View source for Angina

{{Short description|Chest discomfort due to disorder of the heart muscles}}
{{cs1 config|name-list-style=vanc|display-authors=6}}
{{other uses}}
{{Infobox medical condition (new)
| name = Angina
| pronounce = {{IPAc-en|æ|n|ˈ|dʒ|aɪ|n|ə|,_|ˈ|æ|n|dʒ|ɪ|n|ə}} {{respell|ann|JY|nə|,_|AN|jin|ə}}<ref>{{cite web|title=The definition of angina|url=http://www.dictionary.com/browse/angina?s=t}}</ref>
| synonyms = Stenocardia, angina pectoris
| image = File:A man having a Heart Attack.png
| caption = Illustration depicting angina
| field = [[Cardiology]]
| symptoms =
| complications = [[Myocardial infarction]], [[unstable angina]]
| onset =
| duration =
| causes =
| risks =
| diagnosis =
| differential =
| prevention =
| treatment =
| medication =
| prognosis =
| frequency =
| deaths =
}}

<!-- Definition -->
'''Angina''', also known as '''angina pectoris''', is [[chest pain]] or pressure, usually caused by [[ischemia|insufficient blood flow]] to the [[Cardiac muscle|heart muscle]] (myocardium).<ref name="CDC1">{{cite web |title=Coronary Heart Disease, Myocardial Infarction, and Stroke — A Public Health Issue {{!}} CDC |url=https://www.cdc.gov/aging/publications/coronary-heart-disease-brief.html |website=www.cdc.gov |access-date=16 January 2022 |language=en-us |date=31 July 2019}}</ref> It is most commonly a symptom of [[coronary artery disease]].<ref name=CDC1/>

<!-- Cause -->
Angina is typically the result of partial [[vascular occlusion|obstruction]] or [[vasospasm|spasm]] of the [[coronary arteries|arteries that supply blood to the heart muscle]].<ref>{{cite book |title=Dorland's Illustrated Medical Dictionary |date=2003 |publisher=Saunders |location=Philadelphia, PA |isbn=0-7216-0146-4 |pages=82 |url=https://archive.org/details/dorlandsillustra0000unse_q9t6 |access-date=24 August 2022}}</ref> The main mechanism of [[Coronary arteries|coronary artery]] obstruction is [[atherosclerosis]] as part of coronary artery disease. Other causes of angina include [[cardiac arrhythmia|abnormal heart rhythm]]s, [[heart failure]] and, less commonly, [[anemia]].<ref>{{cite journal |author1=Perera, Chanaka Aravinda |author2=Biggers, Richard Peters |author3=Robertson, Alan |title=Deceitful red-flag: angina secondary to iron deficiency anaemia as a presenting complaint for underlying malignancy |journal=BMJ Case Reports |date=1 August 2019 |volume=12 |issue=7 |pages=e229942 |doi=10.1136/bcr-2019-229942 |pmid=31371333 |pmc=6677945}}</ref> The term derives {{ety|la|angere|to strangle||pectus|chest}}, and can therefore be translated as "a strangling feeling in the chest".

An urgent medical assessment is suggested to rule out serious medical conditions.<ref name=":0">{{Cite web |title=Angina |url=https://www.heartandstroke.ca/heart-disease/conditions/angina |access-date=2024-11-26 |website=Heart and Stroke Foundation of Canada |language=en}}</ref> There is a relationship between severity of angina and degree of [[oxygen deprivation]] in the heart muscle. However, the severity of angina does not always match the degree of oxygen deprivation to the heart or the risk of a [[heart attack]] (myocardial infarction). Some people may experience severe pain even though there is little risk of a heart attack whilst others may have a heart attack and experience little or no pain.<ref>{{cite journal |author1=Björck, Lena |author2=Nielsen, Susanne |author3=Jernberg, Tomas |author4=Zverkova-Sandström, Tatiana |author5=Giang, Kok Wai |author6=Rosengren, Annika |title=Absence of chest pain and long-term mortality in patients with acute myocardial infarction |journal= Open Heart|date=26 November 2018 |volume=5 |issue=2 |pages=e000909 |doi=10.1136/openhrt-2018-000909 |pmid=30564376 |pmc=6269644 |url=https://openheart.bmj.com/content/5/2/e000909 |access-date=27 August 2022}}</ref><ref>{{cite journal |author1=Canto, John G. |author2=Goldberg, Robert J. |author3=Hand, Mary M. |title=Symptom Presentation of Women With Acute Coronary Syndromes: Myth vs Reality |journal=Archives of Internal Medicine |date=10 December 2007 |volume=167 |issue=22 |pages=2405–2413 |doi=10.1001/archinte.167.22.2405 |pmid=18071161 |url=https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/770038 |archive-url=https://web.archive.org/web/20220827021734/https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/770038 |access-date=27 August 2022|archive-date=2022-08-27 |doi-access=free |url-access=subscription }}</ref> In some cases, angina can be quite severe. Worsening 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 precede a heart attack, they require urgent medical attention and are, in general, treated similarly to heart attacks.<ref name="AHA-Angina">{{cite web |author1=American Heart Association |title=Angina (Chest Pain) |url=https://www.heart.org/en/health-topics/heart-attack/angina-chest-pain |website=American Heart Association |access-date=27 August 2022 |archive-url=https://web.archive.org/web/20220827013807/https://www.heart.org/en/health-topics/heart-attack/angina-chest-pain |archive-date=27 August 2022 |date=8 November 2021}}</ref>

In the early 20th century, severe angina was seen as a sign of impending death.<ref>{{cite book| vauthors = White PD |title=Heart Disease|date=1931|publisher=Macmillan|edition=1st}}</ref>  However, modern medical therapies have improved the outlook substantially. [[Middle-age]] patients who experience moderate to severe angina ([[Canadian Cardiovascular Society grading of angina pectoris#Functional gradation|grading by classes II, III, and IV]]) have a five-year survival rate of approximately 92%.<ref>{{cite journal | vauthors = Boden WE, O'Rourke RA, Teo KK, Hartigan PM, Maron DJ, Kostuk WJ, Knudtson M, Dada M, Casperson P, Harris CL, Chaitman BR, Shaw L, Gosselin G, Nawaz S, Title LM, Gau G, Blaustein AS, Booth DC, Bates ER, Spertus JA, Berman DS, Mancini GB, Weintraub WS | title = Optimal medical therapy with or without PCI for stable coronary disease | journal = The New England Journal of Medicine | volume = 356 | issue = 15 | pages = 1503–16 | date = April 2007 | pmid = 17387127 | doi = 10.1056/NEJMoa070829 | doi-access = free }}</ref>

==Classification==

===Stable angina<!--stable angina redirects here-->===
Also known as 'effort angina', this refers to the classic type of angina related to [[myocardial ischemia]]. A typical presentation 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 or after administration of [[Sublingual administration|sublingual]] [[nitroglycerin (medication)|nitroglycerin]].<ref name="Stable"/> Symptoms typically diminish several minutes after activity and recur when activity resumes. In this way, stable angina may be thought of as being similar to intermittent [[claudication]] symptoms. Other recognized precipitants of stable angina include cold weather, heavy meals, and [[anxiety|emotional stress]].

