|Other names||Angina pectoris|
|Diagram of discomfort caused by coronary artery disease. Pressure, fullness, squeezing or pain in the center of the chest. Can also feel discomfort in the neck, jaw, shoulder, back or arm|
Angina is usually due to obstruction or spasm of the coronary arteries. Other causes include anemia, abnormal heart rhythms and heart failure. The main mechanism of coronary artery obstruction is an atherosclerosis as part of coronary artery disease. The term derives from the Latin angere (“to strangle”) and pectus (“chest”), and can therefore be translated as “a strangling feeling in the chest”.
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 myocardial infarction (heart attack) and a heart attack can occur without pain). In some cases, angina can be quite severe, and in the early 20th century this was a known sign of impending death. However, given current medical therapies, the outlook has improved substantially. People with an average age of 62 years, who have moderate to severe degrees of angina (grading by classes II, III, and IV) have a 5-year survival rate of approximately 92%.
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 in similar fashion to myocardial infarction.
- 1 Classification
- 2 Signs and symptoms
- 3 Cause
- 4 Pathophysiology
- 5 Diagnosis
- 6 Treatment
- 7 Epidemiology
- 8 History
- 9 References
- 10 External links
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 nitroglycerin. Symptoms typically abate 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 emotional stress.
It has at least one of these three features:
- 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 crescendo pattern (i.e., distinctly more severe, prolonged, or frequent than before).
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. The pathophysiology of unstable angina is the reduction of coronary flow due to transient platelet aggregation on apparently normal endothelium, coronary artery spasms, or coronary thrombosis. 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). Studies show that 64% of all unstable anginas occur between 22:00 and 08:00 when patients are at rest.
In stable angina, the developing atheroma 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. This explains why, in many cases, unstable angina develops independently of activity.
Cardiac syndrome X
Cardiac syndrome X, sometimes known as microvascular angina 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 tests. The primary cause of cardiac syndrome X 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. Since microvascular angina is not characterized by major arterial blockages, it is harder to recognize and diagnose. 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 women than in men, as well as their predilection towards ischemia and acute coronary syndromes in the absence of obstructive coronary artery disease.
Signs and symptoms
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 due to the fact that 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, 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.
A variant form of angina—Prinzmetal’s angina—occurs in patients with normal coronary arteries or insignificant atherosclerosis. It is believed caused by spasms of the artery. It occurs more in younger women.
Major risk factors
- Age (≥ 45 years for men, ≥ 55 for women)
- Diabetes mellitus
- Family history of premature cardiovascular disease (men <55 years, female <65 years old)
- Kidney disease (microalbuminuria or GFR<60 mL/min)
- Obesity (BMI ≥ 30 kg/m2)
- Physical inactivity
- Prolonged psychosocial stress
Routine counselling of adults to advise them to improve their diet and increase their physical activity has not been found to significantly alter behaviour, and thus is not recommended.
- Conditions that exacerbate or provoke angina
One study found that smokers with coronary artery disease had a significantly increased level of 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 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 smoking men 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.
Other medical problems
- Esophageal disorders
- Gastroesophageal Reflux Disease (GERD)
- Profound anemia
- Uncontrolled hypertension
Other cardiac problems
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. This can be caused by narrowing of the blood vessels; a decrease in radius. Blood flow is proportional to the radius of the artery to the fourth power.
- reduced oxygen-carrying capacity of the blood, due to several factors such as a decrease in oxygen tension and hemoglobin concentration. This decreases the ability of hemoglobin to carry oxygen to myocardial tissue.
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 severe anemia (low number of red blood cells), or long-term smoking.
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).
Angina should be suspected in people presenting tight, dull, or heavy chest discomfort that is:
- 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.
Anginal pain is not usually sharp or stabbing or influenced by respiration. Antacids and simple analgesics 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.
In angina patients 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 his/her maximum ability before fatigue, breathlessness, or pain intervenes; if characteristic ECG changes are documented (typically more than 1 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 conclusion 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 thallium scintigram or sestamibi scintigram (in patients unable to 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 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.
