Saadeldeen majeed Professor of cardiology and internal medicine

Saadeldeen majeed Professor of cardiology and internal medicine

Aortic form of atherosclerosis Various forms of aorta lesion 4

What Does It Look Like? • The coronary artery is narrowed reducing the flow of oxygen to the heart. • It is easier for plaque to get inside a narrower artery.

CEREBRAL FORM OF ATHEROSCLEROSIS Acute form may be as Hemorrhage within The brain due to rupture Of atherosclerotic aneurism 7

CEREBRAL FORM OF ATHEROSCLEROSIS • Chronic form may be as encephalopathy With cerebral atrophy (decreasing memory) 8

Extremity form of atherosclerosis • Acute form may be as gangrenous necrosis. 10

RENAL FORM OF ATHEROSCLEROSIS • Acute form may be as infarction • Chronic form is called Atherosclerotic Nephrosclerosis or Primary contracted kidney 11

Intestinal form of atherosclerosis • Acute form may be as gangrenous necrosis of the intestine • Chronic form may be as ischemic enterocolitis 12

Pathogenesis of Atherosclerosis • According to injury hypothesis considers atherosclerosis to be a chronic inflammatory response of the arterial wall initiated by injury: 14

Pathogenesis of Atherosclerosis 1. Chronic endothelial injury. 2. Insudation of lipoproteins [LDL]. 3. Modification of lipoproteins by oxidation. 4. Adhesion of blood monocytes. 5. Adhesion of platelets. 15

Pathogenesis of Atherosclerosis 6. migration of smooth muscle cells from the media into the intima. 7. proliferation of smooth muscle cells in the intima. 8. enhanced accumulation of intra and extra cellular lipids. 16

ATHEROSCLEROTIC PLAQUE • The change of the large arterial intima is called atherosclerotic plaque or atheroma • atherosclerotic plaque is the intimal thickening with lipid accumulation • It consists of fibrous cap, necrotic core and fibrous basis. 17

Atherosclerotic plaque • It has three principle components: 1 - cells –smooth muscle cells, macrophages, other leukocytes. 2 - Extra cellular matrix- collagen, elastic fibers, and proteoglycans. 3 - Intra cellular and extra cellular lipids. 18

Normal coronary artery Lumen has been distended at a pressure of 100 mm. Hg with 10% formal saline used with permission from M. J. Davies Atlas of Coronary Artery Disease 1998 Lippincott-Raven Publishers

Early coronary atherosclerosis Eccentric plaque with a central zone containing yellow lipid used with permission from M. J. Davies Atlas of Coronary Artery Disease 1998 Lippincott-Raven Publishers

Stable angina. Eccentric coronary stenosis used with permission from M. J. Davies Atlas of Coronary Artery Disease 1998 Lippincott-Raven Publishers

Stable angina. Eccentric coronary stenosis thick cap used with permission from M. J. Davies Atlas of Coronary Artery Disease 1998 Lippincott-Raven Publishers

Unstable angina with plaque disruption used with permission from M. J. Davies Atlas of Coronary Artery Disease 1998 Lippincott-Raven Publishers

Unstable angina with plaque disruption The plaque cap is torn, projects into the lumen, exposing a mass of thrombus filling the lipid core used with permission from M. J. Davies Atlas of Coronary Artery Disease 1998 Lippincott-Raven Publishers

Development of Atherosclerotic Plaques Fatty streak Normal Lipid-rich plaque Foam cells Fibrous cap Thrombus Ross R. Nature. 1993; 362: 801 -809. Lipid core

Vulnerable Versus Stable Atherosclerotic Plaques Vulnerable Plaque Lumen Fibrous Cap Lipid Core • Thin fibrous cap • Inflammatory cell infiltrates: proteolytic activity • Lipid-rich plaque Stable Plaque Lumen Lipid Core Fibrous Cap Libby P. Circulation. 1995; 91: 2844 -2850. • Thick fibrous cap • Smooth muscle cells: more extracellular matrix • Lipid-poor plaque