===Unstable angina===
{{main|Unstable angina}}
{{See also|Variant angina}}

[[Unstable angina]] (UA) (also "''crescendo angina''"; this is a form of [[acute coronary syndrome]]) is defined as angina pectoris that changes or worsens or begins suddenly at rest.<ref name="urlMerckMedicus : Dorlands Medical Dictionary">{{cite web |url=http://merckmedicus.com/pp/us/hcp/thcp_dorlands_content_split.jsp?pg=/ppdocs/us/common/dorlands/drlnd/one_04/000004949.htm#000004949 |title=MerckMedicus: Dorland's Medical Dictionary |access-date=2009-01-09}}</ref> Unstable angina is a medical emergency and requires urgent medical treatment from a doctor.<ref name=":0" />

It has at least one of these three features:<ref>{{Cite web |title=Unstable Angina |url=https://www.heart.org/en/health-topics/heart-attack/angina-chest-pain/unstable-angina |access-date=2023-10-23 |website=www.heart.org |language=en}}</ref>
# it occurs at rest (or with minimal exertion), usually lasting more than 10 minutes
# it is severe and of new-onset (i.e., within the prior 4–6 weeks)
# it occurs with a [[wikt:crescendo|crescendo]] pattern (i.e., distinctly more severe, prolonged, or frequent than before).

UA may occur often unpredictably and even at rest, which may be a serious indicator of an impending heart attack. The primary factor differentiating unstable angina from stable angina (other than symptoms) is the underlying [[pathophysiology]] of the [[atherosclerosis]]. The pathophysiology of unstable angina is the reduction of coronary blood flow due to transient [[platelet aggregation]] on apparently normal [[endothelium]], coronary artery spasms, or [[coronary thrombosis]].<ref>{{cite journal | vauthors = Hombach V, Höher M, Kochs M, Eggeling T, Schmidt A, Höpp HW, Hilger HH | title = Pathophysiology of unstable angina pectoris--correlations with coronary angioscopic imaging | journal = European Heart Journal | volume = 9 Suppl N | pages = 40–5 | date = December 1988 | pmid = 3246255 | doi = 10.1093/eurheartj/9.suppl_N.40 }}</ref><ref name="Simons2000">{{cite web| vauthors = Simons M |title=Pathophysiology of unstable angina |date=March 8, 2000 |url=http://cmbi.bjmu.edu.cn/uptodate/coronary%20heart%20disease/Pathophysiology/Pathophysiology%20of%20unstable%20angina.htm |access-date=April 28, 2010 |url-status = dead|archive-url=https://web.archive.org/web/20100330044046/http://cmbi.bjmu.edu.cn/uptodate/coronary%20heart%20disease/Pathophysiology/Pathophysiology%20of%20unstable%20angina.htm |archive-date=March 30, 2010 }}</ref>

The process starts with atherosclerosis, progresses through inflammation to yield an active unstable plaque, which undergoes thrombosis and results in acute myocardial ischemia, which, if not reversed, results in cell necrosis (infarction).<ref name="Simons2000" /> Studies show that 64% of all unstable anginas occur between 22:00 and 08:00 when patients are at rest.<ref name="Simons2000" /><ref name="nhlbi">{{cite web |publisher=National Heart Lung and Blood Institute |title=What Is Angina? |access-date=April 28, 2010 |url=http://www.nhlbi.nih.gov/health/dci/Diseases/Angina/Angina_SignsAndSymptoms.html}}</ref>

In stable angina, the developing [[atheroma]] (a fatty plaque) is protected with a [[fibrous cap]]. This cap may rupture in unstable angina, allowing [[blood clots]] to precipitate and further decrease the area of the coronary vessel's [[Lumen (anatomy)|lumen]]  or the interior open space within an artery. This explains why, in many cases, unstable angina develops independently of activity.<ref name="Simons2000" />

===Microvascular angina===

{{main|Microvascular angina}}

[[Microvascular angina]], also known as ''cardiac syndrome X'', is characterized by angina-like chest pain, in the context of normal epicardial coronary arteries (the largest vessels on the surface of the heart, prior to significant branching) on [[angiography]]. The original definition of cardiac syndrome X also mandated that ischemic changes on exercise (despite normal coronary arteries) were displayed, as shown on [[cardiac stress test]]s.<ref>{{cite book| veditors = Kaski JC |title=Chest pain with normal coronary angiograms: pathogenesis, diagnosis and management| date=1999| publisher=Kluwer| location=Boston| isbn=978-0-7923-8421-2| pages=5–6}}</ref> The primary cause of microvascular angina is unknown, but factors apparently involved are endothelial dysfunction and reduced flow (perhaps due to spasm) in the tiny "resistance" blood vessels of the heart.<ref>Guyton, Arthur. "Textbook of Medical Physiology" 11th edition. Philadelphia; Elsevier, 2006.{{page needed|date=February 2013}}</ref> Since microvascular angina is not characterized by major arterial blockages, it is harder to recognize and diagnose.<ref name="HeartHealthyWomen.org">{{cite web
 |title=Cardiac Syndrome X |date=14 August 2022 |publisher=HeartHealthyWomen.org |url=http://www.hearthealthywomen.org/cardiovascular-disease/cardiac-syndrome-x/cardiac-syndrome-x.html}}{{MEDRS|date=February 2013}}</ref><ref>{{cite web| url=http://www.americanheart.org/presenter.jhtml?identifier=4591 |title=Heart Attack and Angina Statistics. |access-date=2010-04-13 |url-status = dead|archive-url=https://web.archive.org/web/20100413012434/http://www.americanheart.org/presenter.jhtml?identifier=4591 |archive-date=2010-04-13 }} {{failed verification|date=March 2013}}.</ref><ref>
{{cite web |title=Angina |publisher=Texas Heart Institute |date=October 2012 |url=http://www.texasheartinstitute.org/hic/topics/cond/angina.cfm |access-date=2010-05-04 |archive-url=https://web.archive.org/web/20140817121322/http://www.texasheartinstitute.org/HIC/Topics/Cond/Angina.cfm |archive-date=2014-08-17 |url-status = dead}}
</ref>

Microvascular angina was previously considered a rather benign condition, but more recent data has changed this attitude. Studies, including the Women's Ischemia Syndrome Evaluation (WISE), suggest that microvascular angina is part of the pathophysiology of ischemic heart disease, perhaps explaining the higher rates of angina in females than in males, as well as their predilection towards [[ischemia]] and acute coronary syndromes in the absence of obstructive coronary artery disease.<ref>{{cite journal | vauthors = Gulati M, Shaw LJ, Bairey Merz CN | title = Myocardial ischemia in women: lessons from the NHLBI WISE study | journal = Clinical Cardiology | volume = 35 | issue = 3 | pages = 141–8 | date = March 2012 | pmid = 22389117 | pmc = 3297966 | doi = 10.1002/clc.21966 }}</ref>

==Signs and symptoms==
{{More citations needed section|date=June 2013}}

[[File:Angina pectoris.png|thumb|left| Diagram of discomfort caused by coronary artery disease. Pressure, fullness, squeezing or pain in the center of the chest. Discomfort can also be felt in the neck, jaw, shoulders, back or arms.]]

Angina pectoris can be quite painful, but many 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 area, jaw, or shoulders. This is explained by the concept of [[referred pain]] and is because the spinal level that receives visceral sensation from the heart simultaneously receives cutaneous sensation from parts of the skin specified by that spinal nerve's [[Dermatome (anatomy)|dermatome]], without an ability to discriminate the two. Typical locations for referred 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. In this case, the pulse rate and the blood pressure increases. Chest pain lasting only a few seconds is normally not angina (such as [[precordial catch syndrome]]).

