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Angina pectoris refers to a strangling or pressure-like pain caused by cardiac ischemia. The pain is usually located substernally but is sometimes perceived in the neck, shoulder and arm, or epigastrium. Women develop angina at a later age than men and are less likely to have classic substernal pain. Drugs used in angina utilize two main strategies: reduction of oxygen demand and increase of oxygen delivery to the myocardium.
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PATHOPHYSIOLOGY OF ANGINA
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1. Atherosclerotic angina
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Atherosclerotic angina is also known as angina of effort or classic angina. It is associated with atheromatous plaques that partially occlude one or more coronary arteries. When cardiac work increases (eg, in exercise), the obstruction of flow and inadequate oxygen delivery results in the accumulation of metabolites, for example, lactic acid, and ischemic changes that stimulate myocardial pain endings. Rest, by reducing cardiac work, usually leads to complete relief of the pain within 15 min. Atherosclerotic angina constitutes about 90% of angina cases.
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2. Vasospastic angina
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Vasospastic angina, also known as rest angina, variant angina, or Prinzmetal angina, is responsible for less than 10% of angina cases. It involves reversible spasm of coronaries, usually at the site of an atherosclerotic plaque. Spasm may occur at any time, even during sleep. Vasospastic angina may deteriorate into unstable angina.
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A third type of angina—unstable or crescendo angina, one manifestation of acute coronary syndrome—is characterized by increased frequency and severity of attacks that result from a combination of atherosclerotic plaques, platelet aggregation at fractured plaques, and vasospasm. Unstable angina is thought to be the immediate precursor of a myocardial infarction and is treated as a medical emergency.
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