Angina pectoris

"Angina" redirects here. For other uses, see Angina (disambiguation).

Angina pectoris
Classification and external resources
ICD-10	I20
ICD-9	413
DiseasesDB	8695
eMedicine	med/133
MeSH	D000787

Angina pectoris, commonly known as angina, is chest pain^[1] due to ischemia (a lack of blood, thus a lack of oxygen supply) of the heart muscle, generally due to obstruction or spasm of the coronary arteries (the heart's blood vessels). Coronary artery disease, the main cause of angina, is due to atherosclerosis of the cardiac arteries. The term derives from the Latin angina ("infection of the throat") from the Greek ἀγχόνη ankhonē ("strangling"), and the Latin 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 heart attack, and a heart attack can occur without pain).

Worsening ("crescendo") 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 herald myocardial infarction (a heart attack), they require urgent medical attention and are generally treated as a presumed heart attack.

Classification

Stable angina

Also known as effort angina, this refers to the more common understanding of angina related to myocardial ischemia. Typical presentations 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. Symptoms typically abate several minutes following cessation of precipitating activities and stops when activity resumes. In this way, stable angina may be thought of as being similar to claudication symptoms.

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.^[1]

It has at least one of these three features:

1. it occurs at rest (or with minimal exertion), usually lasting >10 min;
2. it is severe and of new onset (i.e., within the prior 4–6 weeks); and/or
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.^[2][3] The process starts with atherosclerosis, and when inflamed leads to an active plaque, which undergoes thrombosis and results in acute ischemia, which finally results in cell necrosis after calcium entry.^[4] Studies show that 64% of all unstable anginas occur between 10 PM and 8 AM when patients are at rest.^[5][6]

In stable angina, the developing atheroma is protected with a fibrous cap. This cap (atherosclerotic plaque) may rupture in unstable angina, allowing blood clots to precipitate and further decrease the lumen of the coronary vessel. This explains why an unstable angina appears to be independent of activity.

Microvascular angina

Microvascular Angina or Angina Syndrome X is characterized by angina-like chest pain, but have different causes.The cause of Microvascular Angina is unknown, but it appears to be the result of poor function in the tiny blood vessels of the heart, arms and legs.^[7] Since microvascular angina isn't characterized by arterial blockages, it's harder to recognize and diagnose, but its prognosis is excellent. ^{[8] [9] [10]}

Signs and symptoms

Most 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 spinal level that receives visceral sensation from the heart simultaneously receiving 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.

Myocardial ischemia comes about when the myocardia (the heart muscles) receive insufficient blood and oxygen to function normally either because of increased oxygen demand by the myocardia or by decreased supply to the myocardia. This inadequate perfusion of blood and the resulting reduced delivery of oxygen and nutrients is 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 thought to be caused by spasms of the artery. It occurs more in younger women.

Cause

Major risk factors

^[11]

• Age (≥ 55 years for men, ≥ 65 for women)
• Cigarette smoking
• Diabetes mellitus (DM)
• Dyslipidemia
• Family History of premature Cardiovascular Disease (men <55 years, female <65 years old)
• Hypertension (HTN)
• Kidney disease (microalbuminuria or GFR<60 mL/min)
• Obesity (BMI ≥ 30 kg/m2)
• Physical inactivity

Conditions that exacerbate or provoke angina

^[12]

• Medications
• vasodilators
• excessive thyroid replacement
• vasoconstrictors
• polycythemia which thickens the blood causing it to slow its flow through the heart muscle

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. Additionally, 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 who had quit smoking compared to those who continued. Studies have found that there are short term and long term benefits to smoking cessation.^{[13][14][15][16]}

Other medical problems

• profound anemia
• uncontrolled HTN
• hyperthyroidism
• hypoxemia

Other cardiac problems

• tachyarrhythmia
• bradyarrhythmia
• valvular heart disease
• hypertrophic cardiomyopathy ^[17][18]

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,.^[19] Blood flow is inversely proportional to the radius of the artery to the fourth power ^[20]
3. reduced oxygen-carrying capacity of the blood, due to several factors such as a decrease in oxygen tension and hemoglobin concentration.^[21] This decreases the ability to of hemoglobin to carry oxygen to myocardial tissue.^[22]

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

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).

Diagnosis

Suspect angina in people presenting with tight, dull, or heavy chest discomfort which is:^[23]

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 burping. These atypical symptoms are particularly likely in older people, women, and those with diabetes.^[23]

Angina pain is not usually sharp or stabbing or influenced by respiration. Antacids and simple analgesia 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.^[23]

In angina patients who are momentarily not feeling any one 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 their maximum ability before fatigue, breathlessness or, importantly, 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 us to some conclusion regarding the angina. The exercise test is also useful in looking for other markers of myocardial ischaemia: blood pressure response (or lack thereof, particularly a drop in systolic pressure), dysrhythmia and chronotropic response. Other alternatives to a standard exercise test include a thallium scintigram (in patients who cannot 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. There has been research which concludes that a frequency is attained when there is increase in the blood pressure and the pulse rate. This frequency varies normally but the range is 45–50 kHz for the cardiac arrest or for the heart failure. In patients who are in hospital 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

