Angina pectoris agents

Other agents are also used for the treatment of manic-depressive disorders based on preliminary clinical results (177). The antiepileptic carbamazepine [298-46-4] has been reported in some clinical studies to be therapeutically beneficial in mild-to-moderate manic depression. Carbamazepine treatment is used especially in bipolar patients intolerant to lithium or nonresponders. A majority of Hthium-resistant, rapidly cycling manic-depressive patients were reported in one study to improve on carbamazepine (178). Carbamazepine blocks noradrenaline reuptake and inhibits noradrenaline exocytosis. The main adverse events are those found commonly with antiepileptics, ie, vigilance problems, nystagmus, ataxia, and anemia, in addition to nausea, diarrhea, or constipation. Carbamazepine can be used in combination with lithium. Several clinical studies report that the calcium channel blocker verapamil [52-53-9] registered for angina pectoris and supraventricular arrhythmias, may also be effective in the treatment of acute mania. Its use as a mood stabilizer may be unrelated to its calcium-blocking properties. Verapamil also decreases the activity of several neurotransmitters. Severe manic depression is often treated with antipsychotics or benzodiazepine anxiolytics. 

Other P"Adrenoceptor Blocking Agents. Carteolol hydrochloride (Table 1) is also a Class II antiarrhythmic agent. In three separate studies in patients having angina pectoris, carteolol was considered effective as evidenced by a reduction in the frequency and severity of anginal episodes, reduction in the amount of nitroglycerin consumed, improvement of ECG parameters, or an increase in the duration of trea dmill exercise (42). 

The therapeutic use of these agents is in control of cardiac arrhythmias, angina pectoris, and in essential and renovascular hypertension. The various ancillary activities lead to side effects and much... 

The mechanism by which organic nitrates relieve the pain of angina pectoris was not discovered until nitric oxide was identified as the agent which was responsible for vasodilation of arteries. It was known for many years that endothelial cells released a factor that resulted in vasodilation a factor appropriately called endothelial relaxing factor (EDRF). It was, however, some time before the factor was identified, probably because it turned out to be a gas - nitric oxide - which was totally unexpected. Nitric oxide is now known to be a very important messenger molecule involved in the regulation of many other systems. The mechanism by which it causes vasodilation is described in Chapter 13. 

Uses. Manufacture of dynamite, gun powder and rocket propellants, and as a therapeutic agent primarily to alleviate angina pectoris. Note Workers engaged in the production or use of dynamite are potentially exposed to mixed vapors of nitroglycerin (NG) and ethylene glycol dinitrate (EGDN). 

Minoxidil may produce serious adverse effects. It can cause pericardial effusion, occasionally progressing to tamponade it can exacerbate angina pectoris. Reserve for hypertensive patients who do not respond adequately to maximum therapeutic doses of a diuretic and 2 other antihypertensive agents. 

The 3-receptor blocking agents have widespread and important uses in the management of cardiac arrhythmias, angina pectoris, and hypertension. Their uses in these conditions are reviewed in Chapters 16, 17, and 20, respectively. Even though acute administration of 3-blockers can precipitate congestive heart failure in patients who are largely dependent on enhanced sym-... 

Verapamil (Isoptin, Covera), in addition to its use as an antiarrhythmic agent, has been employed extensively in the management of variant (Prinzmetal s) angina and effort-induced angina pectoris (see Chapters 17 and 19). It selectively inhibits the voltage-gated calcium channel that is vital for action potential genesis in slow-response myocytes, such as those found in the sinoatrial and A-V nodes. 

Oral minoxidil is a potent agent which has significant side effects including pericardial effusion leading to tamponade and angina pectoris. 

Another cardioselective beta, blocking agent devoid of intrinsic sympathomimetic activity given once daily in the treatment of hypertension and angina pectoris. 

Grines, C.L., M.W. Watkins, G. Helmer, W. Penny, J. Brinker, ID. Marmur, A. West, II Rade, P. Marrott, H.K. Hammond, and R.L. Engler, Angiogenic Gene Therapy (AGENT) trial in patients with stable angina pectoris. Circulation, 2002.105(11) 1291-7. 

Chapter 12 Vasodilators the Treatment of Angina Pectoris Chapter 13 Drugs Used in Heart Failure Chapter 14 Agents Used in Cardiac Arrhythmias Chapter 15 Diuretic Agents... 

The calcium channel blockers currently used to treat angina pectoris are listed in Table 22-3. Although the chemistry and exact mechanism of action of each drug are somewhat distinct, all of these agents exert their effects by limiting calcium entry into specific cardiovascular tissues. Certain calcium channel blockers are said to be selective if they affect vascular smooth muscle, but have little or no affect on the heart. Nonselective calcium channel blockers affect the vasculature and inhibit calcium entry into cardiac muscle cells. Individual agents are discussed below. 

In addition to their antianginal (see Chapter 12 Vasodilators the Treatment of Angina Pectoris) and antiarrhythmic effects (see Chapter 14 Agents Used in Cardiac Arrhythmias), calcium channel blockers also dilate peripheral arterioles and reduce blood pressure. The mechanism of action in hypertension (and, in part, in angina) is inhibition of calcium influx into arterial smooth muscle cells. 

---