ISCHAEMIC HEART DISEASE STABLE ANGINA & ACUTE CORONARY SYNDROME (ACS) By Dr. Zahoor

ISCHAEMIC HEART DISEASE (IHD) Why myocardial ischaemia occurs? Myocardial Ischaemia occurs when there is less supply of oxygen to the heart Less supply of oxygen may be due to decreased blood flow because of coronary artery disease

Diagram of coronary circulation

ISCHAEMIC HEART DISEASE (IHD) Coronary artery disease may be due to - Atheroma - Thrombosis - Embolus - Spasm - Coronary ostial stenosis

ISCHAEMIC HEART DISEASE (IHD) Coronary Artery Disease (cont) Decrease in oxygenated blood flow to coronary artery due to - Anaemia - Carboxyhaemoglubinaemia - Hypotension Increased demand of oxygen due to - increase cardiac output e.g. Throtoxicosis - myocardial hypertrophy e.g. Hypertension, Aortic Stenosis

ISCHAEMIC HEART DISEASE (IHD) Myocardial Ischemia occurs most commonly due to obstructive coronary artery disease (CAD) in the form of coronary Atherosclerosis CAD is the largest cause of death in UK and many parts of the world In 2009 in UK, 1:5 male and 1:8 female death were from coronary artery disease Sudden death can occur

ISCHAEMIC HEART DISEASE (IHD) We will study the process of Atherosclerosis in coronary artery, which causes CAD. Coronary Atherosclerosis is characterized by accumulation of lipid, macrophages and smooth muscle cells in the intimal plaques in large and medium size coronary arteries Process of Atherosclerosis - Endothelial injury - Accumulation of lipoprotein (LDL) - LDL are taken by macrophages - Formation of foam cells – macrophages which have taken LDL - Proliferation of smooth muscle cell

ISCHAEMIC HEART DISEASE (IHD) Formation of Plaque - Proliferation of smooth muscle cells with collagen formation, lipid deposition, macrophages, inflammatory cells, endothelial cell proliferation all make fibro lipid plaque - Plaque may be stable unstable (can rupture) - Plaque can obstruct the blood vessel - Plaque can undergo thrombosis

ISCHAEMIC HEART DISEASE (IHD) Coronary artery disease (CAD) gives rise to 1. Stable angina 2. Acute coronary syndrome - Unstable angina - Non ST elevation myocardial infarction (NSTEMI) - ST elevation myocardial infarction (STEMI)

Mechanism for development of thrombosis on plaque

ISCHAEMIC HEART DISEASE (IHD) Risk Factors Fixed IHD risk factors (that can not be changed) Age – CAD increases with age Male sex – higher incidence than premenopausal women Positive family history

ISCHAEMIC HEART DISEASE (IHD) Risk Factors (Potentially changeable risk factors) Hyperlipidaemia Hypertension Diabetes mellitus Cigarette smoking Diet and obesity Lack of exercise It is recommended that adult should do a minimum of 30mins of moderate activity e.g. Brisk walking, cycling on 5 days of the week

ISCHAEMIC HEART DISEASE (IHD) Risk factors for Coronary Artery Disease

ISCHAEMIC HEART DISEASE (IHD) Primary and Secondary Prevention Primary Prevention - It is prevention of atherosclerotic disease process Secondary Prevention - It is treatment of atherosclerosis that is treatment of disease or its complication

ISCHAEMIC HEART DISEASE (IHD) Important Point Blood Pressure should be maintained below 140/90 mmHg (in Diabetes, BP 130/80 mmHg) Serum cholesterol should be below 4.0 mmol/L HDL should be more than 1 mmol/L LDL should be less than 2 mmol/L

Stable Angina

ISCHAEMIC HEART DISEASE (IHD) Stable Angina The most common symptom associated with angina is central chest pain on exertion Pain of angina pectoris and myocardial infarction is due to myocardial hypoxia Pain in angina is retrosternal, heavy, tight or gripping, with radiation to left arm, neck, jaw , epigastrium. Pain last for 2-10 minute, may be mild or severe

ISCHAEMIC HEART DISEASE (IHD) Pain is provoked by physical exertion, after meal, cold, windy weather, excitement Pain is relieved by rest or sublingual nitrates ( GTN )

