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A 67-year-old woman presents in the emergency department of a small rural hospital with a history of chest pain and shortness of breath while watching television. While nasal oxygen is administered and an ECG is recorded, blood is drawn for high-sensitivity troponin measurement. Her husband provides the history that she has a history of exercise-induced angina pectoris and has taken nitroglycerin for relief in the past. Two doses of nitroglycerin have not relieved her pain on this occasion. She smokes and has a history of hyperlipidemia with elevated “bad cholesterol” (low-density lipoprotein [LDL]) and hypertension. Her father survived a “heart attack” at age 55, and an uncle died of some cardiac disease at age 60. On physical examination, the patient’s blood pressure is 145/90 mm Hg, and her heart rate is 100 bpm. The ECG shows no ST elevation, but ST depression is present in several leads. Assuming that a dioagnosis of acute coronary syndrome (ACS) is correct, what treatment should be implemented?

Ischemic heart disease is one of the most common cardiovascular diseases in developed countries, and angina pectoris is the most common condition involving tissue ischemia in which vasodilator drugs are used. The name angina pectoris denotes chest pain caused by accumulation of metabolites resulting from myocardial ischemia. The organic nitrates, eg, nitroglycerin, are the mainstay of therapy for the immediate relief of angina. Another group of vasodilators, the calcium channel blockers, is also important, especially for prophylaxis, and β blockers, which are not vasodilators, are also useful in prophylaxis. Several newer drugs are available, including drugs that alter myocardial ion currents and selective cardiac rate inhibitors.

The most common cause of angina is atheromatous obstruction of the large coronary vessels (coronary artery disease, CAD). Inadequate blood flow in the presence of CAD results in effort angina, also known as classic angina. Diagnosis is usually made on the basis of the history and stress testing, sometimes supplemented by coronary angiography. Some patients have typical symptoms of angina in spite of normal epicardial coronary vessels. Previously labeled “coronary syndrome X,” this condition is coronary microvascular dysfunction. Both types of angina are associated with diminished coronary fractional flow reserve, the fractional increase in coronary flow that can be achieved by maximal coronary dilation.

Transient spasm of localized portions of these vessels, usually associated with underlying atheromas, can also cause significant myocardial ischemia and pain (vasospastic or variant angina). Vasospastic angina is also called Prinzmetal angina. Diagnosis is usually made on the basis of history but can be confirmed by tests that provoke temporary spasm.

The primary cause of angina pectoris is an imbalance between the oxygen requirement of the heart and the oxygen supplied to it via the coronary vessels. In effort angina, the imbalance occurs when the myocardial oxygen requirement increases, especially during exercise, and coronary blood flow does not increase proportionately. ...

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