The most specific medicine to treat angina is nitroglycerin. It is a potent vasodilator that decreases myocardial oxygen demand by decreasing the heart’s workload. Beta blockers and calcium channel blockers act to decrease the heart’s workload, and thus its requirement for oxygen. 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 a serious drop in blood pressure. Treatments for angina are balloon angioplasty, in which the balloon is inserted at the end of a catheter and inflated to widen the arterial lumen. Stents 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.
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 death. Beta blockers (e.g., carvedilol, propranolol, atenolol) have a large body of evidence in morbidity and mortality benefits (fewer symptoms, less disability and longer life) and short-acting nitroglycerin medications have been used since 1879 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 leading to major anti-ischemic and antianginal efficacy. ACE inhibitors are also vasodilators with both symptomatic and prognostic benefit. Statins are the most frequently used lipid/cholesterol modifiers, which probably also stabilize existing atheromatous plaque. 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.
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), probably working by complex mechanisms such as 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), and encouraging smoking cessation and 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.
Microvascular angina in women
Women with myocardial ischemia often have either no or atypical symptoms, such as palpitations, anxiety, weakness, and fatigue. Additionally, many women 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 women with myocardial ischemia suffer from 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 assessment of the microcirculatory response to adenoside 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, women with this condition have less coronary microvascular dilation in response to nitrates than do those without MVA. Women 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 nonnitrate vasodilators, such as calcium channel blockers and angiotensin converting enzyme (ACE) inhibitors along with HMG-CoA reductase inhibitors (statins), also has been shown to be 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.     
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.
In the United States, 10.2 million are estimated to experience angina with approximately 500,000 new cases occurring each year. Angina is more often the presenting symptom of coronary artery disease in women than in men. The prevalence of angina rises with increasing age, with a mean age of onset of 62.3 years. After five years post-onset, 4.8% of individuals with angina subsequently died from coronary heart disease. Men 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 disease of affluence. The adoption of a rich, Westernized diet and subsequent increase of smoking, obesity, and other risk factors has led to an increase in angina and related diseases in countries such as China
There is disagreement as to how to pronounce angina. It could either be pronounced “an-JAHY-nuh” or “AN-juh-nuh”.
- “MerckMedicus: Dorland’s Medical Dictionary”. Retrieved 2009-01-09.
- White, PD (1931). Heart Disease (1st ed.). Macmillan.
- COURAGE Trial Research Group (2007). “Optimal Medical Therapy with or without PCI for Stable Coronary Disease”. N Engl J Med. 356 (15): 1503–1516. doi:10.1056/NEJMoa070829. PMID 17387127.
- Tobin, Kenneth J. (2010). “Stable Angina Pectoris: What Does the Current Clinical Evidence Tell Us?”. The Journal of the American Osteopathic Association. 110 (7): 364–70. PMID 20693568.
- “MerckMedicus: Dorland’s Medical Dictionary”. Retrieved 2009-01-09.
- Hombach, V.; Höher, M.; Kochs, M.; Eggeling, T.; Schmidt, A.; Höpp, H. W.; Hilger, H. H. (1988). “Pathophysiology of unstable angina pectoris—correlations with coronary angioscopic imaging”. European Heart Journal. 9: 40–5. doi:10.1093/eurheartj/9.suppl_N.40. PMID 3246255.
- Simons, Michael (March 8, 2000). “Pathophysiology of unstable angina”. Archived from the original on March 30, 2010. Retrieved April 28, 2010.
- “What Is Angina?”. National Heart Lung and Blood Institute. Retrieved April 28, 2010.
- Kaski (editor), Juan Carlos (1999). Chest pain with normal coronary angiograms: pathogenesis, diagnosis and management. Boston: Kluwer. pp. 5–6. ISBN 978-0792384212.CS1 maint: Extra text: authors list (link)
- Guyton, Arthur. “Textbook of Medical Physiology” 11th edition. Philadelphia; Elsevier, 2006.[page needed]
- “Cardiac Syndrome X”. HeartHealthyWomen.org.[unreliable medical source?]
