Angina Pectoris

Angina pectoris, commonly known as angina, is severe chest pain due to ischemia (a lack of blood, hence a lack of oxygen supply) of the heart muscle, generally due to obstruction or spasm of the coronary arteries (the heart's blood vessels). The term derives from the Latin angina ("infection of the throat") from the Greek ἀγχόνη ankhone ("strangling"), and the Latin pectus ("chest"), and can therefore be translated as "a strangling feeling in the chest".

Angina pectoris may be classified as either

• Stable
• Unstablle

Stable angina (induced by effort, relieved by rest)

Stable angina(also known as effort angina ) is the most common angina, and the type most people mean when they refer to angina. 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

Unstable angina (also "crescendo angina;") is less common. Angina symptoms are unpredictable and often occur at rest. Therefore it may be a serious indicator of an impending heart attack.

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 previously).

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. 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.Studies show that 64% of all unstable anginas occur between 10 PM and 8 AM when patients are at rest.

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.

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.

Signs and Symptoms

Angina itself is a symptom (or set of symptoms), not a disease. Any of the following may signal angina:

• An uncomfortable pressure, fullness, squeezing, or pain in the center of the chest
  
• It may also feel like tightness, burning, or a heavy weight.
  
• The pain may spread to the shoulders, neck, or arms.
  
• It may be located in the upper abdomen, back, or jaw.
  
• The pain may be of any intensity from mild to severe.

• Shortness of breath
  
• Lightheadedness
  
• Fainting
  
• Anxiety or nervousness
  
• Sweating or cold, sweaty skin
  
• Nausea
  
• Rapid or irregular heart beat
  
• Pallor (pale skin)
  
• Feeling of impending doom

Treatment

As with many other conditions, the way angina is treated depends on how severe it is. 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. 

• Nitroglycerin medications have been used since 1879 for symptomatic relief of angina. It is a potent vasodilator that makes more oxygen available to the heart muscle.

• Calcium channel blockers -such as nifedipine (Adalat) and amlodipine), isosorbide mononitrate and nicorandil are vasodilators commonly used in chronic stable angina. They reduce transmembrane flux of calcium via calcium channels. Cause smooth muscle relaxation, resulting in peripheral arterial vasodilation and afterload reduction. Indicated when symptoms persist despite treatment with beta-blockers or when beta-blockers are contraindicated. Also indicated in patients with Prinzmetal angina with or without nitrates.

• Beta blockers (e.g., carvedilol, propranolol, atenolol). Work by competing with endogenous catecholamines for beta-adrenergic receptors. Reduce myocardial oxygen consumption via several effects, including decrease in resting and exercise heart rates and reductions in myocardial contractility and afterload. Classified as nonselective, beta-1 selective, and having intrinsic sympathomimetic effects.
• ACE inhibitors are also vasodilators with both symptomatic and prognostic benefit. Angiotensin-converting enzyme (ACE) Inhibitors have been shown to reduce rates of death, MI, stroke, and need for revascularization procedures in patients with coronary artery disease or diabetes mellitus and at least oneother cardiovascular risk factor, irrespective of the presence of hypertension or heart failure. The 2009 Canadian Hypertension Education Program recommends  beta-blockers and ACE inhibitors as first-line therapy that patients with angina, recent myocardial infarction or heart failure.
• Anti Platelet Agents- Prevent thrombus formation by inhibiting platelet aggregation. Aspirin is proven beneficial in primary and secondary prevention of coronary artery disease. In patients with aspirin intolerance, use clopidogrel. Clopidogrel is also used in combination with aspirin after coronary stent placement. Recently, clopidogrel use in addition to aspirin has been shown to be significantly superior to aspirin alone in patients with acute coronary syndrome without ST-segment elevation MI.

Apart from medical intervention, some other surgical manipulations may also be recommended. These include:

• balloon angioplasty
• Stents (to maintain the arterial widening are often used)

• Coronary bypass surgery ( bypassing constricted arteries with venous grafts)
• Enhanced external counterpulsation (EECP)-works by stimulating blood vessels to literally branch out thereby creating a natural bypass that circumvents the clogged arteries