A 56-year-old woman presents in the office with a history of recent-onset chest discomfort when jogging or swimming vigorously*. The pain is dull but poorly localized; it disappears after 5–10 minutes of rest. She has never smoked but has a history of hyperlipidemia (total cholesterol level of 245 mg/dL and low-density lipoprotein [LDL] of 160 mg/dL recorded 1 year ago) and admits that she has not been following the recommended diet. 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 80 bpm. She is in no acute distress, and there are no other significant physical findings; an electrocardiogram is normal except for slight left ventricular hypertrophy. Assuming that a diagnosis of stable effort angina is correct, what medical 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 a 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. The resulting ischemia with accumulation of acidic metabolites usually leads to pain. ...