Angina

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For other uses, see Angina (disambiguation).

Angina

Other names Stenocardia, angina pectoris

Illustration depicting angina

 /ænˈdʒaɪnə, ˈændʒɪnə/ ann-JY-nə,  AN-jin-ə[1]
Pronunciation

Specialty Cardiology

Complications Heart attack, unstable angina

Angina, also known as angina pectoris, is chest pain or pressure, usually due
to insufficient blood flow to the heart muscle (myocardium).
Angina is usually due to obstruction or spasm of the arteries that supply blood to the
heart muscle.[2] Other causes include anemia, abnormal heart rhythms, and heart failure.
The main mechanism of coronary artery obstruction is 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, where 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. In the early 20th century this was a known sign of
impending death.[3] 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 five-year survival rate of
approximately 92%.[4]
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 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]
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.[5] 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. [6]
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.[7][8] 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). [8] Studies
show that 64% of all unstable anginas occur between 22:00 and 08:00 when patients
are at rest.[8][9]
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.[8]
See also: variant angina
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.[10] 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. [11] Since microvascular angina is not
characterized by major arterial blockages, it is harder to recognize and diagnose. [12][13]
[14]
 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. [15]

Signs and symptoms[edit]

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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, 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, 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.[16]
Coital angina, also known as angina d'amour, is angina subsequent to sexual
intercourse.[17] It is generally rare, except in patients with severe coronary artery disease.
[17]

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[18]
Routine counseling of adults to advise them to improve their diet and increase their
physical activity has not been found to significantly alter behavior and thus is not
recommended.[19]
Conditions that exacerbate or provoke angina [20]

 Medications
o Vasodilators
o 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.[21][22][23][24]
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[25][26]
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.[27] Blood flow is proportional to
the radius of the artery to the fourth power. [28]
3. reduced oxygen-carrying capacity of the blood,
due to several factors such as a decrease in
oxygen tension and hemoglobin concentration.
[29]
 This decreases the ability of hemoglobin to
carry oxygen to myocardial tissue.[30]
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 the 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.[31] Non-obstructive coronary disease is more common in females. [32][33]

Diagnosis[edit]
Angina should be suspected in people presenting tight, dull, or heavy chest discomfort
that is:[34]

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.[34]
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.[34]
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
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 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 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]
Further information: 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 inaqedate 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 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 medications have been used since 1879 for symptomatic relief
of angina.[35] 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 blockers, specifically B1 adrenergic blockers without intrinsic sympathomimetic
activity are the most preferred for the 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 and Bisoprolol, which result in blocking cAMP in
the heart muscle cells. The cAMP which plays a vital role in phosphorylating the
ryanodine receptor and LTCC will usually increase Ca+2 levels in the heart muscle
cells, which will then result in contraction is blocked. Therefore, B1 blockade decreases
the HR and contraction of the heart muscle, making it need less oxygen demand. 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 instrinsic 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 instrinsic 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 blockers 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 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 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.
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 heart rate reduction without affecting
contractility[36] 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.[37] 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.[38]
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), [39] 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.[40]
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. [41]
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
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, 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 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.[42][43][44][45][46][47]
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.[48]

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%).[49]
In the United States, 10.2 million are estimated to experience angina with approximately
500,000 new cases occurring each year.[5][50] 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. [51] 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.

History[edit]
This section needs expansion. You
can help by adding to
it. (November 2020)

The condition was named "hritshoola" in ancient India and was described
by Sushruta (6th century BC).[52]
The first clinical description of angina pectoris was by a British physician Dr. William
Heberden in 1768.[53]

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 External links[edit]
 Treatment of stable angina recommendations for
patients in layman's 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

Classification D

 ICD-10: I20

 ICD-9-CM: 413

 MeSH: D000787

 DiseasesDB: 8695

External resources  MedlinePlus: 000198

 eMedicine: med/133

show

Signs and symptoms relating to the circulatory system

show

Cardiovascular disease (heart)

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