Angina
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For other uses, see Angina (disambiguation).
Angina
Angina pectoris
Synonyms
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
Pronunciation
Specialty

/ænˈdʒaɪnə/ ann-JY-nə
Cardiology
Angina, also known as angina pectoris, is chest pain or pressure, usually due to not enough
blood flow to the heart muscle.
Angina is usually due to obstruction or spasm of the coronary arteries.[1] Other causes
include anemia, abnormal heart rhythmsand 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.[2] 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%.[3]
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.
Contents

1Classification
o
1.1Stable angina
o
1.2Unstable angina
o
1.3Cardiac syndrome X

2Signs and symptoms

3Cause
o
3.1Major risk factors
o
3.2Other medical problems
o
3.3Other cardiac problems

4Pathophysiology

5Diagnosis

6Treatment
o
6.1Microvascular angina in women
o
6.2Suspected angina

7Epidemiology

8History

9References

10External links
Classification[edit]
Illustration depicting angina
Stable angina[edit]
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.[4] 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.
Unstable angina[edit]
Unstable angina (UA) (also "crescendo angina"; this is a form of acute coronary syndrome) is
defined as angina pectoris that changes or worsens.[5]
It has at least one of these three features:
1. it occurs at rest (or with minimal exertion), usually lasting
more than 10 minutes
2. it is severe and of new onset (i.e., within the prior 4–6 weeks)
3. 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.[6][7] 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).[7] Studies show that 64% of all unstable anginas occur between 22:00 and 08:00
when patients are at rest.[7][8]
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.[7]
Cardiac syndrome X[edit]
Main article: 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.[9] 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.[10] Since microvascular angina is
not
characterized
by
major
arterial
blockages,
it
is
harder
to
recognize
and
diagnose.[11][12][13] 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.[14]
Signs and symptoms[edit]
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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.
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 believed caused by spasms of the artery. It occurs more in
younger women.[15]
Coital angina, also known as angina d'amour, is angina subsequent to sexual intercourse.[16] It is
generally rare, except in patients with severe coronary artery disease.[16]
Cause[edit]
Major risk factors[edit]
[citation needed]

Age (≥ 45 years for men, ≥ 55 for women)

Smoking

Diabetes mellitus

Dyslipidemia

Family history of premature cardiovascular disease (men <55
years, female <65 years old)

Hypertension

Kidney disease (microalbuminuria or GFR<60 mL/min)

Obesity (BMI ≥ 30 kg/m2)

Physical inactivity

Prolonged psychosocial stress[17]
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.[18]
Conditions that exacerbate or provoke angina
[19]

Medications

Vasodilators

Excessive thyroid hormone replacement

Vasoconstrictors

Polycythemia, which thickens the blood, slowing its flow
through the heart muscle

Hypothermia

Hypervolemia

Hypovolemia
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.[20][21][22][23]
Other medical problems[edit]

Esophageal disorders

Gastroesophageal Reflux Disease (GERD)

Hyperthyroidism

Hypoxemia

Profound anemia

Uncontrolled hypertension
Other cardiac problems[edit]

