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1 Dr. Zahoor Ali Shaikh. 2 CORONARY ARTERY DISEASE (CAD)  CAD is most common form of heart disease and causes premature death.  In UK, 1 in 3 men and.

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Presentation on theme: "1 Dr. Zahoor Ali Shaikh. 2 CORONARY ARTERY DISEASE (CAD)  CAD is most common form of heart disease and causes premature death.  In UK, 1 in 3 men and."— Presentation transcript:

1 1 Dr. Zahoor Ali Shaikh

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3 CORONARY ARTERY DISEASE (CAD)  CAD is most common form of heart disease and causes premature death.  In UK, 1 in 3 men and 1 in 4 women die from coronary heart disease.  Approximately 1.3 million people have angina every year. 3

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5 CORONARY ARTERY DISEASE Stable Angina  It is due to transient myocardial ischemia and occurs when there is increased demand of oxygen by heart. 5

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7 7 CORONARY ARTERY DISEASE

8 STABLE ANGINA RISK FACTOR FOR STABLE ANGINA  Hypertension  Diabetes Mellitus  Aortic valve disease - Angina is precipitated by - Anemia - Throtoxicosis 8

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10 INVESTIGATIONS  ECG  Exercise ECG – Exercise tolerance test (ETT). We monitor ECG, BP, and general condition of patient. 10

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12 12 INVESTIGATIONS  Myocardial Perfusion Scan - Thallium stress test

13 INVESTIGATIONS  Coronary Arteriography - Usually performed with a view to percutaneus coronary intervention (PCI) or coronary artery bypass graft (CABG) NOTE – PCI is done under local anesthesia in cardiac cath lab. - CABG surgery is done using left internal mammary artery or Saphenous vein. 13

14 14 INVESTIGATIONS

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16 16 MANAGEMENT OF ANGINA PECTORIS  Assessment of patient  Look for risk factors  Advise to the patient

17 MANAGEMENT OF ANGINA PECTORIS  Antiplatelet therapy – aspirin  Antianginal drugs -Nitrate -Beta blocker -Calcium antagonist 17

18 ASPIRIN  Inhibits platelet aggregation  Inhibits synthesis of prostaglandin Thromboxone A2 and promotes reperfusion and reduces likelihood of thrombosis 18

19 NITRORGLYCERINE (NTG) Action  It is venous and arteriolar dilator, therefore, decreases venous return and preload  Decreases intraventricular volume and ventricular wall tension, therefore, decreases myocardial oxygen demand  Sublingual NTG – peak action 4-8 minute, action last for 10-30 minute  Side effect - headache 19

20 BETA BLOCKER  Beta blocker are very good for angina associated with effort  Beta blocker decrease heart rate, blood pressure, and contractility of heart  Therefore, decrease oxygen demand 20

21 CALCIUM CHANNEL BLOCKER Action  Cause coronary dilatation and increase coronary flow  Decrease myocardial contractility therefore decrease oxygen demand 21

22 CORONARY ARTERY SPASM  It is called variant angina or Vasospastic or prinzmetal angina.  Angina pain is due to spasm of coronary artery.  ECG may show transient ST-elevation  Treatment is with calcium blocker, nitrates. 22

23 ACUTE CORONARY SYNDROME (ACS)  ACS is term used for 1. Unstable Angina 2. Myocardial infarction [MI] – NSTEMI 3. Myocardial infarction [MI] – STEMI  Unstable Angina occurs at rest or minimal exertion in absence of myocardial damage.  MI symptoms occur at rest and there is evidence of myocardial damage, demonstrated by increased level of cardiac Troponin or creatinine kinase-MB. IMPORTANT – Troponin is more specific 23

24 UNSTABLE ANGINA  There is partial/intermittent occlusion of coronary artery  Chest pain occurs at rest and lasts for more than 20 minutes  ECG – ST depression, T wave changes (T inversion)  Cardiac enzyme – Troponin T & I are normal Because No myocardial damage has occurred 24

25 NSTEMI  Chest pain occurs at rest and lasts for more than 20 minutes  ECG – ST depression, T wave changes (T inversion)  Cardiac enzyme – Troponin T & I are increased Because myocardial damage has occurred 25

26 STEMI  Severe Chest pain occurs at rest and lasts for 30 minutes to 1 hour  ECG – ST elevation, T wave changes later Q wave appear  Cardiac enzyme –Troponin T & I are increased and CK-MB increased 26

27 STEMI (cont)  In STEMI, there is severe damage to the myocardium due to occlusion of blood flow in the coronary artery that causes death of myocardial tissue  Sudden death from ventricular fibrillation or asystole within 1 hour can occur. 27

28 Patient with chest pain 28

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31 ACUTE CORONARY SYNDROME (ACS) Diagnosis  Evaluation of ECG  Measurement of biochemical markers of cardiac damage e.g. Troponin I and T, creatine kinase  Cardiac Troponin T and I are most sensitive and specific marker of myocardial cell damage NOTE – Cardiac Biochemical markers are raised in MI. There is no rise in cardiac markers in angina. 31

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33 ACUTE CORONARY SYNDROME (ACS)  Other blood test - WBC count - ESR - C-reactive protein - X-ray chest - Echo cardiography 33

34 MANAGEMENT  Admit the patient  Morphine IV for pain  Aspirin  Nitrate  Beta-blocker  Calcium channel blocker  Reperfusion therapy  Percutaneous Coronary Intervention (PCI) 34

35 35 PCI

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38 38 COMPLICATIONS OF ACUTE CORONARY SYNDROME

39 THANK YOU 39


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