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 (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 & Symptoms:
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.
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.
Treatment:
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 (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 & Symptoms:
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.
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.
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.
Ranolazine (Ranexa) is a new class of anti anginal drug that was approved by the Food and Drug Administration (FDA).
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