Myocardial [[ischemia]] comes about when the myocardium (the heart muscle) receives insufficient blood and oxygen to function normally either because of increased oxygen demand by the myocardium or because of decreased supply to the myocardium. This inadequate [[perfusion]] of blood and the resulting reduced delivery of oxygen and nutrients are 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 [[tobacco smoking|cigarette smoking]], [[Diabetes mellitus|diabetes]], [[Hypercholesterolemia|high cholesterol]], [[hypertension|high blood pressure]], [[sedentary lifestyle]], and [[family history (medicine)|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 believed caused by [[vasospasm|spasms of the artery]]. It occurs more in younger women.<ref name="pmid11869851">{{cite journal | vauthors = Sun H, Mohri M, Shimokawa H, Usui M, Urakami L, Takeshita A | title = Coronary microvascular spasm causes myocardial ischemia in patients with vasospastic angina | journal = Journal of the American College of Cardiology | volume = 39 | issue = 5 | pages = 847–51 | date = March 2002 | pmid = 11869851 | doi = 10.1016/S0735-1097(02)01690-X | doi-access = free }}</ref>

Coital angina, also known as ''angina d'amour'', is angina subsequent to [[sexual intercourse]].<ref name=AHA>{{cite journal | vauthors = Levine GN, Steinke EE, Bakaeen FG, Bozkurt B, Cheitlin MD, Conti JB, Foster E, Jaarsma T, Kloner RA, Lange RA, Lindau ST, Maron BJ, Moser DK, Ohman EM, Seftel AD, Stewart WJ | title = Sexual activity and cardiovascular disease: a scientific statement from the American Heart Association | journal = Circulation | volume = 125 | issue = 8 | pages = 1058–72 | date = February 2012 | pmid = 22267844 | doi = 10.1161/CIR.0b013e3182447787 | doi-access = free }}</ref>  It is generally rare, except in patients with severe [[coronary artery disease]].<ref name=AHA/>

==Cause==
===Major risk factors===
{{columns-list|colwidth=30em|
{{citation needed|reason=previous source was not relevant|date=March 2016}}
* Age (≥ 45 years for men, ≥ 55 for women)
* [[Smoking]]
* [[Diabetes mellitus]]
* [[Dyslipidemia]]
* Family history of premature [[cardiovascular disease]] (males <55 years, females <65 years old)
* [[Hypertension]]
* [[Kidney disease]] ([[microalbuminuria]] or [[Glomerular filtration rate|GFR]]<60 mL/min)
* [[Obesity]] ([[Body mass index|BMI]] ≥ 30&nbsp;kg/m2)
* [[Physical inactivity]]
* Prolonged [[psychosocial]] [[stress (psychological)|stress]]<ref name="pmid8615707">{{cite journal | vauthors = Linden W, Stossel C, Maurice J | title = Psychosocial interventions for patients with coronary artery disease: a meta-analysis | journal = Archives of Internal Medicine | volume = 156 | issue = 7 | pages = 745–52 | date = April 1996 | pmid = 8615707 | doi = 10.1001/archinte.1996.00440070065008 }}</ref>
}}
Routine counseling of adults by physicians to advise them to improve their diet and increase their physical activity has, in general, been found to induce only small changes in actual behavior. Therefore, as of 2012, [[The U.S. Preventive Services Task Force]] does not recommend routine lifestyle counseling of all patients without known cardiovascular disease, hypertension, hyperlipidemia, or diabetes, and instead recommends selectively counseling only those patients who seem most ready to make lifestyle changes and using available time with other patients to explore other types of intervention that would be more likely to have a preventative impact.<ref>{{cite journal | vauthors = Moyer VA | title = Behavioral counseling interventions to promote a healthful diet and physical activity for cardiovascular disease prevention in adults: U.S. Preventive Services Task Force recommendation statement | journal = Annals of Internal Medicine | volume = 157 | issue = 5 | pages = 367–71 | date = September 2012 | pmid = 22733153 | doi = 10.7326/0003-4819-157-5-201209040-00486 | doi-access = free }}</ref>

; Conditions that exacerbate or provoke angina<ref>{{cite book | vauthors = Wells B, DiPiro J, Schwinghammer T, DiPiro C |year=2008 |title=Pharmacotherapy Handbook |url=https://archive.org/details/pharmacotherapyh00well_572 |url-access=limited |edition=7th |location=New York |publisher=McGraw-Hill |page=[https://archive.org/details/pharmacotherapyh00well_572/page/n152 140] |isbn=978-0-07-148501-2}}</ref>
{{columns-list|colwidth=30em|
* [[Medications]]
** [[Vasodilation|Vasodilators]]
** Excessive [[thyroid hormone replacement]]
* [[Vasoconstrictor]]s
* [[Polycythemia]], which thickens the blood, slowing its flow through the heart muscle
* [[Hypothermia]]
* [[Hypervolemia]]
* [[Hypovolemia]]
}}
One study found that [[Tobacco smoking|smokers]] with coronary artery disease had a significantly increased level of [[sympathetic nervous system|sympathetic nerve]] activity when compared to those without. This is in addition to increases in blood pressure, heart rate, and peripheral vascular resistance associated with nicotine, which may lead to recurrent angina attacks. In addition, the [[Centers for Disease Control and Prevention]] (CDC) reports that the risk of CHD (Coronary heart disease), stroke, and [[Peripheral vascular disease|PVD (Peripheral vascular disease)]] is reduced within 1–2 years of smoking cessation. In another study, it was found that, after one year, the prevalence of angina in smokingmales under 60 after an initial attack was 40% less in those having quit smoking compared to those that continued.  Studies have found that there are short-term and long-term benefits to smoking cessation.<ref>{{cite web |publisher= U.S. Centers for Disease Control and Prevention |title=Health Benefits of Cessation |url=https://www.cdc.gov/tobacco/data_statistics/fact_sheets/cessation/quitting/index.htm |date=January 3, 2013}}</ref><ref>{{cite journal | vauthors = Daly LE, Graham IM, Hickey N, Mulcahy R | title = Does stopping smoking delay onset of angina after infarction? | journal = British Medical Journal | volume = 291 | issue = 6500 | pages = 935–7 | date = October 1985 | pmid = 3929970 | pmc = 1417185 | doi = 10.1136/bmj.291.6500.935 }}</ref><ref>{{cite journal | vauthors = Daly LE, Mulcahy R, Graham IM, Hickey N | title = Long term effect on mortality of stopping smoking after unstable angina and myocardial infarction | journal = British Medical Journal | volume = 287 | issue = 6388 | pages = 324–6 | date = July 1983 | pmid = 6409291 | pmc = 1548591 | doi = 10.1136/bmj.287.6388.324 }}</ref><ref>{{cite journal | vauthors = Shinozaki N, Yuasa T, Takata S | title = Cigarette smoking augments sympathetic nerve activity in patients with coronary heart disease | journal = International Heart Journal | volume = 49 | issue = 3 | pages = 261–72 | date = May 2008 | pmid = 18612184 | doi = 10.1536/ihj.49.261 | doi-access = free }}</ref>

