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16-September-2008 16:15:06 - Angina pectoris November 2007 Angina pectoris Classification and external resources ICD-10 I20. ICD-9 413 DiseasesDB 8695 eMedicine med/133 MeSH D000787 This article is about chest pain due to oxygen shortage in the heart. For angina tonsillaris see tonsillitis. For the infection of the soft tissues in the floor of the mouth, see Ludwig's angina. Angina pectoris, commonly known as angina, is severe chest pain due to ischemia a lack of blood and hence oxygen supply of the heart muscle, generally due to obstruction or spasm of the coronary arteries the heart's blood vessels. Coronary artery disease, the main cause of angina, is due to atherosclerosis of the cardiac arteries. The term derives from the Greek ankhon strangling and the Latin pectus chest, and can therefore be translated as a strangling feeling in the chest. It is common to equate severity of angina with risk of fatal cardiac events. There is a weak relationship between severity of pain and degree of oxygen deprivation in the heart muscle i.e. there can be severe pain with little or no risk of a heart attack, and a heart attack can occur without pain. Worsening crescendo angina attacks, sudden-onset angina at rest, and angina lasting more than 15 minutes are symptoms of unstable angina usually grouped with similar conditions as the acute coronary syndrome. As these may herald myocardial infarction a heart attack, they require urgent medical attention and are generally treated as a presumed heart attack. Contents 1 Symptoms 2 Subtypes 2.1 Stable angina 2.2 Unstable angina 3 Diagnosis 4 Pathophysiology 5 Epidemiology 6 Treatment 7 References 8 Major studies 9 External links Symptoms Most patients with angina complain of chest discomfort rather than actual pain: the discomfort is usually described as a pressure, heaviness, tightness, squeezing, burning, or choking sensation. Apart from chest discomfort, anginal pains may also be experienced in the epigastrium upper central abdomen, back, neck, jaw, or shoulders. Typical locations for radiation of pain are arms often inner left arm, shoulders, and neck into the jaw. Angina is typically precipitated by exertion or emotional stress. It is exacerbated by having a full stomach and by cold temperatures. Pain may be accompanied by breathlessness, sweating and nausea in some cases. It usually lasts for about 1 to 5 minutes, and is relieved by rest or specific anti-angina medication. Chest pain lasting only a few seconds is normally not angina. Myocardial ischemia comes about when the myocardia the heart muscles receive insufficient blood and oxygen to function normally either because of increased oxygen demand by the myocardia or by decreased supply to the myocardia. This inadequate perfusion of blood and the resulting reduced delivery of oxygen and nutrients, is directly correlated to blocked or narrowed blood vessels. Some experience autonomic symptoms related to increased activity of the autonomic nervous system such as nausea, vomiting and pallor. Major risk factors for angina include cigarette smoking, diabetes, high cholesterol, high blood pressure, sedentary lifestyle and family history of premature heart disease. A variant form of angina Prinzmetal's angina occurs in patients with normal coronary arteries or insignificant atherosclerosis. It is thought to be caused by spasms of the artery. It occurs more in younger women. Subtypes Stable angina This refers to the more common understanding of angina related to myocardial ischemia. Typical presentations of stable angina is that of chest discomfort and associated symptoms precipitated by some activity running, walking, etc with minimal or non-existent symptoms at rest. Symptoms typically abate several minutes following cessation of precipitating activities and resume when activity resumes. In this way, stable angina may be thought of as being similar to claudication symptoms. Unstable angina Unstable angina UAis defined as angina pectoris or equivalent ischemic discomfort with at least one of three features: 1 it occurs at rest or with minimal exertion, usually lasting 10 min; 2 it is severe and of new onset i.e., within the prior 4-6 weeks; and/or 3 it occurs with a crescendo pattern i.e., distinctly more severe, prolonged, or frequent than previously.UA may occur unpredictably at rest which may be a serious indicator of an impending heart attack. What differentiates stable angina from unstable angina other than symptoms is the pathophysiology of the atherosclerosis. In stable angina, the developing atheroma is protected with a fibrous cap. This cap atherosclerotic plaque may rupture in unstable angina, allowing blood clots to precipitate and further decrease the lumen of the coronary vessel. This explains