- “Heart Attack and Angina Statistics”. Archived from the original on 2010-04-13. Retrieved 2010-04-13.[not in citation given].
- “Angina”. Texas Heart Institute. October 2012.
- Gulati, M; Shaw, LJ; Bairey Merz, C. Noel (2012). “Myocardial ischemia in women: lessons from the NHLBI WISE study”. Clinical Cardiology. 35 (3): 141–148. doi:10.1002/clc.21966. PMC 3297966. PMID 22389117.
- Sun, Hongtao; Mohri, Masahiro; Shimokawa, Hiroaki; Usui, Makoto; Urakami, Lemmy; Takeshita, Akira (28 February 2002). “Coronary microvascular spasm causes myocardial ischemia in patients with vasospastic angina”. Journal of the American College of Cardiology. 39 (5): 847–851. doi:10.1016/S0735-1097(02)01690-X. PMID 11869851.
- Levine, Glenn N.; Steinke, Elaine E.; Bakaeen, Faisal G.; Bozkurt, Biykem; Cheitlin, Melvin D.; Conti, Jamie Beth; Foster, Elyse; Jaarsma, Tiny; Kloner, Robert A. (2012-02-28). “Sexual Activity and Cardiovascular Disease A Scientific Statement From the American Heart Association”. Circulation. 125 (8): 1058–1072. doi:10.1161/CIR.0b013e3182447787. ISSN 0009-7322. PMID 22267844.
- Linden, Wolfgang; Stossel, Carmen; Maurice, Jeffrey (1996). “Psychosocial Interventions for Patients with Coronary Artery Disease: A Meta-analysis”. Archives of Internal Medicine. 156 (7): 745–52. doi:10.1001/archinte.1996.00440070065008. PMID 8615707.
- Moyer, Virginia A.; U.S. Preventive Services Task Force (2012). “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”. Annals of Internal Medicine. 157 (5): 367–71. doi:10.7326/0003-4819-157-5-201209040-00486. PMID 22733153.
- Wells, Barbara; DiPiro, Joseph; Schwinghammer, Terry; DiPiro, Cecily (2008). Pharmacotherapy Handbook (7th ed.). New York: McGraw-Hill. p. 140. ISBN 978-0-07-148501-2.
- “Health Benefits of Cessation”. Centers for Disease Control and Prevention. January 3, 2013.
- Daly, L E; Graham, I M; Hickey, N; Mulcahy, R (1985). “Does stopping smoking delay onset of angina after infarction?”. BMJ. 291 (6500): 935–7. doi:10.1136/bmj.291.6500.935. PMC 1417185. PMID 3929970.
- Daly, L E; Mulcahy, R; Graham, I M; Hickey, N (1983). “Long term effect on mortality of stopping smoking after unstable angina and myocardial infarction”. BMJ. 287 (6388): 324–6. doi:10.1136/bmj.287.6388.324. PMC 1548591. PMID 6409291.
- Shinozaki, Norihiko; Yuasa, Toyoshi; Takata, Shigeo (2008). “Cigarette Smoking Augments Sympathetic Nerve Activity in Patients with Coronary Heart Disease”. International Heart Journal. 49 (3): 261–72. doi:10.1536/ihj.49.261. PMID 18612184.
- Gibbons, Raymond J; Abrams, Jonathan; Chatterjee, Kanu; Daley, Jennifer; Deedwania, Prakash C; Douglas, John S; Ferguson Jr, T.Bruce; Fihn, Stephan D; Fraker Jr, Theodore D; Gardin, Julius M; O’Rourke, Robert A; Pasternak, Richard C; Williams, Sankey V; American College Of, Raymond J; Alpert, Joseph S; Antman, Elliott M; Hiratzka, Loren F; Fuster, Valentin; Faxon, David P; Gregoratos, Gabriel; Jacobs, Alice K; Smith, Sidney C (2003). “ACC/AHA 2002 guideline update for the management of patients with chronic stable angina—summary article”. Journal of the American College of Cardiology. 41 (1): 159–68. doi:10.1016/S0735-1097(02)02848-6. PMID 12570960.
