Summary:
Current evidence strongly suggests that coronary atherosclerosis is a common denominator in
patients with stable effort angina pectoris. The concept of pathophysiology of coronary atheros-
clerosis is presented - angiographic and pathologic evidence now suggest presence of eccentric
and irregular atherosclerotic lesions (sometimes associated with plaque rupture) and simultane-
ously present endothelial dysfunction increases sensitivity of vascular smooth muscles to physical
and biochemical stimuli with propensity to spasm. Ischemia is due to an increased myocardial
oxygen demand (increased heart rate or blood pressure) that cannot be met because of fixed
coronary reserve.
The organic nitrates are important drugs for the treatment of patients wit angina. The mecha-
nism(s) of their action is presented - biotransformation and liberation of nitric oxide which
stimulates guanylyl cyclase and conversion of GTP (by guanylyl cyclase) to cGMP, which causes
vasodilatation but reduces platelet adhesion and aggregation too. Sublingual nitroglycerin and
isosorbide dinitrate are effective in the treatment of acute episodes of angina. Long-acting nitrate
preparations are effectiveness include intermittent transdermal nitroglycerin, standard formula-
tion and sustained - release isosorbid dinitrate (but better isosorbid-5-mononitrate because of
longer duration of action of action and no 1st pass hepatic metabolism) (nitrate-free interval
should be of 8-10 hours duration). The place of the therapy with betablockers and calcium chan-
nel blockers in angina pectoris is presented as well and their combination with nitrates.
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