===Other medical problems===
* [[Esophageal motility disorder|Esophageal disorders]]
* [[Gastroesophageal Reflux Disease|Gastroesophageal reflux disease]] (GERD)
* [[Hyperthyroidism]]
* [[Hypoxemia]]
* Profound [[anemia]]
* Uncontrolled [[hypertension]]

===Other cardiac problems===
* [[Bradyarrhythmia]]
* [[Hypertrophic cardiomyopathy]]
* [[Tachyarrhythmia]]
* [[Valvular heart disease]]<ref>{{cite journal | vauthors = Gibbons RJ, Abrams J, Chatterjee K, Daley J, Deedwania PC, Douglas JS, Ferguson TB, Fihn SD, Fraker TD, Gardin JM, O'Rourke RA, Pasternak RC, Williams SV | title = ACC/AHA 2002 guideline update for the management of patients with chronic stable angina--summary article: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines (Committee on the Management of Patients With Chronic Stable Angina) | journal = Journal of the American College of Cardiology | volume = 41 | issue = 1 | pages = 159–68 | date = January 2003 | pmid = 12570960 | doi = 10.1016/S0735-1097(02)02848-6 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Fraker TD, Fihn SD, Gibbons RJ, Abrams J, Chatterjee K, Daley J, Deedwania PC, Douglas JS, Ferguson TB, Gardin JM, O'Rourke RA, Pasternak RC, Williams SV, Smith SC, Jacobs AK, Adams CD, Anderson JL, Buller CE, Creager MA, Ettinger SM, Halperin JL, Hunt SA, Krumholz HM, Kushner FG, Lytle BW, Nishimura R, Page RL, Riegel B, Tarkington LG, Yancy CW | title = 2007 chronic angina focused update of the ACC/AHA 2002 guidelines for the management of patients with chronic stable angina: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Writing Group to develop the focused update of the 2002 guidelines for the management of patients with chronic stable angina | journal = Journal of the American College of Cardiology | volume = 50 | issue = 23 | pages = 2264–74 | date = December 2007 | pmid = 18061078 | doi = 10.1016/j.jacc.2007.08.002 | author3 = 2002 Chronic Stable Angina Writing Committee | first22 = SM | first21 = MA | first20 = CE | first27 = BW | first26 = FG | first25 = HM | first29 = RL | first28 = R | first19 = JL | first30 = B | first18 = CD | first24 = SA | first16 = SC | first17 = AK | first14 = RA | first15 = SV | doi-access = free }}</ref>

[[Myocardial ischemia]] can result from:
# a reduction of blood flow to the heart that can be caused by [[stenosis]], [[spasm]], or acute [[Vascular occlusion|occlusion]] (by an [[Embolism|embolus]]) of the heart's arteries.
# resistance of the blood vessels. This can be caused by narrowing of the blood vessels; a decrease in radius.<ref>{{cite book |vauthors=Kusumoto FM |chapter=Chapter 10: Cardiovascular Disorders: Heart Disease |veditors=McPhee SJ, Hammer GD |title=Pathophysiology of Disease: An Introduction to Clinical Medicine |edition=6th |chapter-url=http://www.accesspharmacy.com/content.aspx?aID=5367630 |isbn=978-0-07-162167-0 |page=276 |date=2009-10-20 |publisher=McGraw-Hill Education |access-date=2010-04-28 |archive-date=2011-07-27 |archive-url=https://web.archive.org/web/20110727134638/http://www.accesspharmacy.com/content.aspx?aID=5367630 |url-status=dead }}</ref> Blood flow is proportional to the radius of the artery to the fourth power.<ref>{{cite book | vauthors = Michel T |chapter=Treatment of Myocardial Ischemia | veditors = Brunton LL, Lazo JS, Parker KL |title=Goodman & Gilman's The Pharmacological Basis of Therapeutic |edition=11th |page=823 |isbn=978-0-07-142280-2|date=2005-09-13 |publisher=McGraw-Hill Companies,Incorporated }}</ref>
# reduced oxygen-carrying capacity of the blood, due to several factors such as a decrease in oxygen tension and hemoglobin concentration.<ref name="podrid2012">{{cite web | vauthors = Podrid PJ |title=Pathophysiology and clinical presentation of ischemic chest pain |work=[[UpToDate]] |date=November 28, 2012 |publisher=[[Wolters Kluwer]] |url=http://www.uptodate.com/contents/pathophysiology-and-clinical-presentation-of-ischemic-chest-pain }}{{registration required}}</ref> This decreases the ability of hemoglobin to carry oxygen to myocardial tissue.<ref>{{cite web | vauthors = Traverso M | date = 8 August 2004 | url = http://www.chemistry.wustl.edu/~courses/genchem/Tutorials/Ferritin/IronBody.htm | archive-url = https://web.archive.org/web/20100607124022/http://www.chemistry.wustl.edu/~courses/genchem/Tutorials/Ferritin/IronBody.htm | archive-date = 7 June 2010 | title = The Crucial Role of Iron in the Body | work = Washington University in St Louis }}</ref>

[[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 [[Cardiac syndrome X|syndrome X]].

Myocardial ischemia also can be the result of factors affecting blood composition, such as the reduced oxygen-carrying capacity of [[blood]], as seen with severe [[anemia]] (low number of red blood cells), or long-term [[tobacco smoking|smoking]].

==Pathophysiology==
Angina results when there is an imbalance between the heart's oxygen demand and supply. This imbalance can result from an increase in demand (e.g., during exercise) without a proportional increase in supply (e.g., due to obstruction or atherosclerosis of the coronary arteries).

However, the pathophysiology of angina in females varies significantly as compared to males.<ref name="pmid20160161">{{cite journal | vauthors = Vaccarino V | title = Ischemic heart disease in : many questions, few facts | journal = Circulation: Cardiovascular Quality and Outcomes | volume = 3 | issue = 2 | pages = 111–5 | date = March 2010 | pmid = 20160161 | pmc = 3012351 | doi = 10.1161/CIRCOUTCOMES.109.925313 }}</ref> Non-obstructive coronary disease is more common in females.<ref name="pmid16923752">{{cite journal | vauthors = Shaw LJ, Merz CN, Pepine CJ, Reis SE, Bittner V, Kip KE, Kelsey SF, Olson M, Johnson BD, Mankad S, Sharaf BL, Rogers WJ, Pohost GM, Sopko G | title = The economic burden of angina in women with suspected ischemic heart disease: results from the National Institutes of Health--National Heart, Lung, and Blood Institute--sponsored Women's Ischemia Syndrome Evaluation | journal = Circulation | volume = 114 | issue = 9 | pages = 894–904 | date = August 2006 | pmid = 16923752 | doi = 10.1161/CIRCULATIONAHA.105.609990 | doi-access = free | others = Women's Ischemia Syndrome Evaluation (WISE), Investigators }}</ref><ref name="pmid21286281">{{cite journal | vauthors = Banks K, Lo M, Khera A | title = Angina in Women without Obstructive Coronary Artery Disease | journal = Current Cardiology Reviews | volume = 6 | issue = 1 | pages = 71–81 | date = February 2010 | pmid = 21286281 | pmc = 2845797 | doi = 10.2174/157340310790231608 }}</ref>

==Diagnosis==
Angina should be suspected in people presenting tight, dull, or heavy chest discomfort that is:<ref name="cks.nhs.uk">NHS Clinical Knowledge Summaries (2009) Angina - stable. {{cite web|url=http://www.cks.nhs.uk/angina |title=Clinical topic - Angina |access-date=2010-01-04 |url-status = dead|archive-url=https://web.archive.org/web/20100310180036/http://www.cks.nhs.uk/angina |archive-date=2010-03-10 }} Date site accessed: 04/01/2009</ref>
# Retrosternal or left-sided, radiating to the left arm, neck, jaw, or back.
# Associated with exertion or emotional stress and relieved within several minutes by rest.
# Precipitated by cold weather or a meal.