why angina appears to be independent to activity. Diagnosis In angina patients who are momentarily not feeling any chest pain, an electrocardiogram ECG is typically normal, unless there have been other cardiac problems in the past. During periods of pain, depression or elevation of the ST segment may be observed. To elicit these changes, an exercise ECG test treadmill test may be performed, during which the patient exercises to their maximum ability before fatigue, breathlessness or, importantly, pain supervenes; if characteristic ECG changes are documented typically more than 1 mm of flat or downsloping ST depression, the test is considered diagnostic for angina. The exercise test is also useful in looking for other markers of myocardial ischaemia: blood pressure response or lack thereof, particularly a drop in systolic pressure, dysrhythmia and chronotropic response. Other alternatives to a standard exercise test include a thallium scintigram in patients that cannot exercise enough for the purposes of the treadmill tests, e.g., due to asthma or arthritis or in whom the ECG is too abnormal at rest or Stress Echocardiography. In patients in whom such noninvasive testing is diagnostic, a coronary angiogram is typically performed to identify the nature of the coronary lesion, and whether this would be a candidate for angioplasty, coronary artery bypass graft CABG, treatment only with medication, or other treatments. In patients who are in hospital with unstable angina or the newer term of high risk acute coronary syndromes, those with resting ischaemic ECG changes or those with raised cardiac enzymes such as troponin may undergo coronary angiography directly. Pathophysiology Increase in heart rate results in increased oxygen demand by the heart. The heart has a limited ability to increase its oxygen intake during episodes of increased demand. Therefore, an increase in oxygen demand by the heart eg, during exercise has to be met by a proportional increase in blood flow to the heart. Myocardial ischemia can result from: a reduction of blood flow to the heart that can be caused by stenosis, spasm, or acute occlusion by an embolus of the heart's arteries resistance of the blood vessels reduced oxygen-carrying capacity of the blood. Atherosclerosis is the most common cause of stenosis narrowing of the blood vessels of the heart's arteries and, hence, angina pectoris. Some people with chest pain have normal or minimal narrowing of heart arteries; in these patients, vasospasm is a more likely cause for the pain, sometimes in the context of Prinzmetal's angina and syndrome X. Myocardial ischemia also can be the result of factors affecting blood composition, such as reduced oxygen-carrying capacity of blood, as seen with seven anemia low number of red blood cells, or long-term smoking. Epidemiology Roughly 6.3 million Americans are estimated to experience angina. Angina is more often the presenting symptom of coronary artery disease in women than in men. The prevalence of angina rises with an increase in age. Similar figures apply in the remainder of the Western world. All forms of coronary heart disease are much less-common in the Third World, as its risk factors are much more common in Western and Westernized countries; it could therefore be termed a disease of affluence. The increase of smoking, obesity and other risk factors has already led to an increase in angina and related diseases in countries such as China. Treatment The main goals of treatment in angina pectoris are relief of symptoms, slowing progression of the disease, and reduction of future events, especially heart attacks and of course death. An aspirin 75 mg to 100 mg per day has been shown to be beneficial for all patients with stable angina that have no problems with its use. Beta blockers eg. carvedilol, propranolol, atenolol etc. are some few examples have a large body of evidence in morbidity and mortality benefits fewer symptoms and disability and live longer and short-acting nitroglycerin medications are used for symptomatic relief of angina. Calcium channel blockers such as nifedipine Adalat and amlodipine, Isosorbide mononitrate and nicorandil are vasodilators commonly used in chronic stable angina. A new therapeutic class, called If inhibitor, has recently been made available: ivabradine provides pure heart rate reduction,.1 leading to major anti-ischemic and antianginal efficacy. ACE inhibitors are also vasodilators with both symptomatic and prognostic benefit and lastly, statins are the most frequently used lipid/cholesterol modifiers which probably also stabilise existing atheromatous plaque. Surprising perhaps is that exercise is also a very good long term treatment for angina but only particular regimes - gentle and sustained exercise rather than dangerous intense