Anginal Pain - Radiation

ISCHAEMIC HEART DISEASE (IHD) Diagnosis of angina is largely based on clinical history

TYPES OF ANGINA Stable angina – pain related to exertion Unstable angina – pain occurs at rest, it is part of acute coronary syndrome and we will discuss later with acute coronary syndrome Refractory angina – when anginal pain is not controlled by medical therapy, patient is having severe coronary disease

TYPES OF ANGINA (cont) Variant (Prinzmetal’s) angina - Angina usually at rest - It is due to coronary artery spasm - More in women - There is ST elevation on ECG during pain 5. Cardiac syndrome X - Patient has history of angina, positive exercise test but on angiography coronary arteries are normal. Prognosis is good.

STABLE ANGINA Examination No abnormal finding in angina Look for - Anaemia - Throtoxicosis - Hyperlipidaemia (Xanthelasma, Tendon Xanthoma) - Check blood pressure for hypertension - Examine CVS, exclude aortic stenosis as possible cause of angina

STABLE ANGINA (cont) Investigations ECG – 12 lead ECG is normal between attacks During attack, transient ST-depression, T-wave inversion may appear Cardiac enzymes – Troponin T and Troponin I normal Exercise (Stress) ECG – ST- depression of 1 mm is taken as positive test CT – coronary angiography

STABLE ANGINA (cont) Investigations (cont) Functional imaging – SPECT Stress Echocardiography Stress Magnetic resonance imaging (MRI) Cardiac catheterization Note – SPECT – Single Photon Emission Computed Tomography – it is scan of heart, non invasive nuclear imaging test after radioactive tracer injection given IV

STABLE ANGINA (cont) Management of Stable Angina Inform the patient about the nature of disease and reassure that prognosis is good Annual mortality < 2% Treat underlying problem e.g. anemia or hyperthyroidism

STABLE ANGINA (cont) Management of Stable Angina (cont) Manage DM, hypertension if present Look for risk factors e.g. smoking, obesity, hypercholesterolaemia, advice and treat Regular exercise should be encouraged

STABLE ANGINA (cont) Pharmacological therapy Vasodilator – GTN (Glyceryl Trinitrate 0.3-1mg sublingual) Isosorbide mononitrate – 10-60mg orally twice daily Beta Blocker Atenolol (Tenormin) 25-100mg daily Bisoprolol (Concor) 2.5-10mg/day Beta blocker decrease heart rate, decrease BP, and decrease myocardial O2 demand

STABLE ANGINA (cont) Pharmacological therapy (cont) 3. Calcium channel blocker -Verapamil – 80-120mg three times per day - Diltiazem – 60-120mg three times per day - Amlodipine (mainly vasodilator) – 5-10mg per day Verapamil and Diltiazem decrease force of cardiac contraction and inhibit cardiac conductive tissue, therefore, they are contraindicated in severe bradycardia, left ventricular failure, second or third degree heart block - Side effect – Verapamil - Constipation

STABLE ANGINA (cont) Pharmacological therapy (cont) Secondary Prevention Aspirin 75mg daily – it is anti platelet, side effect is GI bleeding ACE inhibitors – used if hypertension, heart failure. Statins (Lipitor ) used to reduce total cholesterol to 4mmol/L and LDL to blow 2mmol/L

STABLE ANGINA (cont) Revascularization PCI – Percutaneous Coronary Intervention It is process to dilate coronary artery stenosis, using inflatable balloon and metallic stent introduced via femoral, radial, or brachial artery

Intra Coronary Stent

STABLE ANGINA (cont) Revascularization (cont) Complication – bleeding, hematoma, pseudo aneurysm Serious Complication – Acute MI 2% – Stroke 0.4% – Death 1% When metallic Drug – eluting stent are used, patients are advised to take Aspirin, Plavix for 1 year

Percutaneous Transluminal Coronary Angioplasty PTCA A. Right coronary artery (RCA) occluded B. Soft wire passed C. Balloon is inflated to dilate stenosis D. RCA reopened

STABLE ANGINA (cont) Coronary Artery Bypass Grafting (CABG) Autologus veins or arteries are anastomosed Saphanous vein or internal memory artery are used Operative mortality < 1%