Some people present with atypical symptoms, including breathlessness, nausea, or epigastric discomfort, or burning. These atypical symptoms are particularly likely in older people, women, and those with diabetes.<ref name="cks.nhs.uk"/>

Anginal pain is not usually sharp or stabbing or influenced by respiration. [[Antacid]]s and simple [[analgesic]]s do not usually relieve the pain. If chest discomfort (of whatever site) is precipitated by exertion, relieved by rest, and relieved by glyceryl trinitrate, the likelihood of angina is increased.<ref name="cks.nhs.uk"/>

In angina patients momentarily not feeling any chest pain, an [[Electrocardiography|electrocardiogram]] (ECG) is typically normal unless there have been other cardiac problems in the past. During periods of pain, depression, or elevation of the [[Electrocardiography#ST segment|ST segment]] may be observed. To elicit these changes, an [[Cardiac stress test|exercise ECG test]] ("treadmill test") may be performed, during which the patient exercises to his/her maximum ability before fatigue, breathlessness, or pain intervenes; if characteristic ECG changes are documented (typically more than 1&nbsp;mm of flat or downsloping ST depression), the test is considered diagnostic for angina. Even constant monitoring of the blood pressure and the pulse rate can lead to some conclusions regarding angina. The exercise test is also useful in looking for other markers of myocardial ischemia: blood pressure response (or lack thereof, in particular, a drop in systolic blood pressure), dysrhythmia, and chronotropic response. Other alternatives to a standard exercise test include a [[Cardiac stress test|thallium scintigram or sestamibi scintigram]] (in patients unable to exercise enough for 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 catheterization|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 surgery|coronary artery bypass graft]] (CABG), treatment only with medication, or other treatments. In hospitalized patients 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.

==Treatment==
{{Further|Antianginal}}

Angina pectoris occurs as a result of coronary blood flow insufficiency in the face of increased oxygen demand. The principal goal in the prevention and relief of angina is to limit the oxygen requirement of the heart so it can meet the inadequate oxygen supply derived through the blood supplied from the stenosed or constricted arteries. The main goals of treatment in angina pectoris are relief of symptoms, slowing progression of the disease, and reduction of future events, especially [[myocardial infarction|heart attacks]] and death. Beta blockers (e.g., [[carvedilol]], [[metoprolol]], [[propranolol]]) have a large body of evidence in morbidity and mortality benefits (fewer symptoms, less disability, and longer life) and short-acting [[nitroglycerin (medication)|nitroglycerin]] medications have been used since 1879 for symptomatic relief of angina.<ref>{{cite book|title=Drug discovery: a history|vauthors=Sneader W|year=2005|publisher=Wiley |isbn=978-0-471-89980-8}}{{page needed|date=February 2013}}</ref> There are differing course of treatments for the patient depending on the type of angina the patient has. However, this second can provide a brief overview of the types of medications provided for angina and the purpose by which they are prescribed.

[[Beta blocker]]s, specifically B1 adrenergic blockers without intrinsic sympathomimetic activity, are preferred for angina treatment, out of B1 selective and non-selective as well as B1 ISA agents. B1 blockers are cardioselective blocking agents (such as nevibolol, atenolol, metoprolol, bisoprolol, etc.) which result in blocking cAMP in the heart muscle cells. cAMP, which plays a vital role in phosphorylating the ryanodine receptor and LTCC, will usually increase Ca<sup>+2</sup> levels in the heart muscle cells, blocking contraction. Therefore, B1 blockade decreases the HR and contraction of the heart muscle, making it demand less oxygen. An important thing to note is that the B1 cardioselective blockers are cardioselective and not cardio-specific. This means that if the beta-adrenergic antagonist is prescribed in higher doses, it can lose the selectivity aspect and begin causing hypertension from B2 adrenergic stimulation of smooth muscle cells. This is why in therapy for patients with angina, the vasodilatory organonitrates complement the use of B-blockers when prescribed the use of angina. The preference for Beta-1 cardioselective blockers is for B1 cardioselective blockers without intrinsic sympathetic activity. Beta blockers with intrinsic sympathetic activity will still do the beta blockade of the heart muscle cells and have a decreased ionotrophic and chronotropic effect, but this effect will be to a lesser extent than if the beta blocker did not have the intrinsic sympathetic activity. A common beta-blocker with ISA prescribed for the treatment of angina is Acebutolol.

Non-selective beta-adrenergic antagonists will yield the same action on B1 receptors, however will also act on B2 receptors. These medications, such as Propranolol and Nadolol, act on B1 receptors on smooth muscle cells as well. B1 blockade occurs in the smooth muscle cells. Specifically cAMP is responsible for inhibiting Myosin Light Kinase, the enzyme responsible for acting on Actin-Myosin. The inhibition of B1 will result in decreased levels of cAMP which will lead to increased levels of  Myosin Light Chain Kinase in the smooth muscle cells, the enzyme responsible for acting on Actin-Myosin and leading to contraction of the smooth muscle cell. This increased contraction of the smooth muscle cell from B1 blockade is not desirable since it explains the hypertension that may arise with patients taking that medication.

[[Calcium channel blocker]]s act to decrease the heart's [[workload]], and thus its requirement for oxygen by blocking the calcium channels of the heart muscle cell. With decreased intracellular calcium, the calcium-troponin complex does not form in the heart muscle cell and it does not contract, therefore reducing the need for oxygen.

The other class of medication that can be used to treat angina are the organic nitrates. Organic nitrates are used extensively to treat angina. They improve coronary blood flow of the coronary arteries (arteries which supply blood to the heart muscle) by reversing and preventing vasospasm, which increases the blood flow to the heart, improving perfusion and oxygen delivery to the heart associated with the pain of angina. These drugs also reduce systemic vascular resistance, of both veins and arteries but the veins to a greater extent. The decrease in the resistance of the arteries and veins decreases the myocardial oxygen demand, which also reduces myocardial oxygen demand.  [[nitroglycerin (medication)|Nitroglycerin]] is a potent [[vasodilator]] that decreases myocardial oxygen demand by decreasing the heart's workload. Nitroglycerin should not be given if certain inhibitors such as [[sildenafil]], [[tadalafil]], or [[vardenafil]] have been taken within the previous 12 hours as the combination of the two could cause [[vasodilatory shock|a serious drop in blood pressure.]]

Treatments for angina are [[Angioplasty|balloon angioplasty]], in which the balloon is inserted at the end of a [[catheter]] and inflated to widen the arterial [[lumen (anatomy)|lumen]]. [[Stent]]s to maintain the arterial widening are often used at the same time. [[Coronary bypass surgery]] involves bypassing constricted arteries with venous grafts. This is much more invasive than [[angioplasty]].