Bradyarrhythmia

Hypertrophic cardiomyopathy

Tachyarrhythmia

Valvular heart disease[24][25]
Myocardial ischemia can result from:
1. 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.
2. resistance of the blood vessels. This can be caused by
narrowing of the blood vessels;
a decrease in
radius.[26] Blood flow is proportional to the radius of the
artery to the fourth power.[27]
3. reduced oxygen-carrying capacity of the blood, due to
several factors such as a decrease in oxygen tension and
hemoglobin concentration.[28] This decreases the ability
of hemoglobin to carry oxygen to myocardial tissue.[29]
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.
Pathophysiology[edit]
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.[30] Non-obstructive coronary
disease is more common in females.[31][32]
Diagnosis[edit]
Angina should be suspected in people presenting tight, dull, or
heavy chest discomfort that is:[33]
1. Retrosternal or left-sided, radiating to the left arm, neck,
jaw, or back.
2. Associated with exertion or emotional stress and relieved
within several minutes by rest.
3. 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.[33]
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.[33]
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.
Treatment[edit]
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.[34] Calcium channel blockers (such
as nifedipine (Adalat)
and amlodipine), isosorbide
mononitrate and nicorandil are vasodilators commonly used in
chronic stable angina.[citation needed] A new therapeutic class, called
If
inhibitor,
has
recently
been
made
available: Ivabradine provides
pure
heart
rate
reduction[35] 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.[36] 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 strokeand gastrointestinal bleeding
offsets any benefits and it is no longer advised unless the risk of
myocardial infarction is very high.[37]
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),[38] 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 herbal products (THCP) for
angina.[39]
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
blood, diabetes and hypertension (high
blood
fats
in
pressure),
the
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.[40]
Microvascular angina in women[edit]
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 stong 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
resonance
imaging
(PET)
(MRI),
scanning,
and
cardiac
magnetic
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.[41] [42] [43] [44][45] [46]
Suspected angina[edit]
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.[47]
Epidemiology[edit]
As of 2010, angina due to ischemic heart disease affects
approximately 112 million people (1.6% of the population) being
slightly more common in men than women (1.7% to 1.5%).[48]
In the United States, 10.2 million are estimated to experience
angina with approximately 500,000 new cases occurring each
year.[4][49] 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.[50] 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
History[edit]
The condition was named "hritshoola" in ancient India and was
described by Sushruta (6th century BC).[51]
There is disagreement as to how to pronounce angina. It could
either be pronounced “an-JAHY-nuh” or “AN-juh-nuh”.[52]
References[edit]
1. ^ "MerckMedicus:
Dorland's
Medical
Dictionary".
Retrieved 2009-01-09.
2. ^ White, PD (1931). Heart Disease (1st ed.). Macmillan.
3. ^ 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.
4. ^ Jump up to:a b 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.
5. ^ "MerckMedicus:
Dorland's
Medical
Dictionary".
Retrieved 2009-01-09.
6. ^ Hombach, V.; Höher, M.; Kochs, M.; Eggeling, T.;
Schmidt, A.; Höpp, H. W.; Hilger, H. H. (1988).
"Pathophysiology
of
unstable
angina
pectoris—
correlations
with
imaging". European
coronary
Heart
angioscopic
Journal. 9:
40–
5. doi:10.1093/eurheartj/9.suppl_N.40. PMID 3246255.
7. ^ Jump
up
to:a b c d Simons,
Michael
(March
8,
2000). "Pathophysiology of unstable angina". Archived
from the original on March 30, 2010. Retrieved April
28, 2010.
8. ^ "What Is Angina?". National Heart Lung and Blood
Institute. Retrieved April 28, 2010.
9. ^ Kaski (editor), Juan Carlos (1999). Chest pain with
normal coronary angiograms: pathogenesis, diagnosis
and management. Boston: Kluwer. pp. 5–6. ISBN 9780792384212.
10. ^ Guyton, Arthur. "Textbook of Medical Physiology"
11th edition. Philadelphia; Elsevier, 2006.[page needed]
11. ^ "Cardiac
Syndrome
X".
HeartHealthyWomen.org.[unreliable medical source?]
12. ^ "Heart Attack and Angina Statistics". Archived
