of the most firmly established risk factors for CAD
• Three types
HDL
LDL
VLDL
HYPERTENSION
• 2nd major risk factor in CAD is HTN
• HTN increases the risk of death from CAD 10 fold in all
people
Tobacco use
• Third major risk factor
• Risk for developing CAD is two to six times higher in those
who smoke than in those who do not smoke
Physical inactivity
Fourth major risk factor for CAD
Increased HDL levels among those who are doing regular
exercise
Obesity
• Mortality statistics high among obese people
• BMI- 30 kg/m2
• waist- more than 40 inches for men ,35 for women
Contributing modifiable risk
factors
• 1.diabetes mellitus
• 2.metabolic syndrome
• 3.psychologic stress
• 4.Homocysteine
• 5.substance abuse
Diabetes mellitus
• Incidence of CAD is two to four times greater among
persons who have diabetes, even with well controlled blood
glucose levels, than general population.
• Person with diabetes has an increased tendency towards
endothelial dysfunction, this may account fatty streaks in
the patients
• These patients have alterations in lipid metabolism and
tend to have high cholesterol and triglyceride levels
Metabolic syndrome
• It is a cluster of risk factors for CAD whose underlying
pathophysiology may be insulin resistance, these include
obesity
increased waist circumference
hypertension
abnormal serum lipids
elevated fasting blood glucose level
Psychololgic states
• Studies proved that type A behavior persons more risk of
developing type B behavior peoples
• During stressful situations results sympathetic nervous
system stimulation leads to release of catecholamines
leades to increased myocardial oxygen demand
Homocysteine
• It is produced by breakdown of essential amino acid
methionie, which is found dietary protien
• High blood levels of homocystiene contribute damaging
inner lining of blood vessels, promoting plaque buildup,
altering clotting mechanism
Substance abuse
• Illicit drugs such as cocaine and methamphetamine can
produce coronary spasm results myocardial ischemia and
spasm,
Management
• Health promotion
identification of high risk people
screen by obtaining health history
family history, dietary habits, physical activity,
unhealthy habits, psychologic stress,
physical examination and blood investigation
• Management of high risk people
Hypertension
monitor BP regularly
take prescribed medications
reduce salt intake
physical activity
everyone should aim for at least 30 minutes of
moderate physical activities on most days of the week
• Nutritional therapy
lowering LDL cholesterol, that is decrease in saturated
fatty acid and cholesterol and increase complex
carbohydrates and fiber
Lipid lowering drug therapy
• Complete lipid profile is recommended every 5 years
beginning at age 20
• Drug therapy
STATINS /HMG-CoA Reductase Inhibitors
Drugs are most widely used lipid lowering drugs, these
inhibit synthesis of cholesterol in the liver
• lower LDL and triglyceride levels, and increase HDL levels.
HMG-CoA Reductase Inhibitors
(statins)
• Lovastatin 20–80 mg
• Simvastatin 20–80 mg
• Fluvastatin - 20–80 mg
• Atorvastatin calcium - 10–80 mg
Nicotinic acids (niacin)
• decrease lipoprotein synthesis,
• lower LDL and triglyceride levels,
• increase HDL levels
• Eg,
• Niacin (Niacor, Niaspan)
Nicotinic acid 1.5–3 g
Fibric acid Derivatives
• Decreases hepatic synthesis and secretion of VLDL
,reduces triglycerides by decreasing VLDL
• Eg- Fenofibrate (Tricor) - 200 mg
Bile acid sequestrants
• Bind cholesterol n the intestine, increase its breakdown,
and lower LDL levels with minimal effect on HDLs and no
effect (or minimal increase) on triglyceride levels.
• Cholestryramine - 4–16 g
• Colestipol 5-20 g

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CORONARY ARTERY DISEASE

  • 2. GLOBAL BURDEN OF CVD • A century ago, Cardio vascular disease (CVD) mortality <10% • Currently, approximately 30% of mortality worldwide - 40% in high income countries - 28% in low and middle income countries -Braunwald’s Heart Disease( 2008)
  • 3. VITAL STATISTICS - WHO • 2 million people die of CVD in India every year • 32 % are in the age group 35-44 • Four Indians die of a heart ailment every minute
  • 4. Atherosclerosis The word atherosclerosis is of Greek origin and literally means focal accumulation of lipid (ie, athere [gruel]) and thickening of arterial intima (ie, sclerosis [hardening]) which is an abnormal accumulation of lipid, or fatty, substances and fibrous tissue in the vessel wall.
  • 5. Definition Atherosclerosis is a disease of large and medium-sized arteries and is characterized by • Endothelial dysfunction • Vascular inflammation • Buildup of lipids, cholesterol, calcium, and cellular debris within the intima of the vessel wall
  • 6. CORONARY ARTERY DISEASE IS ALSO KNOWN AS; ATHEROSCLEROTIC HEART DISEASE CORONARYATHEROSCLEROSIS CORONARYARTERIOSCLEROSIS CORONARY HEART DISEASE
  • 8. DEVELOPMENTAL STAGES • It is progressive disease that develop over many years, when it become symptomatic the disease process usually well advanced • STAGES Formation of fatty streak Formation of fibrous plaque Development of complicated lesion
  • 9. Fatty streak • Earliest lesions of atherosclerosis characterized by lipid filled smooth muscle • As streak develop within smooth muscle cells a yellow tinge appears • Can be seen by the age of 15 and increase surface area when age advances • Reduced LDL cholesterol reverse this process
  • 10.
