Coronary Artery Disease

Coronary Artery Disease

1. Introduction:

• Coronary artery disease (CAD) is a prevalent condition in developed countries.

• Pathogenesis: Fat deposits in the inner lining of the coronary arteries lead to atherosclerosis, progressively forming blood clots that cause obstruction.

• Major complications: Angina pectoris (AP), myocardial infarction (MI), and sudden death.

2. Causes:

• Primary cause: coronary artery disease (atherosclerosis, coronary spasm, vasculitis).

• Other causes: valvular heart disease (stenosis, regurgitation due to atherosclerosis, syphilis), hypertrophic cardiomyopathy (functional coronary insufficiency, non-narrowed coronary arteries).

3. Pathogenesis:

• AP: The heart’s oxygen demand exceeds the coronary system’s supply capacity.

• Pain: A direct manifestation of acute myocardial ischemia and the accumulation of metabolic substances due to oxygen deprivation, leading to rapid pH reduction in the coronary sinus, loss of cellular potassium, increased lactate production, causing electrocardiogram (ECG) abnormalities and impaired ventricular function.

4. Factors Determining Myocardial Oxygen Consumption:

• Heart rate, myocardial contractility, systolic pressure.

• An increase in one or more of these factors along with a decrease in coronary blood flow leads to AP.

5. Relevant Pathogenesis Mechanisms:

• Myocardium and oxygen

• Coronary reserve

• Coronary artery vasomotor capacity

• Myocardial ischemia

6. Myocardial Ischemia:

• Secondary ischemia: due to increased oxygen demand.

• Primary ischemia: due to a sudden decrease in coronary flow.

7. Coronary Reserve:

• The heart’s oxygen uptake capacity, increased 300-400% over normal levels.

• Adaptation and increased oxygen demand lead to increased coronary flow.

• Coronary flow depends on perfusion pressure and resistance (under the epicardium).

8. Peak Coronary Blood Flow:

• Diastole.

9. Decreased Coronary Flow, Primarily Affecting Blood Supply in:

• Subendocardium.

10. Coronary Artery Vasomotor Capacity Depends On:

• Vasoconstricting factors: systolic squeezing force, muscular bridges crossing an epicardial coronary artery, the effect of alpha and beta receptors with dopamine doses above 15 mg/kg/min.

• Vasodilating factors: metabolites due to myocardial ischemia, the effect of alpha and beta receptors with dopamine doses below 5 mg/kg/min.

11. Myocardial Ischemia Occurs When:

• There is an imbalance between oxygen supply and demand.

12. During Exertion, Increased Oxygen Consumption Is Reflected In:

• Heart rate, systolic blood pressure, myocardial contractility.

13. Coronary Artery Narrowing Is Significant When:

• The artery diameter is reduced by more than 70%.

14. Consequences of Myocardial Ischemia:

• Metabolism: lactate production.

• Hemodynamics: impaired relaxation, decreased ventricular compliance, reduced contractility.

• ECG: repolarization abnormalities.

• Clinical: AP.

15. Angina Pectoris Is AP With Characteristics:

• Occurs after exertion, radiating to the inner arm, terminating at the ring and little fingers of the left hand, possibly extending to the shoulder, back, lower jaw, or neck.

• Nature: vague (chest tightness), constricting (a heavy weight).

• Duration: short, a few minutes.

• Relief after exertion, reduced or eliminated with rest or vasodilating drugs.

• Cold is a trigger for pain.

16. Myocardial Infarction:

• Similar to AP but more severe, lasting more than 30 minutes, with less relief after rest and nitroglycerin.

17. Clinical Manifestations of Myocardial Infarction:

• Increased heart rate and blood pressure.

• A systolic murmur in mid- and late systole may be heard due to papillary muscle dysfunction caused by acute myocardial ischemia.

18. Electrocardiogram in Myocardial Infarction:

• ST segment depression is typical.

• Sometimes ST segment elevation.

• Rhythm disturbances, especially ventricular tachycardia.

19. Diagnosis of Myocardial Infarction:

• Clinical: evolving AP.

• ECG: changes according to disease progression.

• Cardiac enzymes: elevated CPK, CPK-MB, GOT, LDH, Troponin T.

20. Complications of Myocardial Infarction:

• Arrhythmias: ventricular tachycardia, ventricular fibrillation, bradycardia, AV block.

• Heart failure.

• Ventricular aneurysm.

21. Treatment Principles:

• Identify and manage risk factors.

• Modify factors that worsen AP.

22. Identifying and Managing Risk Factors:

• Lifestyle changes: moderation, physical activity, weight loss.

• Management of diabetes, hypertension, dyslipidemia.

• Regular lipid testing, annual stress test.

23. Treatment Methods:

• Medical: during attack, between attacks.

• Percutaneous coronary intervention.

• Coronary artery bypass surgery.

24. Medical Management:

• During attack: sublingual nitroglycerin 0.3-0.6 mg.

• Between attacks: long-acting nitrates, beta-blockers, calcium channel blockers, aspirin, clopidogrel.

25. Percutaneous Coronary Intervention:

• Success rate of 85-90% in the initial stage.

• Drawback: restenosis within 6 months in 25-40% of cases.

• Objective: to prevent restenosis after angioplasty.

• There are two types of stents: drug-eluting and bare metal.

26. Coronary Artery Bypass Surgery:

• Grafting of saphenous vein or internal mammary artery onto the affected coronary artery.

• Improves prognosis and symptoms of myocardial infarction.

• Preferred when: narrowing of the coronary artery trunk, poor left ventricular function, multi-vessel disease, diabetic patients with multi-vessel disease, concurrent valvular heart disease requiring open-heart surgery.

27. Stable Angina Pectoris Management:

• During attack: rest, avoidance of exertion, sublingual nitroglycerin 0.3-0.6 mg.

• Between attacks: long-acting nitrates, beta-blockers, calcium channel blockers, potassium channel activators, amiodarone, trimetazidine, analgesics, and sedatives.

• Angioplasty and stent placement.

• Aorto-coronary bypass surgery.

28. Prinzmetal Angina Management:

• During attack: sublingual and intravenous nitrates, rapid-acting calcium channel blockers.

• Long-term: long-acting nitrates and calcium channel blockers, selective alpha-adrenoceptor blockers, endothelin antagonists.

• Non-selective beta-blockers can worsen coronary spasm.

• If coronary spasm is resistant to drug treatment: consider coronary intervention or surgery.

29. Unstable Angina Management:

• Rest, monitoring, oxygen.

• Clinical, ECG, and biochemical (CPK) monitoring.

• Sedatives, analgesics.

• Nitrates, calcium channel blockers, beta-blockers, heparin, aspirin.

• If there’s no response despite combined treatment with nitrates + beta-blockers + calcium channel blockers, immediate coronary intervention is required.

30. Silent Myocardial Ischemia Management:

• Intensive anti-anginal treatment.

• Coronary assessment.

31. Myocardial Infarction Treatment Objectives:

• Pain relief, minimizing infarct size, preventing and treating arrhythmias and mechanical complications.

32. Myocardial Infarction Management:

• Admission to a cardiac intensive care unit.

• Establishment of an emergency intravenous line for medication administration.

• Early thrombolytic therapy.

• Pain control: nitroglycerin, oxygen, mild sedation, light snacks to prevent constipation.

• Beta-blockers, anticoagulants/antiplatelet drugs, angiotensin-converting enzyme inhibitors.

33. Prevention:

• Identification of risk factors.

• Specific recommendations: smoking cessation, blood pressure control, management of high cholesterol, increased exercise and physical activity, diabetes management, limiting oral contraceptive use.