Coronary Heart Disease PDF

CORONARY HEART DISEASE Dr.AMIR AL-MUMIN  CORONARY HEART DISEASE Objectives 1. The student can enumerate the clinical manifestations of coronary heart disease and the mechanism of each. 2. The student can define chronic stable angina and enumerate the factors precipitating...

CORONARY HEART DISEASE Dr.AMIR AL-MUMIN  CORONARY HEART DISEASE Objectives 1. The student can enumerate the clinical manifestations of coronary heart disease and the mechanism of each. 2. The student can define chronic stable angina and enumerate the factors precipitating angina. 3. The student can enumerate the important investigations in stable angina. 4. The student can outline the management of chronic stable angina. 5. The student can define unstable angina and non ST-elevation myocardial infarction  con. on Objectives 6. The student can enumerate the important investigations in unstable angina and non ST-elevation myocardial infarction. 7. The student can outline the management of unstable angina and non ST-elevation myocardial infarction. 8. The student can outline the ECG changes of acute ST- elevation myocardial infarction. 9. The student can enumerate the plasma cardiac markers useful in diagnosing MI. 10. The student can outline the early management of acute ST-elevation myocardial infarction Coronary heart disease Coronary heart disease (CHD) is the most common form of heart disease and the single most important cause of premature death in certain parts of world. Disease of the coronary arteries is almost always due to atheroma and its complications, particularly thrombosis. 1. Stable angina 2. Unstable angina 3. Myocardial infarction 4. Heart failure 5. Arrhythmia 6. Sudden death Ischaemia due to fixed atheromatous stenosis of one or more coronary arteries Ischaemia caused by dynamic obstruction of a coronary artery due to plaque rupture with superimposed thrombosis and spasm Myocardial necrosis caused by acute occlusion of a coronary artery due to plaque rupture and thrombosis Myocardial dysfunction due to infarction or ischaemia Altered conduction due to ischaemia or infarction Ventricular arrhythmia, asystole or massive myocardial infarction Angina pectoris is the symptom complex caused by transient myocardial ischaemia. It may occur whenever there is an imbalance between myocardial oxygen supply and demand. It occurs when coronary perfusion is impaired by fixed or stable atheroma of the coronary arteries.  Independent risk factors for coronary heart disease Increasing age Male sex Family history High blood pressure High total cholesterol Low HDL-cholesterol Cigarette smoking Presence of diabetes/insulin resistance Presence of left ventricular hypertrophy Obesity Lack of physical activity Alcohol hypothyroidism  Lipid Profile Bad cholesterol Good cholesterol LDL HDL Carries 75% of cholesterol to cells It removes cholesterol from the walls of the arteries and returns it to the liver Becomes bad when it gets oxidated It helps prevent oxidation of LDL. In The body releases various fact, it appears to have antioxidant immune factors aimed at properties on its own. protecting the damaged walls. Unfortunately, in excessive Triglycerides – increasing role in IHD quantities they cause development inflammation and promote Triglycerides appear to interact with HDL cholesterol in such a way that further injury to the areas they HDL levels fall as triglyceride levels target rise. Low HDL is known to be harmful to the heart FACTORS INFLUENCING MYOCARDIAL OXYGEN SUPPLY AND DEMAND Increased Oxygen Demand (cardiac work) 1. ↑Heart rate 2. ↑ Blood pressure 3. ↑ Myocardial contractility 4. Left ventricular hypertrophy 5. Valve disease, e.g. aortic stenosis  Decreased Oxygen Supply ( Coronary Blood Flow) 1. ↓Duration of diastole 2. ↓ Coronary perfusion pressure (aortic diastolic minus coronary sinus or right atrial diastolic pressure) 3. ↑ Coronary vasomotor tone 4. ↓ Oxygenation ↓ Haemoglobin ↓ Oxygen saturation  Clinical features Stable angina is characterized by central chest pain, discomfort or breathlessness that is precipitated by exertion or other forms of stress, and is promptly relieved by rest.  ACTIVITIES PRECIPITATING ANGINA Physical exertion Cold exposure Heavy meals Intense emotion 1. Resting ECG 2. Exercise ECG 3. Myocardial perfusion scanning 4. Stress echocardiography 5. Coronary arteriography  Management The management of angina pectoris involves: -A careful assessment of the likely extent and severity of arterial disease. -The identification and control of significant risk factors (e.g. smoking, hypertension, hyperlipidaemia). -The use of measures to control symptoms. -The identification of high-risk patients and application of treatments to improve life expectancy  ADVICE TO PATIENTS WITH STABLE ANGINA -Do not smoke -Aim at ideal body weight -Take regular exercise (exercise up to, but not beyond, the point of chest discomfort is beneficial and may promote collateral vessels) -Avoid severe unaccustomed exertion, and vigorous exercise after a heavy meal or in very cold weather -Take sublingual nitrate before undertaking exertion that may induce angina  Drug therapy 1. Antiplatelet therapy Low-dose aspirin or clopidogrel 2. Lipid-lowering therapy Statins 3. Anti-anginal drug treatment Four groups of drugs are used to help relieve or prevent the symptoms of angina: 1. Nitrates 2. β-blockers(metoprolol,bisoprolol,atenolol) 3. Calcium antagonists and(deltiazem,verapamil) 4. Potassium channel activators(nicorandil) The most widely used invasive options for the treatment of ischaemic heart disease include: 1. Percutaneous coronary intervention (PCI) 2. Coronary artery bypass graft (CABG) surgery Unstable angina is a clinical syndrome that is characterized by: -New-onset of severe angina -Rapidly worsening angina (crescendo angina) -Angina on minimal exertion, or -Angina at rest. Non ST-elevation myocardial infarction differs from unstable angina by the presence of elevated markers of myocardial necrosis in blood. The lesion is usually a complex ulcerated or fissured atheromatous plaque with adherent platelet-rich thrombus and local coronary artery spasm. This is a dynamic process whereby the degree of obstruction may either increase or regress  Diagnosis and risk stratification The assessment of acute chest pain depends heavily on: 1. An analysis of the character of the pain and its associated features. 