The most specific medicine to treat angina is nitroglycerin. It is a potent vasodilator that makes more oxygen available to the heart muscle. 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 Viagra, Cialis, or Levitra have been taken by the casualty within the previous 12 hours as the combination of the two could cause a serious drop in blood pressure. Treatments 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, of course, 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.^[24] 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^[25] leading to major anti-ischemic and antianginal efficacy. ACE inhibitors are also vasodilators with both symptomatic and prognostic benefit and, lastly, statins are the most frequently used lipid/cholesterol modifiers which probably also stabilize existing atheromatous plaque^{[citation needed]}. Low-dose aspirin decreases the risk of heart attack in patients with chronic stable angina, and was previously part of standard treatment, however it has since been discovered that the increase in haemorrhagic stroke and gastrointestinal bleeding offsets this gain so they are no longer advised unless the risk of myocardial infarction is very high.^[26]

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),^[27] 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), encouraging stopping smoking and weight optimisation.

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.^[28]

Suspected angina

Hospital admission for people with the following symptoms, as they may have unstable angina: Pain at rest (which may occur at night), pain on minimal exertion, angina that seems to be progressing rapidly despite increasing medical treatment. Refer urgently all people with suspected angina to a chest pain evaluation service, for confirmation of the diagnosis and assessment of the severity of coronary heart disease.^[29]

Epidemiology

Roughly 6.3 million Americans are estimated to experience angina. 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.^[30] 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, as chronicled in The China Study, has already led to an increase in angina and related diseases in countries such as China.

Recently, angina was tied to exposure of Bisphenol-A^[31] among adults in the US.

History

The concept of Hritshoola—literally heart pain—was known to Sushruta (6th century BCE).^[32] Dwivedi & Dwivedi (2007)—on the condition described by Sushruta—hold that: 'It embodies all the essential components of present day definition, i.e. site, nature, aggravating and relieving factors and referral. According to him angina is chest pain which is precordial, temporary, exertional, emotional, burning like and relieved by rest. He also linked this kind of pain to obesity (medoroga).'^[32]

References

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2. ^ V. Hombach, M. Höher, M. Kochs, T. Eggeling, A. Schmidt, H. W. Höpp and H. H. Hilger. (1998). “Pathophysiology of unstable angina pectoris—correlations with coronary angioscopic imaging”. European Heart Journal 9 (N): 40-45.
3. ^ Simons, Michael M.D. “Pathophysiology of unstable angina”. March 8, 2000. http://cmbi.bjmu.edu.cn/uptodate/coronary%20heart%20disease/Pathophysiology/Pathophysiology%20of%20unstable%20angina.htm. Accessed April 28, 2010.
4. ^ Simons, M. Pathophysiology of unstable angina. March 8, 2000. Chinese Medical & Biological Information. Available at http://cmbi.bjmu.edu.cn/uptodate/coronary%20heart%20disease/Pathophysiology/Pathophysiology%20of%20unstable%20angina.htm. Accessed April 28, 2010.
5. ^ Simons, Michael. (2000). “Pathophysiology of unstable Angina”. http://cmbi.bjmu.edu.cn/uptodate/coronary%20heart%20disease/Pathophysiology/Pathophysiology%20of%20unstable%20angina.htm
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7. ^ Guyton, Arthur. "Textbook of Medical Physiology" 11th edition. Philadelphia; Elsevier, 2006.
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12. ^ Wells BG, Dipiro JT, Schwinghammer TL, Dipiro CV. Pharmacotherapy Handbook. 7th Ed. New York: McGraw-Hill; 2009: 140
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14. ^ Daly LE, Graham IM, Hickey N, Mulcahy R (October 1985). "Does stopping smoking delay onset of angina after infarction?". Br Med J (Clin Res Ed) 291 (6500): 935–7. doi:10.1136/bmj.291.6500.935. PMC 1417185. PMID 3929970. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1417185. 
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20. ^ Michel Thomas, "Chapter 31. Treatment of Myocardial Ischemia" (Chapter). Laurence L. Brunton, John S. Lazo, Keith L. Parker: Goodman & Gilman's The Pharmacological Basis of Therapeutic, 11th edition ,http://www.accesspharmacy.com/content.
21. ^ Podrid, P. PathoPathophysiology and clinical presentation of ischemic chest pain. Uptodate Online. Retrieved on April 28, 2010 at: http://www.utdol.com/online/content/topic.do?topicKey=chd/17139&source=preview&selectedTitle=2~150&anchor=H17#H3
22. ^ The Crucial Role of Iron in the Body, http://www.chemistry.wustl.edu/~courses/genchem/Tutorials/Ferritin/IronBody.htm, Retrieved: 2010-4-28
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29. ^ NHS Clinical Knowledge Summaries (2009) Angina - stable: suspected angina Suspected angina Date site accessed: 04/01/2009
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32. ^ ^{a b} Dwivedi, Girish & Dwivedi, Shridhar (2007). History of Medicine: Sushruta – the Clinician – Teacher par Excellence. National Informatics Centre (Government of India).

Further reading

• Information on ACTION - A Coronary Disease Trial Investigating Outcome with Nifedipine GITS in Patients with chronic stable angina pectoris

External links

• British Heart Foundation - Angina
• Angina Pectoris Animation Video 3D