  • 11. Fibrous plaque • Beginning of progressive changes in the endothelium • Changes can appear in coronary arteries by age of 30 • Normally endothelium repairs normally , but this not happen with a person with CAD • LDL and growth factors from platelets stimulate smooth muscle proliferation and thickening of arterial wall • Once injury take place lipoproteins deposits cholesterol in arterial intima forms fibrous plaque • This results narrowing of vessel lumen decreases blood flow
  • 12.
  • 13. Complicated lesion • Dangerous stage • As fibrous plaque grows, continued inflammation can result in plaque instability, ulceration and rupture • Once the integrity of the artery’s inner wall is compromised platelet accumulation leading to a thrombus formation • This leading to further narrowing or total occlusion of artery
  • 14.
  • 16. Nonmodifiable Risk Factors • Family history of coronary heart disease • Increasing age • Gender (heart disease occurs three times more often in men than in premenopausal women) • Race (higher incidence of heart disease in African Americans than in Caucasians)
  • 17. Modifiable Risk Factors • High blood cholesterol level • Cigarette smoking, tobacco use • Hypertension • Diabetes mellitus • Lack of estrogen in women • Physical inactivity • Obesity
  • 18. Age, Gender and Ethinicity • Highest among middle aged men • After 65 men and women equalizes • Family history is a risk factor for CAD • 40-60% Genetic contribution
  • 19. Non modifiable risk factors • Elevated serum lipids • One of the most firmly established risk factors for CAD • Three types HDL LDL VLDL
  • 20. HYPERTENSION • 2nd major risk factor in CAD is HTN • HTN increases the risk of death from CAD 10 fold in all people
  • 21. Tobacco use • Third major risk factor • Risk for developing CAD is two to six times higher in those who smoke than in those who do not smoke
  • 22. Physical inactivity Fourth major risk factor for CAD Increased HDL levels among those who are doing regular exercise
  • 23. Obesity • Mortality statistics high among obese people • BMI- 30 kg/m2 • waist- more than 40 inches for men ,35 for women
  • 24. Contributing modifiable risk factors • 1.diabetes mellitus • 2.metabolic syndrome • 3.psychologic stress • 4.Homocysteine • 5.substance abuse
  • 25. Diabetes mellitus • Incidence of CAD is two to four times greater among persons who have diabetes, even with well controlled blood glucose levels, than general population. • Person with diabetes has an increased tendency towards endothelial dysfunction, this may account fatty streaks in the patients • These patients have alterations in lipid metabolism and tend to have high cholesterol and triglyceride levels
  • 26. Metabolic syndrome • It is a cluster of risk factors for CAD whose underlying pathophysiology may be insulin resistance, these include obesity increased waist circumference hypertension abnormal serum lipids elevated fasting blood glucose level
  • 27. Psychololgic states • Studies proved that type A behavior persons more risk of developing type B behavior peoples • During stressful situations results sympathetic nervous system stimulation leads to release of catecholamines leades to increased myocardial oxygen demand
  • 28. Homocysteine • It is produced by breakdown of essential amino acid methionie, which is found dietary protien • High blood levels of homocystiene contribute damaging inner lining of blood vessels, promoting plaque buildup, altering clotting mechanism
  • 29. Substance abuse • Illicit drugs such as cocaine and methamphetamine can produce coronary spasm results myocardial ischemia and spasm,
  • 30. Management • Health promotion identification of high risk people screen by obtaining health history family history, dietary habits, physical activity, unhealthy habits, psychologic stress, physical examination and blood investigation
  • 31. • Management of high risk people Hypertension monitor BP regularly take prescribed medications reduce salt intake physical activity everyone should aim for at least 30 minutes of moderate physical activities on most days of the week
  • 32. • Nutritional therapy lowering LDL cholesterol, that is decrease in saturated fatty acid and cholesterol and increase complex carbohydrates and fiber
  • 33. Lipid lowering drug therapy • Complete lipid profile is recommended every 5 years beginning at age 20 • Drug therapy STATINS /HMG-CoA Reductase Inhibitors Drugs are most widely used lipid lowering drugs, these inhibit synthesis of cholesterol in the liver • lower LDL and triglyceride levels, and increase HDL levels.
  • 34. HMG-CoA Reductase Inhibitors (statins) • Lovastatin 20–80 mg • Simvastatin 20–80 mg • Fluvastatin - 20–80 mg • Atorvastatin calcium - 10–80 mg
  • 35. Nicotinic acids (niacin) • decrease lipoprotein synthesis, • lower LDL and triglyceride levels, • increase HDL levels • Eg, • Niacin (Niacor, Niaspan) Nicotinic acid 1.5–3 g
  • 36. Fibric acid Derivatives • Decreases hepatic synthesis and secretion of VLDL ,reduces triglycerides by decreasing VLDL • Eg- Fenofibrate (Tricor) - 200 mg
  • 37. Bile acid sequestrants • Bind cholesterol n the intestine, increase its breakdown, and lower LDL levels with minimal effect on HDLs and no effect (or minimal increase) on triglyceride levels. • Cholestryramine - 4–16 g • Colestipol 5-20 g