RE-EVALUATION OF THE MECHANISM AND TREATMENT OF ANGINA DECUBITUS

patients with angina decubitus (AD) were studied during hospitalization. These patients were found to have severe coronary artery obstructive lesions and an increase of myocardial oxygen consumption (MOC) before the onset to AD, indicating that AD belongs to the category of effort angina.18 patients were investigated by continuous hemodynamic monitoring. Three patients had significant increase in pulmonary artery diastolic pressure (PADP) before the onset. In the other 15 patients. PADP increased slightly in 12 and remained unchanged in 3 cases before the onset. Left ventriculography showed ejection fraction (EF)>45% in 25 of the 27 patients. These results indicate that left ventricular (LV) systolic dysfunction is not a major factor in the Pathogenesis of AD. The patients with LVEDP>12 mmHg constituted 60% of 25 patients with EF>45%, suggesting that these patients had ohvious LV diastolic dysfunction, which may be the major factor in the pathogenesis of AD.According to the results of our treatment, beta blockers may be used as the major form of tteatment in the patients with AD.

Pathogenesis of NSAID-induced gastric damage:Importance of cyclooxygenase inhibition and gastric hypermotility

This article reviews the pathogenic mechanism of nonsteroidal anti-inflammatory drug(NSAID)-induced gastric damage,focusing on the relation between cyclooxygenase(COX) inhibition and various functional events.NSAIDs,such as indomethacin,at a dose that inhibits prostaglandin(PG) production,enhance gastric motility,resulting in an increase in mucosal permeability,neutrophil infiltration and oxyradical production,and eventually producing gastric lesions.These lesions are prevented by pretreatment with PGE 2 and antisecretory drugs,and also via an atropine-sensitive mechanism,not related to antisecretory action.Although neither rofecoxib(a selective COX-2 inhibitor) nor SC-560(a selective COX-1 inhibitor) alone damages the stomach,the combined administration of these drugs provokes gastric lesions.SC-560,but not rofecoxib,decreases prostaglandin E 2(PGE 2) production and causes gastric hypermotility and an increase in mucosal permeability.COX-2 mRNA is expressed in the stomach after administration of indomethacin and SC-560 but not rofecoxib.The up-regulation of indomethacin-induced COX-2 expression is prevented by atropine at a dose that inhibits gastric hypermotility.In addition,selective COX-2 inhibitors have deleterious influences on the stomach when COX-2 is overexpressed under various conditions,including adrenalectomy,arthritis,and Helicobacter pylori-infection.In summary,gastric hypermotility plays a primary role in the pathogenesis of NSAID-induced gastric damage,and the response,causally related with PG deficiency due to COX-1 inhibition,occurs prior to other pathogenic events such as increased mucosal permeability;and the ulcerogenic properties of NSAIDs require the inhibition of both COX-1 and COX-2,the inhibition of COX-1 upregulates COX-2 expression in association with gastric hypermotility,and PGs produced by COX-2 counteract the deleterious effect of COX-1 inhibition.