A clinical syndrome due lo myocardial ischemia characterized by episodes of precordial discomfon and pressure, typically precipitated by exertion and relieved by rest or sublingual nitroglycerin.
Angina pectoris is a clinical manifestation of coronary artery disease. The discomfort of angina, which is highly variable, is most commonly felt beneath the sternum. It may be a vague, barely troublesome ache, or il may rapidly become a severe, intense, precordial crushing sensation. Some patients do nol perceive the discomfort as pain.
Angina is usually triggered by physical activity and typically persists for no more than a few minutes, subsiding with rest. Angina is worsened when exertion follows a meal. It is also exaggerated in cold weather. Walking into the wind or first contact with cold air on leaving a warm room may also precipitate an attack. Angina may occur at night (nocturnal angina), which may be ;i sign of recurrent left ventricular failure, ;tn equivalent of nocturnal dyspnea.
Attacks may vary in frequency from several a day lo occasional episodes separated by symptom-free intervals of weeks or months. They may increase in frequency (crescendo angina) to a fatal outcome or may gradually decrease or disappear if an adequate collateral circulation develops, if the ischemic area becomes infarcted, or if heart failure supervenes and limits activity.
Any change in the pattern of symptoms—increased intensity of attacks, decreased threshold of stimulus, longer duration, or occurrence when the patient is sedentary or awakening from sleep—should be viewed as serious. Such changes are termed unstable angina, which may be prodromal to acute myocardial infarction.
Treatment
The treatment of elderly persons wilh angina should begin with an attempt to identify other superimposed and treatable illnesses that may increase myocardial oxygen demand and decrease its supply, such as anemia, infection, hyperthyroidism, and arrhythmias. If any of these conditions are present and treated, the angina may possibly be eliminated.
Pharmacotherapy: The primary drug options are the same for elderly as for younger patients: nitrates, β-blockcrs, and calcium antagonists. Age-associated changes in pharmacokinetics and pharmacodynamics (eg, decreases in serum albumin and lean body mass and increases in cii-acid glycoproteins and body fat) may influence the choice and dose of these drugs. Aging is also associated with a change in the cardiovascular response to certain medications including β-agonisls and digitalis. Older persons are also more likely to be laking other medications that may alter the pharmacokinetics of cardiovascular agents.
Nitrates act primarily by lowering preload through venous dilation, which decreases venous return and hence ventricular cavity size, and to a lesser extern by reducing aflerload through arteriolar dilation. They may also produce coronary vasodilation. Nitroglycerin given sqb-lingually 0.3 to 0.6 nig or as a lingual aerosol spray 0.4 mg provides relief during an acute ischemic episode and is useful for prophylaxis. Unforlunately. the anli-ischemie effect of both oral (20 to 40 mg qid) and topical (5 )o 20 mg/24 h) nitrate preparations is significantly attenuated if the drug is given continuously. This can be ;ivoided by intermittent dosing. Removing Ihc transdermal patch overnight or using oral preparations bid or tid may prevent Ihc development of nitrate tolerance. However, this may leave the patient insufficiently protected between doses.
Preexisting diminished intravascular volume, impaired venous valves, and a diminished barorcceptor reflex make older patients more susceptible (o the hypotensive effecls of nitrates. Thus, it is important lo begin with a low dose, increase the dose slowly, and instruct palients to lie down when they first take any nitrate preparation.
P-Blockers work primarily by reducing myocardial oxygen demand; they decrease heart rate, myocardial contractility, and blood pressure. Secondarily, they increase myocardial oxygen supply through the reduction in hear! rate (since most of the coronary flow occurs during diastole). In addition, propranolol has been shown lo produce a right-ward shift of the oxyhemoglobin dissociation curve, thus increasing release of oxygen to ischemic tissues.
The choice of β-blocker should be based on the drug’s associated properties. Low doses of relatively cardioseleclive drugs (atenolol 50 mg/day or metoprolol 100 mg/day) may be used when blockade of p2-receptors is undesirable. However, the selectivity is only relative because blockade of P2-rcceptors occurs at moderate to high doses. Hy-drophilic β-blockers (atenolol 50 to 200 mg/day or nadolol 40 to 80 mg/day) should be considered when treating patients with hepalic disease or when CNS side effects need to be minimized. Lipophilic β-blockers (propranolol 80 to 240 mg/day, metoprolol 50 to 100 mg bid, or timolol 10 to 20 mg bid) may be preferable in patients with coexisting renal disease.
Secondary prevention is an important additional benefit of some β-blockers. Studies have shown that timolol (20 mgAlay), propranolol UfiO to 240 mg/day), and metoprolol (100 to 200 mg/day) decrease the risk of subsequent infarction and death when given after myocardial infarction.
Because of pharmacodynamic and pharmacokinetic changes (described in Ch. 21), the β-blocking properties of these drugs are diminished in the elderly. The age-related reduction in cardiovascular responsiveness to β-agonist stimulation results in less reliance on catecholamines and more dependence on the Frank-Starling mechanism to increase cardiac work during times of stress (see Chs, 33 and 41). This suggests that β-blockers as anti-ischemic agents may be less effective in elderly than in younger patients.
Preexisting disease, such as bronchospaslic pulmonary disease, claudication, insulin-dependent diabetes mellitus, impaired ventricular function, and conduction system disease, may render the elderly more sensitive to the side effects of β-blockers. Prolonged therapy may result in tip-regulation of cardiac β-receptors and hence produce an increased sensitivity to endogenous catecholamines if β-blockers are abruptly withdrawn. Thus, ^-blockers should be withdrawn slowly, if possible, when therapy is discontinued in angina patients.
Calcium antagonists are useful for treating stable and unstable angina. This group of drugs includes nifedipine 30 lo 120 mg/day. dil-liazem 90 to 360 mg/day, verapamil 120 to 480 mg/day, and the newer dihydropyridines, amlodipinc 5 to 10 mg/day and felodipine 5 to 10 mg/day.
Calcium antagonists act primarily by decreasing coronary and peripheral vascular resistance, although verapamil (and to a considerably less extent, dilliazcm) has negative inotropic and chronotropic effects. These agents exert an anti-ischemic effect (I) by decreasing coronary artery resislancc and preventing spasm, which increases myocardial oxygen supply, and (2) by inducing peripheral vasodilation, which decreases myocardial oxygen demand. They also have antiplatelet properties and an antihypertensive cffecl. which makes them useful in palients wilh coexisting hyperlension.
Because calcium antagonists have a peripheral vasodilating effect, they should be given cautiously to elderly palients. Hypotension can occur with peripheral vasodilation, especially in patients who are volume depleted. A sympalhctic reflex-induced increase in cardiac work may also occur, which can be prevented by the concomitant administration of a relatively small dose of β-blocker. Some calcium antagonists also have negative inotropic, chronotropic, and dromolropic effects, which affect primarily persons with preexisting impaired ventricular function or conduction system disease or those taking fairly high doses of β-blockers. No significant rebound phenomenon appears to occur on withdrawal of calcium antagonists.
Aspirin (325 mg/day) has been shown to reduce by 50% the rate of myocardial infarction and death in patients wilh unstable angina, to provide secondary prevention after myocardial infarction, and to improve patency of saphenous vein grafts after bypass surgery.