Angina pectoris effort

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. 

Toyosaki N, Toyo-oka T, Natsume T, Katsuki T, Tateishi T, Yaginuma T, Hosoda S. Combination therapy with diltiazem and nifedipine in patients with effort angina pectoris. Circulation 1988 77(6) 1370-5. 

Ruzyllo, W, Tendera, M., Eord, I., Fox, K. M. Antianginal efficacy and safety of ivabradine compared with amlodipine in patients with stable effort angina pectoris a 3-month randomised, double-blind, multicentre, noninferiority trial. Drugs 2007, 67, 393 05. 

Dipyridamole is a potent coronary vasodilator. Despite the fact that it causes a substantial increase in CBF, its value for the acute relief or prevention of angina pectoris has been seriously questioned. Considerable effort has been expended in the study of this drug. Deutllcke reports dipyridamole to inhibit adenosine deaminase which results in an accumulation of adenosine. Since adenosine is a potent vasodilator, there is an increase in CBF. Emmons found dipyridamole to inhibit platelet agglutination and proposed that dipyridamole prevents the uptake of adenosine by red blood cells, thereby delaying its deamination. Stafford feels that dipyridamole inhibition of adenosine deaminase is unlikely, as high concentrations are necessary to produce inhibition of deaminase from intestinal mucosa. Much lower concentrations of dipyridamole potentiate the action of adenosine on myocardial tissue. Stafford proposes that dipyridamole prevents the uptake of adenosine by myocardial tissue or red blood... 

Angina of effort, ciassic angina, atheroscierotic angina Angina pectoris (crushing, strangling chest pain) that is precipitated by exertion and caused by increased Oj demand that cannot be met because of irreversible atherosclerotic obstruction of coronary arteries... 

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