- Fraker, Theodore D.; Fihn, Stephan D.; 2002 Chronic Stable Angina Writing Committee; American College Of, Cardiology; American Heart, Association; Gibbons, RJ; Abrams, J; Chatterjee, K; Daley, J; Deedwania, PC; Douglas, JS; Ferguson Jr, TB; Gardin; O’Rourke, RA; Williams, SV; Smith Jr, SC; Jacobs, AK; Adams, CD; Anderson, JL; Buller, CE; Creager, MA; Ettinger, SM; Halperin; Hunt, SA; Krumholz, HM; Kushner, FG; Lytle, BW; Nishimura, R; Page, RL; Riegel, B (2007). “2007 Chronic Angina Focused Update of the ACC/AHA 2002 Guidelines for the Management of Patients with Chronic Stable Angina”. Journal of the American College of Cardiology. 50 (23): 2264–74. doi:10.1016/j.jacc.2007.08.002. PMID 18061078.
- Kusumoto, Fred M (2009-10-20). “Chapter 10: Cardiovascular Disorders: Heart Disease”. In McPhee, SJ; Hammer, GD (eds.). Pathophysiology of Disease: An Introduction to Clinical Medicine (6th ed.). p. 276. ISBN 978-0-07-162167-0.
- Thomas, Michel (2005-09-13). “Treatment of Myocardial Ischemia”. In Brunton, Laurence L.; Lazo, John S.; Parker, Keith L. (eds.). Goodman & Gilman’s The Pharmacological Basis of Therapeutic (11th ed.). p. 823. ISBN 978-0071422802.
- Podrid, Philip J (November 28, 2012). “Pathophysiology and clinical presentation of ischemic chest pain”. UpToDate. Wolters Kluwer.(registration required)
- The Crucial Role of Iron in the Body
- Vaccarino, V. (16 February 2010). “Ischemic Heart Disease in Women: Many Questions, Few Facts”. Circulation: Cardiovascular Quality and Outcomes. 3 (2): 111–115. doi:10.1161/CIRCOUTCOMES.109.925313. PMC 3012351. PMID 20160161.
- 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 (Aug 29, 2006). Women’s Ischemia Syndrome Evaluation (WISE), Investigators. “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”. Circulation. 114 (9): 894–904. doi:10.1161/CIRCULATIONAHA.105.609990. PMID 16923752.
- Banks, Kamakki; Lo, Monica; Khera, Amit (1 February 2010). “Angina in Women without Obstructive Coronary Artery Disease”. Current Cardiology Reviews. 6 (1): 71–81. doi:10.2174/157340310790231608. PMC 2845797. PMID 21286281.
- NHS Clinical Knowledge Summaries (2009) Angina – stable. “Archived copy”. Archived from the original on 2010-03-10. Retrieved 2010-01-04.CS1 maint: Archived copy as title (link) Date site accessed: 04/01/2009
- Sneader, Walter (2005). Drug discovery: a history. ISBN 978-0-471-89980-8.[page needed]
- Sulfi, S.; Timmis, A. D. (2006). “Ivabradine – the first selective sinus node if channel inhibitor in the treatment of stable angina”. International Journal of Clinical Practice. 60 (2): 222–8. doi:10.1111/j.1742-1241.2006.00817.x. PMC 1448693. PMID 16451297.
- Nissen SE; Nicholls SJ; Sipahi I; et al. (2006). “Effect of very high-intensity statin therapy on regression of coronary atherosclerosis: The asteroid trial”. JAMA. 295 (13): 1556–1565. doi:10.1001/jama.295.13.jpc60002. PMID 16533939.
- Barnett, H.; Burrill, P.; Iheanacho, I. (2010). “Don’t use aspirin for primary prevention of cardiovascular disease”. BMJ. 340: c1805. doi:10.1136/bmj.c1805. PMID 20410163.
- Ades, P. A.; Waldmann, M. L.; Poehlman, E. T.; Gray, P.; Horton, E. D.; Horton, E. S.; Lewinter, M. M. (1993). “Exercise conditioning in older coronary patients. Submaximal lactate response and endurance capacity”. Circulation. 88 (2): 572–7. doi:10.1161/01.CIR.88.2.572. PMID 8339420.
