Angina
Angina | |
---|---|
Other names | Stenocardia, angina pectoris |
Heart attack, unstable angina |
Angina, also known as angina pectoris, is chest pain or pressure, usually caused by insufficient blood flow to the heart muscle (myocardium).[2] It is most commonly a symptom of coronary artery disease.[2]
Angina is typically the result of partial
There is a relationship between severity of angina and degree of
In the early 20th century, severe angina was seen as a sign of impending death.
Classification
Stable angina
Also known as 'effort angina', this refers to the classic type of angina related to
Unstable Angina
Unstable angina (UA) (also "crescendo angina"; this is a form of acute coronary syndrome) is defined as angina pectoris that changes or worsens.[11]
It has at least one of these three features:[12]
- 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 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
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).[14] Studies show that 64% of all unstable anginas occur between 22:00 and 08:00 when patients are at rest.[14][15]
In stable angina, the developing
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 tests.[16] 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.[17] Since microvascular angina is not characterized by major arterial blockages, it is harder to recognize and diagnose.[18][19][20]
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.[21]
Signs and symptoms
This section needs additional citations for verification. (June 2013) |
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
of premature heart disease.A variant form of angina—
Coital angina, also known as angina d'amour, is angina subsequent to sexual intercourse.[23] It is generally rare, except in patients with severe coronary artery disease.[23]
Cause
Major risk factors
- 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 GFR<60 mL/min)
- Obesity (BMI ≥ 30 kg/m2)
- Physical inactivity
- Prolonged stress[24]
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.[25]
- Conditions that exacerbate or provoke angina[26]
- 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
Other medical problems
- Esophageal disorders
- Gastroesophageal reflux disease(GERD)
- Hyperthyroidism
- Hypoxemia
- Profound anemia
- Uncontrolled hypertension
Other cardiac problems
- Bradyarrhythmia
- Hypertrophic cardiomyopathy
- Tachyarrhythmia
- Valvular heart disease[31][32]
- 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.[33] Blood flow is proportional to the radius of the artery to the fourth power.[34]
- reduced oxygen-carrying capacity of the blood, due to several factors such as a decrease in oxygen tension and hemoglobin concentration.[35] This decreases the ability of hemoglobin to carry oxygen to myocardial tissue.[36]
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
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.[37] Non-obstructive coronary disease is more common in females.[38][39]
Diagnosis
Angina should be suspected in people presenting tight, dull, or heavy chest discomfort that is:[40]
- 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.[40]
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.[40]
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
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 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.[41] 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 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+2 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 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.
Treatments for angina are
Calcium channel blockers (such as
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),[45] 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.[46]
Identifying and treating risk factors for further coronary heart disease is a priority in patients with angina. This means testing for
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.[47]
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.[48][49][50][51][52][53]
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.[54]
Epidemiology
As of 2010, angina due to
In the United States, 10.2 million are estimated to experience angina with approximately 500,000 new cases occurring each year.[10][56] 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.[57] 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 disease of affluence.
History
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).[58]
The first clinical description of angina pectoris was by a British physician Dr. William Heberden in 1768.[59]
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External links
- Treatment of stable angina recommendations for patients in layman's terms
- British Heart Foundation - Angina Archived 2017-12-22 at the Wayback Machine
- Angina Pectoris Animation Video 3D Archived 2011-02-21 at the Wayback Machine
- 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
- Encyclopædia Britannica. Vol. II (9th ed.). 1878. p. 29. .