IHD (Stable Angina) PDF

 Definition Ischemic heart disease (IHD) is a condition in which there is an inadequate supply of blood and o2 to a part of the myocardium.It typically occurs when there is an imbalance between myocardial oxygen supply and demand. IHD may present as: Stable...

 Definition Ischemic heart disease (IHD) is a condition in which there is an inadequate supply of blood and o2 to a part of the myocardium.It typically occurs when there is an imbalance between myocardial oxygen supply and demand. IHD may present as: Stable Angina Unstable angina Myocardial infarction -Chromic coronary syndrome is term used to describe stable angina -Acute coronary syndrome is a term that encompasses both UA and MI.  Angina Definition & Cause & Sx Angina pectoris is a symptom complex caused by transient myocardial ischaemia, which occurs whenever there is an imbalance between myocardial oxygen supply and demand. Most common Cause is atherosclerosis. The history is the most important factor in making the diagnosis. Stable angina is characterized by central chest pain, discomfort or breathlessness precipitated by exertion and relieved by rest. Some patients nd the discomfort comes when they start walking and that later it does not return despite greater effort (‘warm-up angina’=Second Wind). When occur at rest while the patient is recumbent (angina decubitus). When oocur at night (Nocturnal angina) fi  Physical examination Physical examination is frequently unremarkable but should include a careful search for evidence of: Valve disease (particularly aortic). Important risk factors (hypertension, DM). LV dysfunction (cardiomegaly, gallop rhythm). Manifestations of arterial disease (carotid bruits, peripheral arterial disease). Unrelated conditions that may exacerbate angina (anaemia, thyrotoxicosis).  Investigations 1-ELECTROCARDIOGRAM A 12-lead ECG recorded at rest may be normal in patients with typical angina pectoris, but there may also be signs of an old myocardial infarction. Repolarization abnormalities, i.e., ST-segment and T- wave changes, as well as LVH and disturbances of cardiac rhythm or intraventricular conduction are suggestive of IHD Dynamic ST-segment and T-wave changes that accompany episodes of angina pectoris and disappear thereafter are more speci c. fi 2-Exercise ECG Should be performed using a standard treadmill or bicycle ergometer protocol while monitoring the patient’s pulse, BP and general condition. Planar or downsloping ST segment depression of 1 mm or more is indicative of ischaemia.Up-sloping ST depression is less speci c; it often occurs in normal individuals. False-positive results can occur with digoxin therapy, left ventricular hypertrophy, bundle branch block and WPW syndrome.However, exercise testing may be normal in a signi fi fi 3-Stress echocardiography Medical or exercise stress may show a regional wall hypokinesia in the left ventricle during stress,this may indicate ischemia. 4-Myocardial perfusion scanning A perfusion defect present during stress but not at rest provides evidence of reversible myocardial ischaemia whereas a persistent perfusion defect seen during both phases of the study is usually indicative of previous MI. 5-CT coronary arteriography CT coronary arteriography is being used to document the presence or absence of CAD in patients with suspected angina. 6-Coronary angiography Coronary angiography provides detailed anatomical information about the extent and nature of CAD. It is usually performed when coronary artery bypass graft surgery or percutaneous coronary intervention is being considered. 7-Cardiac biomarkers (serum troponin ,CK-MB) are usually not used in patient with stable angina (but it is highly indicated in patient with acute coronary syndrome).  NON Specific Investigation Blood sugar Urinalysis (sugar , albumin urea) Lipid profile Renal function test (blood urea,serum creatinine) Thyroid function test Complete blood count (anemia) Chest X-ray high-sensitivity C-reactive protein (CRP)  Management This should begin with a careful explanation of the problem and a discussion of the lifestyle and medical interventions that can be deployed to relieve symptoms and improve prognosis. The principles of management involve: 1 A careful assessment of the extent and severity of arterial disease. 2 Identification and treatment of risk factors. 3 Advice on smoking cessation. 4 Introduction of drug treatment for symptom control. 5 identification of high-risk patients for treatment to improve life expectancy.  Medication 1-Antiplatlet All patients with angina secondary to CAD should receive antiplatelet therapy. Low-dose (75 mg) aspirin should be prescribed for all patients and continued indefinitely since it reduces the risk of MI. Clopidogrel (75 mg daily) is an equally effective alternative if aspirin causes dyspepsia or other side effects. 2-Statin All patients should be prescribed a statin (Rosuvastitin,Atorvastatin,Simvastatin), even if cholesterol is normal. 3-Nitrates Nitrates act directly on vascular smooth muscle to produce venous and arteriolar dilatation. Several preparations are available, They help angina by lowering preload and afterload, which reduces myocardial oxygen demand , and by increasing myocardial oxygen supply through coronary vasodilatation. Sublingual GTN, administered from a metered-dose aerosol (400 μg per spray) or as a tablet (300 or 500 μg), is indicated for acute attacks and will usually relieve an attack in 2–3 minutes. Isosorbide dinitrate (10–20 mg 3 times daily) and isosorbide mononitrate (20–60 mg once or twice daily) can be given by mouth, unlike GTN, which undergoes extensive metabolism in the liver.  