1. Coronary Heart Diseases (Ischemic heart diseases) Definition: “impairment of heart function due to inadequate blood flow to the heart compared to its needs, caused by obstructive changes in the coronary circulation to the heart” WHO→ CHD, CAD or IHD is our modern epidemic or the emerging epidemic. IHD is first leading cause of Death in the World.

2. The lumen of a coronary artery can be narrowed when a segment of the wall thickens (stenosis). Coronary Atherosclerosis: This process of arteries thickening and narrowing is brought about by two linked processes called atherogenesis and thrombogenesis.

3. Atherogenesis: Is the formation of atherosclerotic plaque (atheroma) in the internal layer of the wall of the artery. Thrombogenesis: Is the formation of a blood clot (thrombus) in a vessel by thrombocytes circulating in the blood on atheromatous plaque.

4. Atherogenesis: Is the formation of atherosclerotic plaque (atheroma) in the internal layer of the wall of the artery. Atherogenesis starts with fatty deposits. Fibrous tissue then grows around a fatty deposit creating an atherosclerotic plaque, which protrudes into the lumen of the artery narrowing it. Atherogenesis: Is the formation of atherosclerotic plaque (atheroma) in the internal layer of the wall of the artery. Atherogenesis starts with fatty deposits. Fibrous tissue then grows around a fatty deposit creating an atherosclerotic plaque, which protrudes into the lumen of the artery narrowing it.

5. Thrombogenesis: Is the formation of a blood clot (thrombus) in a vessel by thrombocytes circulating in the blood on atheromatous plaque. When a plaque full of cholesterol ulcerates or desquamates, it releases the cholesterol content and various fragments of the plaque to the circulation. This triggers the formation of a blood clot by thrombocytes circulating in the blood, which leads to varying degrees of obstruction of the lumen.

6. Clinical manifestations of coronary atherosclerosis Usually develop when the coronary arteries are narrowed at least by 75%. 1. Chest pain (angina pectoris ”stable or unstable”). 2. Heart attack (myocardial infarction). 3. Arrhythmia of any kinds. 4. Sudden cardiac death. 5. Congestive heart failure.

7. Irreversible damage to the cells may occur in about 40 minutes. The dead heart muscle cells cannot be replaced by new muscle cells (specialized). They are replaced by scar tissue, which is less elastic and does not contract as the muscle leading to many complications. Irreversible damage to the cells may occur in about 40 minutes. The dead heart muscle cells cannot be replaced by new muscle cells (specialized). They are replaced by scar tissue, which is less elastic and does not contract as the muscle leading to many complications.

8. The role of infection: Certain infectious agents have been implicated based on their isolation from the atheromatous plaques or on the presence of positive serology findings for organisms such as 1. C pneumoniae, 2. Helicobacter pylori, 3. Herpes simplex virus, 4. Cytomegalovirus.

9. Risk factors: The cause of atherosclerosis is not known. Risk factors can be divided into those that cannot be changed (unmodifiable; namely age, sex, race and family history) and those that can be (modified; or managed (such obesity and alcohol consumption). Risk factors multiply each other’s effect of increasing the risk of CHD (multiplicative not additive).

10. Un-modifiable risk factors: Age: 40-45 for men 50-55 for women. Sex: At all age men > women There is about a decade difference in incidence. Family history: Close or primary relatives. Especially premature atherosclerosis. Race: Till now there is no clear data established CHD state.

11. Modifiable risk factors: Dyslipedemia: ↑ LDL ↑ VLDL ↑ TG ↑ Cholesterol ↓ HDL Smoking: Very strong evidence Dose-response relationship 2-4 times risk Passive smokers also at large risk Multiplicative effects by acting on other risk factors

12. Modifiable risk factors: Hypertension: Well established risk factor Both systolic and diastolic hypertension Obesity: Central obesity more harmful than general obesity BMI > 25 (pre-obese) and > 30 (obese) WHR > 1 for men and WHR > 0.85 fro women Waist > 40 inch for men and Waist > 35 inch for women.

13. Modifiable risk factors: Diabetes: Both types IDDM and NIDDM Risk equivalent to established CHD It causes and accelerates atherosclerosis Do not forget “silent MI”. Sedentary life: Because physical activity improves lipid profiles, ↓ BP, controls body weight, controls serum glucose, copes with stress. At least 30 min exercise (moderate) / day for 4-5 times / week.

14. Modifiable risk factors: Metabolic Syndrome: A cluster of Most established heart attack risk factors including: - Diabetes or insulin resistant (± glucose intolerance), + - Raised blood pressure, + - Atherogenic dyslipidemia, + - Abdominal obesity, + - Pro-thrombotic (± pro-inflammatory state) * Main target for intervention. Personality type A Alcohol drinking

15. Dependent / Emerging / Novel Risk Factors: ↑ Homocysteine. ↑ Lp (a). Abnormalities in blood coagulation: – ↑ Plasma fibrinogen. – ↑ Coagulation factors: V, VII, VIII. – Platelets abnormalities. – Impaired fibrinolysis. Inflammatory markers: – C-Reactive protein. – Interlukin. Short stature. Impaired glucose tolerance. Increased oxidative stress. Stress. Tachycardia. Ethnic group. S. creatinine. Ultra-novel risk factors: Plasma Myeloperoxidase. Red Cell Glutathione Peroxidase 1 activity.

16. Prevention: 1. Primary: By eliminating or reducing established risk factors (such as stop smoking and decrease weight) 2. Secondary: Good treatment of established case MI to reduce complication. 3. Tertiary: Rehabilitation of established case of MI to return to normal life. 4. Primordial: Prevention of risk factor before its development (such as healthy diets for baby). Strategies for prevention: 1. Population strategies. 2. High risk strategies.

17. The assessment of overall cardiovascular (CV) risk is a valuable and accepted means of identifying patients who are likely to benefit most from intervention. Risk elimination is central to the management of CV disease. Data from large epidemiological cohort studies have provided the raw data used to evaluate the contribution of individual CV risk factors. Usually, they use 10 years risk (prediction) of large CV events (such MI) for certain person, given as %.

18. Example: Peter has a 5% global risk of CV event, this means, 100 persons, like Peter, 5 of them will get major CV event (like MI) within subsequent 10 years. GLOBAL RISK ASSESSMENT SCORING SYSTEMS FRAMINGHAM Scoring System (USA). PROCAM Scoring System (Germany). SCORE Project (European). INDIANA Project (Latin Americans). Australian Scoring System (Australia). Etc.

19. Effects of aspirin in 1000 men over 10 year 10% risk of CHD in 10 y 5% risk of CHD in 10 y 2.5% risk of CHD in 10 y Events 28126MI prevented 3-5 GIT Bleed 111Stroke Bleed

20. Treatment Threshold Treatment10 years CVD risk No treatment< 5% Statin5-10% Consider Statin + Aspirin 10- 15% Statin + Aspirin > 15%