What is preferable in unstable angina, beta-blockade or calcium-inhibition?
Nifedipine is a strong calcium antagonist; it blocks the excitation-contraction coupling, yet at therapeutic dosage levels it has few side effects. It is said that a single molecule of nifedipine can neutralize the effects of several thousand calcium ions in the excitation-process. Thus this agent reduces the ability of the cardiac cells to develop mechanical tension yet it does not affect electrical excitation. Calcium antagonists are also potent dilators, particularly of the arteries on the periphery of the human body and in the coronary arterial system. The basic mode of action is thought to be the same, i.e. reduction of the calcium transport, this time into the smooth muscle cells of the arterial wall, thus "forcing' the arteriole to dilate. The resultant action is a reduction in afterload, while there is an increase in perfusion of the coronary vascular bed. Thus there is a dual action, the one centrally, the other peripherally both of which will be particularly effective in patients with unstable angina (UA) in whom excess coronary vascular tone is suspected. Beta-blockers, particularly propranolol and metoprolol, with which we have the most experience, work via beta 2 adrenoceptor blockade in the heart. Cardiac frequency decreases, arrhythmias are suppressed, blood pressure may decrease, all reducing cardiac work. If in UA variations in coronary vascular tone and frank spasm do occur then is would be more logical to use Ca-antagonists instead of beta-blockade. Our clinical experience to date has not shown that patients with UA are worsened by propranolol or metoprolol but there are scores of clinical reports showing worsening of chest pain in Prinzmetal's syndrome, presumably because beta-blockade leads to excessive alpha-adrenergic vascular tone. On the other hand, in one year experience with 73 patients with UA, 52 did not experience relief from adequate beta-blockade until nifedipine was added. Within 2 hours, 42 of the 52 became asymptomatic--thus indicating that in UA the need for spasmolytic therapy prevails over the need for beta-blockade. In many cases of UA both drugs may have a place however, their exact relative value remains to be established.
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D000368:Aged; D000787:Angina Pectoris / Q000188:drug therapy* / Q000209:etiology; D000818:Animals; D002121:Calcium Channel Blockers / Q000627:therapeutic use*; D003327:Coronary Disease / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology; D006801:Humans; D008297:Male; D009543:Nifedipine / Q000627:therapeutic use; D005996:Nitroglycerin / Q000627:therapeutic use; D011433:Propranolol / Q000009:adverse effects / Q000627:therapeutic use; D013552:Swine; D014655:Vascular Resistance / Q000187:drug effects; D014700:Verapamil / Q000009:adverse effects / Q000627:therapeutic use
D000319:Adrenergic beta-Antagonists; D002121:Calcium Channel Blockers; D011433:Propranolol; D014700:Verapamil; D005996:Nitroglycerin; D009543:Nifedipine