Prostaglandins and heart disease.
The role of prostaglandins (PGs) in cardiac pathophysiology has been reviewed with special emphasis on clinically applied aspects. Several PGs are synthesized and released by the heart and coronary vessels. Their synthesis is altered by various factors such as physical manipulation of tissue, pharmacological treatments and pathological conditions such as myocardial over-reactivity and ischemia. The involvement of PGs in cardiac dysfunction remains controversial, although it has been proposed that various PGs such as PGI2 or PGB2 may play a role in disaggregating platelets, inhibiting thrombus progression and coronary vasodilatation. The balance between thromboxane A2 (TXA2), a proaggregatory agent released from platelets and PGI2 may have a role in the genesis and management of angina and myocardial infarction. The use of non-steroidal anti-inflammatory agents in these conditions remains controversial; their possible beneficial effects are believed to be due to inhibition of TXA2 synthesis whereas their failure to be effective may be a consequence of concomitant inhibition of PGI2 production. Modulation of endogenous PG synthesis and administration of exogenous PGs or their analogues appear to be two therapeutic approaches in the management of certain cardiac diseases. Accordingly, there is a great need for synthesizing stable and potent PG analogues as well as specific inhibitors of PG synthesis in addition to studying their pharmacology and therapeutics. In this review we have emphasized the involvement of PGs in the pathogenesis of some forms of cardiac disease and have highlighted some therapeutic implications of these substances for the treatment of heart disease.
D000787:Angina Pectoris / Q000503:physiopathology; D000789:Angina, Unstable / Q000503:physiopathology; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology; D003326:Coronary Circulation / Q000187:drug effects; D003327:Coronary Disease / Q000503:physiopathology; D003329:Coronary Vasospasm / Q000503:physiopathology; D006330:Heart Defects, Congenital / Q000503:physiopathology; D006331:Heart Diseases / Q000188:drug therapy / Q000503:physiopathology*; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D009203:Myocardial Infarction / Q000503:physiopathology; D010974:Platelet Aggregation / Q000187:drug effects; D011448:Prostaglandin Antagonists / Q000627:therapeutic use; D011453:Prostaglandins / Q000502:physiology*
D011448:Prostaglandin Antagonists; D011453:Prostaglandins