Calcium channel blockers (such as [[nifedipine]] (Adalat) and [[amlodipine]]), [[isosorbide mononitrate]] and [[nicorandil]] are vasodilators commonly used in chronic stable angina.{{Citation needed| date=June 2009}} A new therapeutic class, called If inhibitor, has recently been made available: [[Ivabradine]] provides heart rate reduction without affecting contractility<ref name="pmid16451297">{{cite journal | vauthors = Sulfi S, Timmis AD | title = Ivabradine -- the first selective sinus node I(f) channel inhibitor in the treatment of stable angina | journal = International Journal of Clinical Practice | volume = 60 | issue = 2 | pages = 222–8 | date = February 2006 | pmid = 16451297 | pmc = 1448693 | doi = 10.1111/j.1742-1241.2006.00817.x }}</ref> leading to major anti-ischemic and antianginal efficacy. [[ACE inhibitor]]s are also vasodilators with both symptomatic and prognostic benefit. [[Statin]]s are the most frequently used lipid/cholesterol modifiers, which probably also stabilize existing atheromatous plaque.<ref name="doi:10.1001/jama.295.13.jpc60002">{{cite journal | vauthors = Nissen SE, Nicholls SJ, Sipahi I, Libby P, Raichlen JS, Ballantyne CM, Davignon J, Erbel R, Fruchart JC, Tardif JC, Schoenhagen P, Crowe T, Cain V, Wolski K, Goormastic M, Tuzcu EM | title = Effect of very high-intensity statin therapy on regression of coronary atherosclerosis: the ASTEROID trial | journal = JAMA | volume = 295 | issue = 13 | pages = 1556–65 | date = April 2006 | pmid = 16533939 | doi = 10.1001/jama.295.13.jpc60002 | doi-access = free }}</ref> Low-dose [[aspirin]] decreases the risk of heart attack in patients with chronic stable angina, and was part of standard treatment. However, in patients without established cardiovascular disease, the increase in [[hemorrhagic stroke]] and gastrointestinal bleeding offsets any benefits and it is no longer advised unless the risk of myocardial infarction is very high.<ref name="pmid20410163">{{cite journal | vauthors = Barnett H, Burrill P, Iheanacho I | title = Don't use aspirin for primary prevention of cardiovascular disease | journal = BMJ | volume = 340 | pages = c1805 | date = April 2010 | pmid = 20410163 | doi = 10.1136/bmj.c1805 | s2cid = 3137720 }}</ref>

Exercise is also a very good long-term treatment for the angina (but only particular regimens – gentle and sustained exercise rather than intense short bursts),<ref name="pmid8339420">{{cite journal | vauthors = Ades PA, Waldmann ML, Poehlman ET, Gray P, Horton ED, Horton ES, LeWinter MM | title = Exercise conditioning in older coronary patients. Submaximal lactate response and endurance capacity | journal = Circulation | volume = 88 | issue = 2 | pages = 572–7 | date = August 1993 | pmid = 8339420 | doi = 10.1161/01.CIR.88.2.572 | doi-access = free }}</ref> probably working by complex mechanisms such as improving blood pressure and promoting coronary artery collateralisation.

Though sometimes used by patients, evidence does not support the use of [[Traditional Chinese medicine|traditional Chinese herbal products]] (THCP) for angina.<ref>{{cite journal | vauthors = Zhuo Q, Yuan Z, Chen H, Wu T | title = Traditional Chinese herbal products for stable angina | journal = The Cochrane Database of Systematic Reviews | issue = 5 | pages = CD004468 | date = May 2010 | volume = 2010 | pmid = 20464731 | pmc = 6718232 | doi = 10.1002/14651858.cd004468.pub2 }}</ref>

Identifying and treating risk factors for further coronary heart disease is a priority in patients with angina. This means testing for [[hypercholesterolemia|elevated cholesterol]] and other fats in the blood, [[diabetes mellitus|diabetes]] and [[hypertension]] (high blood pressure), and encouraging [[smoking cessation]] and [[weight loss|weight optimization]].

The calcium channel blocker [[nifedipine]] prolongs cardiovascular event- and procedure-free survival in patients with coronary artery disease. New overt heart failures were reduced by 29% compared to placebo; however, the mortality rate difference between the two groups was statistically insignificant.<ref name="pmid15351192">{{cite journal | vauthors = Poole-Wilson PA, Lubsen J, Kirwan BA, van Dalen FJ, Wagener G, Danchin N, Just H, Fox KA, Pocock SJ, Clayton TC, Motro M, Parker JD, Bourassa MG, Dart AM, Hildebrandt P, Hjalmarson A, Kragten JA, Molhoek GP, Otterstad JE, Seabra-Gomes R, Soler-Soler J, Weber S | title = Effect of long-acting nifedipine on mortality and cardiovascular morbidity in patients with stable angina requiring treatment (ACTION trial): randomised controlled trial | journal = Lancet | volume = 364 | issue = 9437 | pages = 849–57 | year = 2004 | pmid = 15351192 | doi = 10.1016/S0140-6736(04)16980-8 | collaboration = Coronary disease Trial Investigating Outcome with Nifedipine gastrointestinal therapeutic system investigators | s2cid = 12795811 }}</ref>

===Microvascular angina in women===
Women with myocardial ischemia often have either no or atypical symptoms, such as palpitations, anxiety, weakness, and fatigue. Additionally, many females with angina are found to have cardiac ischemia, yet no evidence of obstructive coronary artery disease on cardiac catheterization. Evidence is accumulating that nearly half of females with myocardial ischemia have coronary microvascular disease, a condition often called microvascular angina (MVA). Small intramyocardial arterioles constrict in MVA causing ischemic pain that is less predictable than with typical epicardial coronary artery disease (CAD).

The pathophysiology is complex and still being elucidated, but there is strong evidence that endothelial dysfunction, decreased endogenous vasodilators, inflammation, changes in adipokines, and platelet activation are contributing factors. The diagnosis of MVA may require catheterization during which there is an assessment of the microcirculatory response to adenosine or acetylcholine and measurement of coronary and fractional flow reserve. New techniques include positron emission tomography (PET) scanning, cardiac magnetic resonance imaging (MRI), and transthoracic Doppler echocardiography.

