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 exploit two main strategies: reduction of oxygen demand and increase of oxygen delivery to the myocardium.
|Angina of effort, classic angina, atherosclerotic angina||Angina pectoris (crushing, strangling chest pain) that is precipitated by exertion|
|Vasospastic angina, variant angina, Prinzmetal's angina||Angina precipitated by reversible spasm of coronary vessels, often at rest|
|Coronary vasodilator||Older, incorrect name for drugs useful in angina; some potent coronary vasodilators are ineffective in angina|
|"Monday disease"||Industrial disease caused by chronic exposure to vasodilating concentrations of organic nitrates in the workplace; characterized by headache, dizziness, and tachycardia on return to work after 2 days absence|
|Nitrate tolerance, tachyphylaxis||Loss of effect of a nitrate vasodilator when exposure is prolonged beyond 10–12 h|
|Unstable angina||Rapidly progressing increase in frequency and severity of anginal attacks; an acute coronary syndrome that often heralds imminent myocardial infarction|
|Preload||Filling pressure of the heart, dependent on venous tone and blood volume; determines end-diastolic fiber length and tension|
|Afterload||Impedance to ejection of stroke volume; determined by arterial blood pressure and arterial stiffness; determines systolic fiber tension|
|Intramyocardial fiber tension||Force exerted by myocardial fibers, especially ventricular fibers at any given time; a primary determinant of O2 requirement|
|Double product||The product of heart rate and systolic blood pressure; an estimate of cardiac work|
|Myocardial revascularization||Mechanical intervention to improve O2 delivery to the myocardium by angioplasty or bypass grafting|
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 acidic metabolites and ischemic changes that stimulate myocardial pain endings. Rest usually leads to complete relief of the pain within 15 min. Atherosclerotic angina constitutes about 90% of angina cases.
Vasospastic angina, also known as rest angina, variant angina, or Prinzmetal's angina, is responsible for less than 10% of 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.
A third type of angina—unstable or crescendo angina, also known as 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, ...