Headache is common with oral nitrates but tends to diminish if the patient perseveres with the treatment. Continuous nitrate therapy can cause pharmacological tolerance but this can be avoided by a 6–8-hour nitrate-free period, best achieved at night when the patient is inactive. If nocturnal angina is a predominant symptom, long- acting nitrates can be given at the end of the day. 4-Beta-blockers These lower myocardial oxygen demand by reducing heart rate,BP and myocardial contractility. A once-daily cardioselective preparation such as slow-release Metoprolol (50–200 mg daily) or Bisoprolol (5–15 mg daily) is preferable. In theory, non-selective β-blockers may aggravate coronary vasospasm (by blocking coronary artery β2-adrenoceptors). Beta-blockers should not be withdrawn abruptly, as rebound effects may precipitate dangerous arrhythmias, worsening angina or MI. This is known as the β-blocker withdrawal syndrome. 5-Calcium channel antagonists These drugs lower myocardial oxygen demand by reducing BP and myocardial contractility. Verapamil and Diltiazem (nondihydropyridine) can be used as monotherapy because they slow SA node firing, inhibit conduction through the AV node and tend to cause bradycardia. Calcium channel antagonists reduce myocardial contractility and must be used with care in patients with poor LV function, Dihydropyridine calcium antagonists, such as Nifedipine and Amlodipine, may cause a reflex tachycardia,so it is best to use them in combination with a β-blocker. 6-Potassium channel activators Nicorandil (10–30 mg twice daily orally). It acts as a vasodilator with effects on the arterial and venous systems, and has the advantage that it does not exhibit the tolerance seen with nitrates. 7-Ion channel antagonist Ivabradine is the first of this class of drug. It induces bradycardia by modulating ion channels in the sinus node. It does not inhibit myocardial contractility and appears to be safe in patients with heart failure. 8-Ranolazine This drug inhibits the late inward sodium current in coronary artery smooth muscle cells, with a secondary effect on calcium flux and vascular tone, reducing angina symptoms.  Non-pharmacological (Surgical) treatments 1-Percutaneous coronary intervention Percutaneous coronary intervention (PCI) involves passing a fine guidewire across a coronary stenosis under radiographic control and using it to position a balloon, which is then inflated to dilate the stenosis. This can be combined with deployment of a coronary stent, which is a piece of metallic ‘scaffolding’ that can be eluted with drugs with ant proliferative properties and that helps to maximize and maintain dilatation of a stenosed vessel. Stenosis in bypass grafts can be dilated, as well as those in the native coronary arteries. 2-Coronary artery bypass grafting (CABG): The internal mammary arteries, radial arteries or reversed segments of the patient’s own saphenous vein can be used to bypass coronary artery stenosis. This usually involves major surgery under cardiopulmonary bypass but, in some cases, grafts can be applied to the beating heart: ‘off-pump’ surgery. The operative mortality is approximately 1.5% but risks are higher in elderly patients, those with poor left ventricular function and those with significant comorbidity, such as renal failure.Arterial grafts have a much better long- term patency rate. Survival is improved by CABG in: 1-Symptomatic patients with left main stem stenosis or 2-Three-vessel coronary disease when the LAD, CX and right coronary arteries are involved, or 3- Two-vessel disease involving the proximal LAD coronary artery.  Prognosis The prognosis of CAD is related to the: 1-Number of diseased vessels. 2-The degree of left ventricular dysfunction. A patient with single-vessel disease and good left ventricular function has a 5- year survival of more than 90%. In contrast, a patient with severe left ventricular dysfunction and extensive three-vessel disease has a 5-year survival of less than 30% unless revascularisation is performed. Symptoms are a poor guide to prognosis, since spontaneous improvement in angina due to the development of collateral vessels is common. Nevertheless, the 5-year mortality of patients with severe angina (CCS angina scale III or IV) is nearly double that of patients with mild symptoms.  Other Causes of Angina Causes of angina: 1. Atherosclerosis (most common cause). 2. Aortic valve disease (mainly stenosis). 3. Hypertrophic cardiomyopathy. 4. Vasculitis or aortitis (Takayasu). 5. Coronary artery spasm. 6. Syndrome X  Coronary artery spasm Angina may result from vasospasm of the coronary arteries. This may coexist with atherosclerosis, especially in unstable angina , but may occur as an isolated phenomenon in less than 1% of cases, in patients with normal coronary arteries on angiography. This is sometimes known as variant angina; and when it is accompanied by transient ST elevation on the ECG, it is termed Prinzmetal’s angina.  Syndrome X The constellation of: 1- Typical angina on effort, 2-Objective evidence of myocardial ischaemia on stress testing, and 3-Normal coronary arteries on angiography is sometimes known as syndrome X. Many of these patients are women and the mechanism of their symptoms is often unclear. This disorder is poorly understood; it carries a good prognosis and may respond to anti-anginal therapy.