short bursts,2 probably working by complex mechanisms such improving blood pressure and promoting coronary artery collateralisation. Identifying and treating risk factors for further coronary heart disease is a priority in patients with angina. This means testing for elevated cholesterol and other fats in the blood, diabetes and hypertension high blood pressure, encouraging stopping smoking and weight optimisation. Ranolazine Ranexa is a new class of anti anginal drug that was approved by the Food and Drug Administration FDA Recently, University of Cincinnati medical researchers in cardiology have tried to use a non-invasive, non-surgical collecting tool to gather harvested erythropoietic bone marrow-based adult stem cells and coax them into regrowing new coronary blood vessels to supply the cardiac muscle's cells cardiac myocytes with oxygenated blood, with some success- leading to larger Phase 2 trials.citation needed The largest randomised trial of an anti-anginal drug to date is the ACTION trial. It included 7,665 patients with stable angina pectoris. ACTION demonstrated that the calcium channel blocker nifedipine Adalat prolongs cardiovascular event- and procedure-free survival in patients with coronary artery disease. For example new overt heart failures were reduced by 29% compared to placebo. This finding confirms the vascular-protective effects of nifedipine.3 References ^ Sulfi S, Timmis AD 2006. Ivabradine -- the first selective sinus node If channel inhibitor in the treatment of stable angina. Int. J. Clin. Pract. 60 2: 222-8. doi:10.1111/j.1742-1241.2006.00817.x. PMID 16451297. ^ Ades PA, Waldmann ML, Poehlman ET, et al 1993. Exercise conditioning in older coronary patients. Submaximal lactate response and endurance capacity. Circulation 88 2: 572-7. PMID 8339420. ^ Poole-Wilson PA, Lubsen J, Kirwan BA, et al 2004. Effect of long-acting nifedipine on mortality and cardiovascular morbidity in patients with stable angina requiring treatment ACTION trial: randomised controlled trial. Lancet 364 9437: 849-57. doi:10.1016/S0140-67360416980-8. PMID 15351192. Major studies Information on ACTION - A Coronary Disease Trial Investigating Outcome with Nifedipine GITS in Patients with chronic stable angina pectoris External links British Heart Foundation - Angina Angina Pectoris Online Resource for nurses and those in similar professions. Angina Pectoris Animation Video 3D v d e Cardiovascular disease: heart disease - Circulatory system pathology I00-I52, 390-429 Ischaemic/ Acute coronary CHD: CAD - Coronary thrombosis - Coronary vasospasm - Coronary artery aneurysm Angina pectoris Prinzmetal's angina - Myocardial infarction heart attack Myocardial rupture - Dressler's syndrome Layers Pericardium Pericarditis Acute, Constrictive - Pericardial effusion - Cardiac tamponade - Hemopericardium Myocardium Myocarditis Cardiomyopathy: Dilated Alcoholic - Hypertrophic - Restrictive Loeffler endocarditis, Cardiac amyloidosis Arrhythmogenic right ventricular dysplasia Endocardium/ valves Endocarditis Subacute bacterial endocarditis, Libman-Sacks endocarditis, Nonbacterial thrombotic endocarditis mitral regurgitation, prolapse, stenosis - aortic stenosis, insufficiency - tricuspid stenosis, insufficiency - pulmonary stenosis, insufficiency Conduction/ arrhythmia Heart block AV 1°, 2°, 3° - Bundle branch Left, Right - Bifascicular/Trifascicular - Sinoatrial - Sick sinus syndrome - Adams-Stokes syndrome Pre-excitation syndrome Wolff-Parkinson-White - Lown-Ganong-Levine Tachycardia Paroxysmal - Supraventricular AV nodal reentrant, Accelerated idioventricular rhythm, Sinus - Ventricular Torsades de pointes, Catecholaminergic polymorphic Premature contraction Atrial - Ventricular Flutter/fibrillation Atrial flutter - Ventricular flutter - Atrial fibrillation Familial - Ventricular fibrillation Pacemaker Wandering pacemaker - Ectopic pacemaker - Parasystole Long QT syndrome Romano-Ward syndrome - Andersen-Tawil syndrome - Jervell and Lange-Nielsen syndrome Cardiac arrest Sudden cardiac death - Asystole Other Cardiomegaly - Ventricular hypertrophy Left, Right/Cor pulmonale Heart failure Cardiac asthma - Rheumatic fever See also congenital, neoplasia Retrieved from http://en..org/wiki/Angina_pectoris Categories: Ischemic heart diseasesHidden categories: Articles needing additional references from November 2007 | All articles with statements | Articles with statements since November 2007 Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages العربية Dansk Deutsch Ελληνικά Español Esperanto Ù?ارسی Français Bahasa Indonesia Italiano עברית Kurdî / كوردی Latina Nederlands ‪Norsk bokmÃ¥l‬ Polski Português Runa Simi РуÑ?Ñ?кий Suomi Svenska Türkçe ä¸æ–‡ This page was last modified on 2 August 2008, at 11:20
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