2. Evaluation of the 12-lead ECG and 3. Serial measurements of biochemical markers of cardiac damage, such as troponin I and T or CPK-MB.  Management - Admission urgently to hospital - Bed rest -Antiplatelet therapy (aspirin and clopidogrel) -Anticoagulant therapy (e.g. unfractionated or fractionated heparin) -A β-blocker (e.g. atenolol or metoprolol). - Calcium channel blocker (verapamil or diltiazem) if a β-blocker is contraindicated. - If pain persists or recurs, infusions of intravenous nitrates - Coronary angiography should be considered with a view to revascularisation in all patients at moderate or high risk. ST ELEVATION MYOCARDIAL INFARCTION Myocardial infarction (MI) is almost always due to the formation of occlusive thrombus at the site of rupture or erosion of an atheromatous plaque in a coronary artery. The process of infarction progresses over several hours and therefore most patients present when it is still possible to salvage myocardium and improve outcome Pain is the cardinal symptom of MI, but breathlessness, vomiting, and collapse or syncope are common features. The pain occurs in the same sites as angina but is usually more severe and lasts longer; it is often described as a tightness, heaviness or constriction in the chest.  INVESTIGATIONS The earliest ECG change is usually ST elevation; later on there is diminution in the size of the R wave and a Q wave begins to develop. Subsequently, the T wave becomes inverted because of a change in ventricular repolarisation; this change persists after the ST segment has returned to normal. The ECG changes are best seen in the leads that 'face' the infarcted area MI causes a detectable rise in the plasma concentration of enzymes and proteins that are normally concentrated within cardiac cells. The biochemical markers that are most widely used in the detection of MI are: Creatine kinase (CK) A more sensitive and cardiospecific isoform of this enzyme (CK-MB) The cardiospecific proteins, troponins T and I Serial (usually daily) estimations are particularly helpful because it is the change in plasma concentrations of these markers that is of diagnostic value.  EARLY MANAGEMENT Patients with suspected acute MI require immediate access to medical/paramedical care and defibrillation facilities. A patient with severe chest pain also requires urgent medical assessment and analgesia. Patients are usually managed in a dedicated cardiac unit because this offers a convenient way of concentrating the necessary expertise, monitoring and resuscitation facilities.  EARLY MANAGEMENT OF ACUTE MYOCARDIAL INFARCTION Provide facilities for defibrillation Immediate measures High-flow oxygen I.V access ECG monitoring 12-lead ECG I.V. analgesia (opiates) and antiemetic Aspirin 300 mg(preferablly chewing) Reperfusion: Primary PCI or thrombolysis Detect and manage acute complications 1 Arrhythmias 2 Ischaemia 3-Heart failure  Maintaining vessel patency Aspirin and clopidogrel Intravenous heparin or subcutaneous low molecular weight heparin Beta-blockers Nitrates and other agents  COMPLICATIONS OF INFARCTION Arrhythmias Ischaemia Acute circulatory failure Pericarditis Mechanical complications: Papillary muscle damage (mitral regurgitation) Rupture of interventricular septum (ventricular septal defect) Rupture of left ventricular free wall (cardiac tamponade) Embolism Ventricular remodelling and aneurysm  Summary -Coronary heart disease can present in various ways. - Stable angina is characterized by central chest pain, discomfort or breathlessness that is precipitated by exertion or other forms of stress, and is promptly relieved by rest. - Activities precipitating angina include physical exertion, cold exposure, heavy meals and intense emotion. - Investigations useful in diagnosis of stable angina include stress ECG, stress perfusion scanning, stress echocardiography and coronary angiography. -Management of stable angina include lifestyle modifications, aspirin, lipid-lowering therapy, anti-anginal therapy and in certain patients coronary revascularization.  Summary - Unstable angina is acute presentation of IHD. - Non ST-elevation MI is acute presentation of IHD with elevated cardiac markers and absence of ST elevation. - Diagnosis of unstable angina/ non ST-elevation MI is based on the analysis of chest pain, 12-lead ECG and cardiac markers. - Management of unstable angina/ non ST-elevation MI involves medical stabilization and, in intermediate to high risk patients, coronary revascularization. - Acute ST-elevation MI is characterized by typical ECG changes and elevated plasma cardiac markers. - Management of acute ST-elevation MI include immediate measures, reperfusion, detection and managing complications. - The are many complications of acute ST-elevation MI. iiiii