- Zhuo, Qi; Yuan, Zhengyong; Chen, Hengxi; Wu, Taixiang (2010-05-12). “Cochrane Database of Systematic Reviews”. Cochrane Database of Systematic Reviews (5): CD004468. doi:10.1002/14651858.cd004468.pub2. PMID 20464731.
- Poole-Wilson, Philip A; Lubsen, Jacobus; Kirwan, Bridget-Anne; Van Dalen, Fred J; Wagener, Gilbert; Danchin, Nicolas; Just, Hanjörg; Fox, Keith AA; Pocock, Stuart J; Clayton, Tim C; Motro, Michael; Parker, John D; Bourassa, Martial G; Dart, Anthony M; Hildebrandt, Per; Hjalmarson, Åke; Kragten, Johannes A; Molhoek, G Peter; Otterstad, Jan-Erik; Seabra-Gomes, Ricardo; Soler-Soler, Jordi; Weber, Simon; Coronary disease Trial Investigating Outcome with Nifedipine gastrointestinal therapeutic system investigators (2004). “Effect of long-acting nifedipine on mortality and cardiovascular morbidity in patients with stable angina requiring treatment (ACTION trial): Randomised controlled trial”. The Lancet. 364 (9437): 849–57. doi:10.1016/S0140-6736(04)16980-8. PMID 15351192.
- Celik T et al: Int J Cardiol 218:233-234, 2016
- Cattaneo M et al: Int J Cardiol 181:376-381, 2015
- Lanza GA et al: Circ J 2016 May 27
- Marinescu MA et al: JACC Cardiovasc Imaging 8(2): 210-220, 2015
- Selthofer-Relatic K, Boxnjak I, Kibel A: Cardiol Res Pract 2016: 8173816, 2016
- Titterington JS, Hung OY, Wenger N: Future Cardiol 11(2): 229-242, 2015
- NHS Clinical Knowledge Summaries (2009) Angina – stable: suspected angina Suspected angina Archived December 14, 2010, at the Wayback Machine Date site accessed: 04/01/2009
- Vos, T; Flaxman, AD; Naghavi, M; Lozano, R; Michaud, C; Ezzati, M; Shibuya, K; Salomon, JA; et al. (Dec 15, 2012). “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”. Lancet. 380 (9859): 2163–96. doi:10.1016/S0140-6736(12)61729-2. PMC 6350784. PMID 23245607.
- Rosamond, W.; Flegal, K.; Furie, K.; Go, A.; Greenlund, K.; Haase, N.; Hailpern, S. M.; Ho, M.; Howard, V.; 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. (17 December 2007). “Heart Disease and Stroke Statistics – 2008 Update: A Report From the American Heart Association Statistics Committee and Stroke Statistics Subcommittee”. Circulation. 117 (4): e25–e146. doi:10.1161/CIRCULATIONAHA.107.187998. PMID 18086926.
- Buckley, B. S; Simpson, C. R; McLernon, D. J; Murphy, A. W; Hannaford, P. C (2009). “Five year prognosis in patients with angina identified in primary care: Incident cohort study”. BMJ. 339: b3058. doi:10.1136/bmj.b3058. PMC 2722695. PMID 19661139.
- Dwivedi, Girish; Dwivedi, Shridhar (2007). “Sushruta – the Clinician – Teacher par Excellence” (PDF). The Indian Journal of Chest Diseases and Allied Sciences. 49: 243–4. Archived from the original (PDF) on 2008-10-10.
- “The definition of angina”.
- Treatment of stable angina recommendations for patients in layman terms
- British Heart Foundation – Angina
- Angina Pectoris Animation Video 3D
- Guidelines on the management of stable angina pectoris – European Society of Cardiology
- Heart Attack and Angina Statistics by American Heart Association : Final 2006 statistics for the United States
- ANGINA: OVERVIEW, SYMPTOMS, DIAGNOSIS AND TREATMENT by WeMa Life (20 April 2018)