from the original on 2010-04-13. Retrieved 2010-0413.[not in citation given].
13. ^ "Angina". Texas Heart Institute. October 2012.
14. ^ 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 22389
117.
15. ^ 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
Cardiology. 39 (5):
American
College
of
847–851. doi:10.1016/S0735-
1097(02)01690-X. PMID 11869851.
16. ^ Jump up to:a b 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 00097322. PMID 22267844.
17. ^ 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.
18. ^ 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:10.7326/0003-4819-157-5-20120904000486. PMID 22733153.
19. ^ Wells, Barbara; DiPiro, Joseph; Schwinghammer,
Terry;
DiPiro,
Handbook (7th
Cecily
ed.).
(2008). Pharmacotherapy
New
p. 140. ISBN 978-0-07-148501-2.
York:
McGraw-Hill.
20. ^ "Health Benefits of Cessation". Centers for Disease
Control and Prevention. January 3, 2013.
21. ^ 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.
22. ^ 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.
23. ^ Shinozaki, Norihiko; Yuasa, Toyoshi; Takata, Shigeo
(2008). "Cigarette Smoking Augments Sympathetic Nerve
Activity
in
Patients
Disease". International
with
Heart
Coronary
Journal. 49 (3):
Heart
261–
72. doi:10.1536/ihj.49.261. PMID 18612184.
24. ^ 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.
25. ^ 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.
26. ^ Kusumoto,
Fred
M
(2009-10-20). "Chapter
10:
Cardiovascular Disorders: Heart Disease". In McPhee,
SJ; Hammer, GD. Pathophysiology of Disease: An
Introduction
to
Clinical
Medicine (6th
ed.).
p. 276. ISBN 978-0-07-162167-0.
27. ^ Thomas,
Michel
(2005-09-13).
"Treatment
of
Myocardial Ischemia". In Brunton, Laurence L.; Lazo,
John S.; Parker, Keith L. Goodman & Gilman's The
Pharmacological
Basis
of
Therapeutic (11th
ed.).
(November
28,
p. 823. ISBN 978-0071422802.
28. ^ Podrid,
Philip
J
2012). "Pathophysiology and clinical presentation of
ischemic
chest
pain". UpToDate. Wolters
Kluwer.(registration required)
29. ^ The Crucial Role of Iron in the Body
30. ^ Vaccarino, V. (16 February 2010). "Ischemic Heart
Disease
in
Women:
Many
Questions,
Few
Facts". Circulation:
Cardiovascular
Quality
Outcomes. 3 (2):
and
111–
115. doi:10.1161/CIRCOUTCOMES.109.925313. PMC 3
012351. PMID 20160161.
31. ^ 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. PMI
D 16923752.
32. ^ 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. P
MID 21286281.
33. ^ Jump up to:a b c NHS Clinical Knowledge Summaries
(2009) Angina - stable. "Archived copy". Archived
from the original on 2010-03-10. Retrieved 2010-0104. Date site accessed: 04/01/2009
34. ^ Sneader,
Walter
(2005). Drug
discovery:
a
history. ISBN 978-0-471-89980-8.[page needed]
35. ^ 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.
36. ^ 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 165339
39.
37. ^ 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.
38. ^ 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.
39. ^ 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. PMI
D 20464731.
40. ^ 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
controlled
(ACTION
trial". The
trial):
Randomised
Lancet. 364(9437):
849–
57. doi:10.1016/S0140-6736(04)169808. PMID 15351192.
41. ^ Celik T et al: Int J Cardiol 218:233-234, 2016
42. ^ Cattaneo M et al: Int J Cardiol 181:376-381, 2015
43. ^ Lanza GA et al: Circ J 2016 May 27
44. ^ Marinescu MA et al: JACC Cardiovasc Imaging 8(2):
210-220, 2015
45. ^ Selthofer-Relatic K, Boxnjak I, Kibel A: Cardiol Res
Pract 2016: 8173816, 2016
46. ^ Titterington JS, Hung OY, Wenger N: Future Cardiol
11(2): 229-242, 2015
47. ^ 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
48. ^ 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)617292. PMC 6350784. PMID 23245607.
49. ^ 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. PM
ID 18086926.
50. ^ 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 19
661139.
51. ^ Dwivedi, Girish; Dwivedi, Shridhar (2007). "Sushruta
– the Clinician – Teacher par Excellence" (PDF). The
Indian
Journal
Sciences. 49:
of
Chest
Diseases
243–4.
and
Archived
Allied
from the
original (PDF) on 2008-10-10.
52. ^ "The definition of angina".
External links[edit]
D
Classification
External resources

ICD-10: I20

ICD-9-CM: 413

MeSH: D000787

DiseasesDB: 8695

MedlinePlus: 000198

eMedicine: med/133

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)
nd signs relating to the cardiovascular system (R00–R03, 785)
lar disease (heart) (I00–I52, 390–429)
NDL: 00567282
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