Relief of Coronary Obstruction By Surgical Techniques

Algorithm for Management of Patient’s with Stable Angina

ACUTE CORONARY SYNDROME

Patient with chest pain

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

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 normal Because No myocardial damage has occurred

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

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

STEMI (cont) IMPORTANT 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. IMPORTANT Thrombolytic therapy is given in STEMI Thrombolytic therapy is NOT GIVEN IN UNSTABLE ANGINA AND NSTEMI

NSTEMI & UNSTABLE ANGINA Investigations and Treatment High risk patient who are likely to progress to MI require urgent coronary angiography in less than 72 Hours Who are high risk patient ? - Patient with persistent angina or recurrent angina with ST changes > 2mm or deep negative T wave changes . - Clinical signs of heart failure - Hemodynamic instability - Life threatening arrhythmias

NSTEMI & UNSTABLE ANGINA (Cont) Patient having high risk score ( CONT ) Increased Troponin Dynamic ST or T wave changes Previous MI PCI within last 6 months Previous CABG

Medical Treatment Unstable Angina &NSTEMI O2 Morphine and anti emetic Aspirin Clopidrogrel (Plavix )- anti platelet agent Enoxaprin- low molecular heparin Beta blocker ACE-Inhibitors Nitrates Statins eg lipitor

ST Elevation MI ( STEMI ) ECG changes in myocardial infarction (STEMI) Leads Showing ST Elevation Infarct Site V2 – V5 Anterior V1 – V3 Anteroseptal V4 – V6, I, aVL Anterolateral I, aVL Lateral II, III, aVF Inferior V1, V2(Reciprocal) Posterior

ST ELEVATION MI COMMENT ON ECG

ST elevation in lead 1 ,aVL, V2, V3 , v4,v5, v6 ANTERO-LATERAL MI

STEMI COMMENT ON ECG

ST ELEVATION IN LEAD II,III,aVF INFERIOR MI

Medical Treatment STEMI O2 Morphine and anti emetic Aspirin Clopidrogrel (Plavix )- anti platelet agent Enoxaprin- low molecular heparin Beta blocker ACE-Inhibitors Nitrates Statins eg lipitor

STEMI PCI PCI is advised , where facilities are available, when patient presented to hospital in 12 hours of pain. THROMBOLYSIS If PCI not availble ( small hospital ) Fibrinolysis (Thrombolysis) is done within 6 hours ( Up to 12 hrs )of STEMI Drugs used for Thrombolysis are Alteplase (human tissue plasminogen activator or tPA ) Streptokinase

STEMI -COMPLICATIONS Heart failure Myocardial rupture Ventricular septal defect Mitral regurgitation due to severe LV dysfunction and dilatatiopn Papillary muscle dysfunction

STEMI – CARDIAC ARRHYTHMIAS Ventricular tachycardia and ventricular fibrillation Cardiac arrest Atrial fibrillation Conduction defect - common with INFERIOR MI as Rt coronary artery supplies Inferior surface and SA & AV nodes.

Post ACS Life style modificatiion Diet- Omega- 3 fatty acid from fish Daily walk 20- 30 min daily Stop smoking Maintain alcohol consumption in safe limits 21 units/ week If over weight – reduce weight Control Hypertension less than 140/90 mmHg , if patient has DM, than BP less than 130/ 90 mmHg Maintain Hb A1c less than 7% in Diabetic patient

CASE HISTORY – A patient with hypertension and chest pain A 50 year old smoker with hypertension develops central crushing chest pain radiating to his jaw. He has vomited and now feels short of breath. ECG was done which is shown.

Questions: What is the diagnosis? a. Posterior MI b. Inferior MI c. Antrolateral MI d. Pericarditis Patient is given Morphine, anti-emetic and aspirin. He is taken immediately to the cardiac cath lab, where he undergoes coronary angiography and stenting to one of the vessels. Which coronary artery is stented? a. Right b. Circumflex c. Diagonal d. Left anterior descending (LAD)

Answers: Answer to Question 1 : c. Antrolateral MI Answer to Question 2: d. Left anterior descending (LAD)

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