Managing MVA can be challenging, for example, females with this condition have less coronary microvascular dilation in response to nitrates than do those without MVA. Females with MVA often have traditional risk factors for CAD such as obesity, dyslipidemia, diabetes, and hypertension. Aggressive interventions to reduce modifiable risk factors are an important component of management, especially smoking cessation, exercise, and diabetes management. The combination of non-nitrate vasodilators, such as calcium channel blockers and angiotensin-converting enzyme (ACE) inhibitors along with HMG-CoA reductase inhibitors (statins), also is effective in many women, and new drugs, such as Ranolazine and Ivabradine, have shown promise in the treatment of MVA. Other approaches include spinal cord stimulators, adenosine receptor blockade, and psychiatric intervention.<ref name="pmid27236120">{{cite journal | vauthors = Celik T, Ozturk C, Balta S, Demirkol S, Iyisoy A | title = Coronary microvascular dysfunction in patients with cardiac syndrome X: Ongoing debate | journal = International Journal of Cardiology | volume = 218 | issue = | pages = 233–234 | date = September 2016 | pmid = 27236120 | doi = 10.1016/j.ijcard.2016.05.050 }}</ref><ref name="pmid25555283">{{cite journal | vauthors = Cattaneo M, Porretta AP, Gallino A | title = Ranolazine: Drug overview and possible role in primary microvascular angina management | journal = International Journal of Cardiology | volume = 181 | issue = | pages = 376–81 | date = February 2015 | pmid = 25555283 | doi = 10.1016/j.ijcard.2014.12.055 }}</ref><ref name="pmid27245239">{{cite journal | vauthors = Lanza GA, Careri G, Stazi A, Villano A, De Vita A, Aurigemma C, Crea F | title = Clinical Spectrum and Outcome of Patients With Non-ST-Segment Elevation Acute Coronary Syndrome and No Obstructive Coronary Atherosclerosis | journal = Circulation Journal | volume = 80 | issue = 7 | pages = 1600–6 | date = June 2016 | pmid = 27245239 | doi = 10.1253/circj.CJ-16-0145 | doi-access = free }}</ref><ref name="pmid25677893">{{cite journal | vauthors = Marinescu MA, Löffler AI, Ouellette M, Smith L, Kramer CM, Bourque JM | title = Coronary microvascular dysfunction, microvascular angina, and treatment strategies | journal = JACC. Cardiovascular Imaging | volume = 8 | issue = 2 | pages = 210–20 | date = February 2015 | pmid = 25677893 | pmc = 4384521 | doi = 10.1016/j.jcmg.2014.12.008  }}</ref><ref name="pmid27092288">{{cite journal | vauthors = Selthofer-Relatić K, Bošnjak I, Kibel A | title = Obesity Related Coronary Microvascular Dysfunction: From Basic to Clinical Practice | journal = Cardiology Research and Practice | volume = 2016 | issue = | pages = 8173816 | date = 2016 | pmid = 27092288 | pmc = 4820617 | doi = 10.1155/2016/8173816 | doi-access = free }}</ref><ref name="pmid25760881">{{cite journal | vauthors = Titterington JS, Hung OY, Wenger NK | title = Microvascular angina: an update on diagnosis and treatment | journal = Future Cardiology | volume = 11 | issue = 2 | pages = 229–42 | date = March 2015 | pmid = 25760881 | doi = 10.2217/fca.14.79 }}</ref>

===Suspected angina===
Hospital admission for people with the following symptoms is recommended, as they may have unstable angina: pain at rest (which may occur at night), pain on minimal exertion, angina that seems to progress rapidly despite increasing medical treatment. All people with suspected angina should be urgently referred to a chest pain evaluation service, for confirmation of the diagnosis and assessment of the severity of coronary heart disease.<ref>{{cite web | work = NHS Clinical Knowledge Summaries | date = 2009 | url = http://www.cks.nhs.uk/angina/management/quick_answers/scenario_suspected_angina | title = Suspected angina | archive-url = https://web.archive.org/web/20101214040716/http://www.cks.nhs.uk/angina/management/quick_answers/scenario_suspected_angina | archive-date=December 14, 2010 | publisher = U.K. National Institute for Health and Clinical Excellence }}</ref>

==Epidemiology==
As of 2010, angina due to [[ischemic heart disease]] affects approximately 112&nbsp;million people (1.6% of the global population) being slightly more common in males than females (1.7% to 1.5%).<ref name=LancetEpi2012>{{cite journal | vauthors = Vos T, Flaxman AD, Naghavi M, Lozano R, Michaud C, Ezzati M, Shibuya K, Salomon JA, Abdalla S, Aboyans V, Abraham J, Ackerman I, Aggarwal R, Ahn SY, Ali MK, Alvarado M, Anderson HR, Anderson LM, Andrews KG, Atkinson C, Baddour LM, Bahalim AN, Barker-Collo S, Barrero LH, Bartels DH, Basáñez MG, Baxter A, Bell ML, Benjamin EJ, Bennett D, Bernabé E, Bhalla K, Bhandari B, Bikbov B, Bin Abdulhak A, Birbeck G, Black JA, Blencowe H, Blore JD, Blyth F, Bolliger I, Bonaventure A, Boufous S, Bourne R, Boussinesq M, Braithwaite T, Brayne C, Bridgett L, Brooker S, Brooks P, Brugha TS, Bryan-Hancock C, Bucello C, Buchbinder R, Buckle G, Budke CM, Burch M, Burney P, Burstein R, Calabria B, Campbell B, Canter CE, Carabin H, Carapetis J, Carmona L, Cella C, Charlson F, Chen H, Cheng AT, Chou D, Chugh SS, Coffeng LE, Colan SD, Colquhoun S, Colson KE, Condon J, Connor MD, Cooper LT, Corriere M, Cortinovis M, de Vaccaro KC, Couser W, Cowie BC, Criqui MH, Cross M, Dabhadkar KC, Dahiya M, Dahodwala N, Damsere-Derry J, Danaei G, Davis A, De Leo D, Degenhardt L, Dellavalle R, Delossantos A, Denenberg J, Derrett S, Des Jarlais DC, Dharmaratne SD, Dherani M, Diaz-Torne C, Dolk H, Dorsey ER, Driscoll T, Duber H, Ebel B, Edmond K, Elbaz A, Ali SE, Erskine H, Erwin PJ, Espindola P, Ewoigbokhan SE, Farzadfar F, Feigin V, Felson DT, Ferrari A, Ferri CP, Fèvre EM, Finucane MM, Flaxman S, Flood L, Foreman K, Forouzanfar MH, Fowkes FG, Franklin R, Fransen M, Freeman MK, Gabbe BJ, Gabriel SE, Gakidou E, Ganatra HA, Garcia B, Gaspari F, Gillum RF, Gmel G, Gosselin R, Grainger R, Groeger J, Guillemin F, Gunnell D, Gupta R, Haagsma J, Hagan H, Halasa YA, Hall W, Haring D, Haro JM, Harrison JE, Havmoeller R, Hay RJ, Higashi H, Hill C, Hoen B, Hoffman H, Hotez PJ, Hoy D, Huang JJ, Ibeanusi SE, Jacobsen KH, James SL, Jarvis D, Jasrasaria R, Jayaraman S, Johns N, Jonas JB, Karthikeyan G, Kassebaum N, Kawakami N, Keren A, Khoo JP, King CH, Knowlton LM, Kobusingye O, Koranteng A, Krishnamurthi R, Lalloo R, Laslett LL, Lathlean T, Leasher JL, Lee YY, Leigh J, Lim SS, Limb E, Lin JK, Lipnick M, Lipshultz SE, Liu W, Loane M, Ohno SL, Lyons R, Ma J, Mabweijano J, MacIntyre MF, Malekzadeh R, Mallinger L, Manivannan S, Marcenes W, March L, Margolis DJ, Marks GB, Marks R, Matsumori A, Matzopoulos R, Mayosi BM, McAnulty JH, McDermott MM, McGill N, McGrath J, Medina-Mora ME, Meltzer M, Mensah GA, Merriman TR, Meyer AC, Miglioli V, Miller M, Miller TR, Mitchell PB, Mocumbi AO, Moffitt TE, Mokdad AA, Monasta L, Montico M, Moradi-Lakeh M, Moran A, Morawska L, Mori R, Murdoch ME, Mwaniki MK, Naidoo K, Nair MN, Naldi L, Narayan KM, Nelson PK, Nelson RG, Nevitt MC, Newton CR, Nolte S, Norman P, Norman R, O'Donnell M, O'Hanlon S, Olives C, Omer SB, Ortblad K, Osborne R, Ozgediz D, Page A, Pahari B, Pandian JD, Rivero AP, Patten SB, Pearce N, Padilla RP, Perez-Ruiz F, Perico N, Pesudovs K, Phillips D, Phillips MR, Pierce K, Pion S, Polanczyk GV, Polinder S, Pope CA, Popova S, Porrini E, Pourmalek F, Prince M, Pullan RL, Ramaiah KD, Ranganathan D, Razavi H, Regan M, Rehm JT, Rein DB, Remuzzi G, Richardson K, Rivara FP, Roberts T, Robinson C, De Leòn FR, Ronfani L, Room R, Rosenfeld LC, Rushton L, Sacco RL, Saha S, Sampson U, Sanchez-Riera L, Sanman E, Schwebel DC, Scott JG, Segui-Gomez M, Shahraz S, Shepard DS, Shin H, Shivakoti R, Singh D, Singh GM, Singh JA, Singleton J, Sleet DA, Sliwa K, Smith E, Smith JL, Stapelberg NJ, Steer A, Steiner T, Stolk WA, Stovner LJ, Sudfeld C, Syed S, Tamburlini G, Tavakkoli M, Taylor HR, Taylor JA, Taylor WJ, Thomas B, Thomson WM, Thurston GD, Tleyjeh IM, Tonelli M, Towbin JA, Truelsen T, Tsilimbaris MK, Ubeda C, Undurraga EA, van der Werf MJ, van Os J, Vavilala MS, Venketasubramanian N, Wang M, Wang W, Watt K, Weatherall DJ, Weinstock MA, Weintraub R, Weisskopf MG, Weissman MM, White RA, Whiteford H, Wiersma ST, Wilkinson JD, Williams HC, Williams SR, Witt E, Wolfe F, Woolf AD, Wulf S, Yeh PH, Zaidi AK, Zheng ZJ, Zonies D, Lopez AD, Murray CJ, AlMazroa MA, Memish ZA | title = Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010 | journal = Lancet | volume = 380 | issue = 9859 | pages = 2163–96 | date = December 2012 | pmid = 23245607 | pmc = 6350784 | doi = 10.1016/S0140-6736(12)61729-2 }}</ref>

