Everything about Angina Pectoris totally explained
Angina pectoris, commonly known as
angina, is
chest pain due to
ischemia (a lack of blood and hence
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
Greek ankhon ("strangling") and the
Latin pectus ("chest"), and can therefore be translated as "a strangling feeling in the chest".
It is common to equate severity of angina with risk of fatal cardiac events. There is a weak relationship between severity of pain and degree of oxygen deprivation in the heart muscle (for example 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.
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, jaw, or shoulders. Typical locations for
radiation of 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. It usually lasts for about 1 to 5 minutes, and is relieved by rest or specific anti-angina medication. 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.
Angina may further be classified as stable or unstable angina.
Stable angina 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 resume when activity resumes. In this way, stable angina may be thought of as being similar to claudication symptoms.
Unstable angina 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. 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 lumen of the coronary vessel. This explains why angina appears to be independent to activity.
Diagnosis
In angina patients who are 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 their maximum ability before fatigue, breathlessness or, importantly, pain supervenes; if characteristic ECG changes are documented (typically more than 1 mm of flat or downsloping ST depression), the test is considered diagnostic for 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 that can't exercise enough for the purposes of the treadmill tests, for example, 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 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.
Pathophysiology
Increase in heart rate results in increased oxygen demand by the heart. The heart has a limited ability to increase its oxygen intake during episodes of increased demand. Therefore, an increase in oxygen demand by the heart (eg, during exercise) has to be met by a proportional increase in blood flow to the heart.
Myocardial ischemia can result from:
- a reduction of blood flow to the heart that can be caused by stenosis, spasm, or acute occlusion (by an embolus) of the heart's arteries
- resistance of the blood vessels
- reduced oxygen-carrying capacity of the blood.
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.
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 an increase in age. 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 increase of
smoking,
obesity and other risk factors has already led to an increase in angina and related diseases in countries such as
China.
Treatment
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. An
aspirin (75 mg to 100 mg) per day has been shown to be beneficial for all patients with stable angina that have no problems with its use.
Beta blockers (eg. carvedilol, propranolol,atenolol etc. are some few examples) have a large body of evidence in morbidity and mortality benefits (fewer symptoms and disability and live longer) and short-acting
nitroglycerin medications are used for symptomatic relief of angina.
Calcium channel blockers (such as
nifedipine (Adalat) and
amlodipine),
Isosorbide mononitrate and
nicorandil are vasodilators commonly used in chronic stable angina. A new therapeutic class, called If inhibitor, has recently been made available:
ivabradine provides pure heart rate reduction,. leading to major anti-ischemic and antianginal efficacy.
ACE inhibitors are also vasodilators with both symptomatic and prognostic benefit and lastly,
statins are the most frequently used lipid/cholesterol modifiers which probably also stabilise existing atheromatous plaque.
Surprising perhaps is that exercise is also a very good long term treatment for angina (but only particular regimes - gentle and sustained exercise rather than dangerous intense short bursts), probably working by complex mechanisms such 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.
Ranolazine (Ranexa) is a new class of anti anginal drug that was approved by the Food and Drug Administration (FDA)
Recently, University of Cincinnati medical researchers in cardiology have tried to use a non-invasive, non-surgical collecting tool to gather harvested erythropoietic bone marrow-based adult stem cells and coax them into regrowing new coronary blood vessels to supply the cardiac muscle's cells (cardiac myocytes) with oxygenated blood, with some success- leading to larger Phase 2 trials.
The largest randomised trial of an anti-anginal drug to date is the ACTION trial. It included 7,665 patients with stable angina pectoris. ACTION demonstrated that the calcium channel blocker nifedipine (Adalat) prolongs cardiovascular event- and procedure-free survival in patients with coronary artery disease. For example new overt heart failures were reduced by 29% compared to placebo. This finding confirms the vascular-protective effects of nifedipine.
Further Information
Get more info on 'Angina Pectoris'.
|
External Link Exchanges
Do you know how hard it is to get a link from a large encyclopaedia? Well we're different and will prove it. To get a link from us just add the following HTML to your site on a relevant page:
<a href="http://angina_pectoris.totallyexplained.com">Angina pectoris Totally Explained</a>
Then simply click through this link from your web page. Our crawlers will verify your link, extract the title of your web page and instantly add a link back to it. If you like you can remove the words Totally Explained and embed the link in article text.
As long as your link remains in place, we'll keep our link to you right here. Please play fair - our crawlers are watching. Your site must be closely related to this one's topic. Any kind of spamming, dubious practises or removing the link will result in your link from us being dropped and, potentially, your whole site being banned. |