Major modifiable Risk Factors • Cigarette smoking (passive smoking? ) • Elevated total or LDL-cholesterol • Hypertension (BP 140/90 mm. Hg or on antihypertensive medication). . Low HDL cholesterol (<40 mg/d. L)† • Obesity: Body Mass Index (BMI) – Weight (kg)/height (m 2) – Weight (lb)/height (in 2) x 703 • Obesity BMI >30 kg/m 2 with overweight defined as 25 -<30 kg/m 2 • Abdominal obesity involves waist circumference >40 in. in men, >35 in. in women • Physical inactivity: most experts recommend at least 30 minutes moderate activity at least 4 -5 days/week † HDL cholesterol 60 mg/d. L counts as a “negative” risk factor; its presence removes one risk factor from the total count.

Nonmodifiable Risk Factors • Age- Age (men 45 years; women 55 years) the older you get, the greater the chance. • Sex- males have a greater rate even after women pass menopause. • Race- minorities have a greater chance. • Family history- if family members have had CHD, there is a greater chance. Family history of premature CHD – – CHD in male first degree relative <55 years CHD in female first degree relative <65 years

Clinical Manifestations of Atherosclerosis • Coronary heart disease – Stable angina, acute myocardial infarction, sudden death, unstable angina • Cerebrovascular disease – Stroke, TIAs • Peripheral arterial disease – Intermittent claudication, increased risk of death from heart attack and stroke American Heart Association, 2000.

FORMS OF ATHEROSCLEROSIS • • • CEREBRAL ARTERIES INJURY CARDIAC ARTERIES INJURY RENAL ARTERIES INJURY AORTA INJURY INTESTINAL ARTERIES INJURY EXTREMITY ARTERIES INJURY 44

The Skinny on Fat • Saturated fats- basically means the fat is saturated with hydrogen, they are solid at room temperature. Examples are lard and butter. • Why are they bad for you? They increase levels of LDL , decrease HDL and increase total cholesterol.

The Skinny on Fat • What are monounsaturated fats? • They are liquid at room temperature but start to solidify in the refrigerator. • Decrease total cholesterol and lower LDL levels.

The Skinny on Fat • What are trans fatty acids? They are unsaturated fats but they tend to raise total and bad cholesterol. • Where do you find them? • In fast-food restaurants • Commercial baked goods. Examples: doughnuts, potato chips, cupcakes.

What about Omega 3? • Type of polyunsaturated fat. • Consistently lowers serum triglycerides and may also have an effect on lowering blood pressure. • Found in oily fish such as salmon, tuna, and herring. • Is available as a supplement.

Physical Inactivity • Increasing physical activity has been shown to decrease blood pressure. • Moderate to intense physical activity for 30 -45 minutes on most days of the week is recommended.

Cigarette Smoking • Causes an increase in blood pressure • Usually have lower levels of HDL • Within 1 year of quitting, CHD risk decreases, within 2 years it reaches the level of a nonsmoker.

Diabetes Mellitus • At any given cholesterol level, diabetic persons have a 2 or 3 x higher risk of atherosclerosis! • Insulin is required to maintain adequate levels of lipoprotein lipase, an enzyme needed to break down bad cholesterols.

Obesity • People who are obese have 2 to 6 times the risk of developing hypertension. • Location of the body fat is significant. • Pears of apples?

Approaches to Primary and Secondary Prevention • Primary prevention involves prevention of onset of disease in persons without symptoms. • Primordial prevention involves the prevention of risk factors causative o the disease, thereby reducing the likelihood of development of the disease. • Secondary prevention refers to the prevention of death or recurrence of disease in those who are already symptomatic

Prevention of atherosclerosis • • Primary prevention: Population strategy. Targeted strategy. Secondary prevention

• Get regular medical checkups. • Control your blood pressure. • Check your cholesterol. • Don’t smoke. • Exercise regularly. • Maintain a healthy weight. • Eat a heart-healthy diet. • Manage stress.