In the United States, 10.2 million are estimated to experience angina with approximately 500,000 new cases occurring each year.<ref name="Stable">{{cite journal | vauthors = Tobin KJ | title = Stable angina pectoris: what does the current clinical evidence tell us? | journal = The Journal of the American Osteopathic Association | volume = 110 | issue = 7 | pages = 364–70 | date = July 2010 | pmid = 20693568 | url = http://www.jaoa.org/cgi/pmidlookup?view=long&pmid=20693568 | access-date = 2013-02-07 | archive-date = 2020-03-11 | archive-url = https://web.archive.org/web/20200311114444/https://jaoa.org/?view=long&pmid=20693568 | url-status = dead }}</ref><ref name="pmid18086926">{{cite journal | vauthors = Rosamond W, Flegal K, Furie K, Go A, Greenlund K, Haase N, Hailpern SM, Ho M, Howard V, Kissela B, Kissela B, Kittner S, Lloyd-Jones D, McDermott M, Meigs J, Moy C, Nichol G, O'Donnell C, Roger V, Sorlie P, Steinberger J, Thom T, Wilson M, Hong Y | title = Heart disease and stroke statistics--2008 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee | journal = Circulation | volume = 117 | issue = 4 | pages = e25-146 | date = January 2008 | pmid = 18086926 | doi = 10.1161/CIRCULATIONAHA.107.187998 | doi-access = free }}</ref> Angina is more often the presenting symptom of coronary artery disease in females than in men. The prevalence of angina rises with increasing age, with a mean age of onset of 62.3 years.<ref>{{cite journal | vauthors = Buckley BS, Simpson CR, McLernon DJ, Murphy AW, Hannaford PC | title = Five year prognosis in patients with angina identified in primary care: incident cohort study | journal = BMJ | volume = 339 | pages = b3058 | date = August 2009 | pmid = 19661139 | pmc = 2722695 | doi = 10.1136/bmj.b3058 }}</ref> After five years post-onset, 4.8% of individuals with angina subsequently died from coronary heart disease. Males with angina were found to have an increased risk of subsequent acute myocardial infarction and coronary heart disease related death than women. 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 [[Diseases of affluence|disease of affluence]].

==History==
{{Expand section|date=November 2020}}
The condition was named "hritshoola" in ancient India and was described by [[Sushruta]] (6th century BC).<ref name="Dwivedi&Dwivedi07">{{cite journal| vauthors = Dwivedi G, Dwivedi S |year=2007 |url=http://medind.nic.in/iae/t07/i4/iaet07i4p243.pdf |title=Sushruta – the Clinician – Teacher par Excellence |journal=The Indian Journal of Chest Diseases and Allied Sciences |volume=49 |pages=243–4 |url-status = dead|archive-url=https://web.archive.org/web/20081010045900/http://medind.nic.in/iae/t07/i4/iaet07i4p243.pdf |archive-date=2008-10-10 }}</ref>

The first clinical description of ''angina pectoris'' was by a British physician [[William Heberden|Dr. William Heberden]] in 1768.<ref>{{Cite journal|date=2002-10-16|title=Angina Pectoris: The Eighteenth-Century Origins of Angina Pectoris: Predisposing Causes, Recognition, and Aftermath|url=https://doi.org/10.1001/jama.288.15.1917-JBK1016-3-1|journal=JAMA|volume=288|issue=15|pages=1917–1918|doi=10.1001/jama.288.15.1917-JBK1016-3-1|issn=0098-7484|url-access=subscription}}</ref>

== References ==
{{reflist|30em}}

== External links ==
* [https://web.archive.org/web/20130921104228/http://www.optiongrid.org/resources/angina_grid.pdf Treatment of stable angina recommendations for patients] in layman's terms
* [https://www.bhf.org.uk/heart-health/conditions/angina British Heart Foundation - Angina] {{Webarchive|url=https://web.archive.org/web/20171222052357/https://www.bhf.org.uk/heart-health/conditions/angina |date=2017-12-22 }}
* [http://www.hipsknees.info/flash31/ypo.swf Angina Pectoris Animation Video 3D] {{Webarchive|url=https://web.archive.org/web/20110221011444/http://www.hipsknees.info/flash31/ypo.swf |date=2011-02-21 }}
* [https://web.archive.org/web/20121114065012/http://eurheartj.oxfordjournals.org/content/27/11/1341.full.pdf+html Guidelines on the management of stable angina pectoris - European Society of Cardiology]
* [https://web.archive.org/web/20100413012434/http://www.americanheart.org/presenter.jhtml?identifier=4591 Heart Attack and Angina Statistics] by American Heart Association: Final 2006 statistics for the United States
* {{cite EB9 |wstitle= Angina Pectoris |volume= II |page=29 |short= 1}}

{{Medical condition classification and resources
 | DiseasesDB     = 8695
 | ICD10          = {{ICD10|I|20||i|20}}
 | ICD9           = {{ICD9|413}}
 | ICDO           =
 | OMIM           =
 | MedlinePlus    = 000198
 | MedlinePlus_mult = {{MedlinePlus2|000201}}
 | eMedicineSubj  = med
 | eMedicineTopic = 133
 | MeshID         = D000787
}}
{{Cardiovascular system symptoms and signs}}
{{Heart diseases}}
{{Authority control}}

{{DEFAULTSORT:Angina Pectoris}}
[[Category:Acute pain]]
[[Category:Ischemic heart diseases]]