PubMed · 3384233
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G F Buja, R Scognamiglio, G Boffa, D Danieli, I Maragno. 1988. [A clinical case].. https://pubmed.ncbi.nlm.nih.gov/3384233/
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BACKGROUND: Estrogen has an antioxidant potential which may contribute to its cardioprotective effect. We sought to determine whether estrogen administration can affect coronary vasomotor tone in patients after angioplasty by reducing 8-iso-prostaglandin (PG) F(2alpha) concentrations, a bioactive product of lipid peroxidation. METHODS: The study was designed to prospectively investigate 30 consecutive patients scheduled for elective coronary angioplasty. Patients were randomized into two groups according to whether they did not (group 1, n = 15) or did have (group 2, n = 15) intracoronary (i.c.) treatment with estrogen prior to coronary angioplasty. RESULTS: There were no significant differences of collateral circulation assessed by intracoronary Doppler flow velocity during balloon inflations between the study groups. The diameters of the coronary artery at the dilated and distal segments were significantly reduced 15 min after dilation compared with those immediately after dilation in group 1 (both P < 0.0001). The vasoconstriction was significantly blunted in group 2. The 8-iso-PGF(2alpha) levels in plasma from the coronary sinus rose significantly from 194 +/- 45 to 390 +/- 97 pg/ml (P < 0.0001, 95% confidence intervals = 142-249 pg/ml) 15 min after angioplasty in group 1, which was attenuated after administering estrogen. Significant correlation was found between the changes of coronary vasomotion of the dilated segment and 8-iso-PGF(2alpha) levels in group 1 (r = 0.73, P = 0.002). CONCLUSIONS: 8-iso-PGF(2alpha) is released into the coronary circulation during angioplasty, and this vasoactive substance may contribute to the occurrence of vasoconstriction. Estrogen administration attenuated vasoconstriction by reducing the 8-iso-PGF(2alpha) levels. This finding may provide a new strategy to treat coronary vasoconstriction after angioplasty.
Angiotensin-converting enzyme inhibition is not an effective antianginal therapy. Experimental data suggest that broader vasopeptidase inhibition may decrease the magnitude of demand-induced myocardial ischemia. A randomized, double-blind, placebo controlled parallel study evaluated omapatrilat, an inhibitor of angiotensin-converting enzyme and neutral endopeptidase. The primary objective was to compare maximum duration of exercise at peak plasma concentrations. Exercise treadmill studies were performed in 348 patients who had chronic angina at baseline and after 4 weeks of therapy with 80 mg/day omapatrilat or placebo. Safety data were collected and reported for all patients. Treadmill exercise duration at peak was significantly prolonged in the omapatrilat group compared with the placebo group (76.6 +/- 84.2 vs 28.7 +/- 82.2 seconds difference from baseline, p <0.001). Similar statistically significant increases were seen in time to onset of level III/IV angina and time to onset of >/=0.1-mV ST-segment depression (p <0.001). The significant improvements in exercise duration and measurements of myocardial ischemia were not sustained 20 to 28 hours after dosing. Omapatrilat was generally well tolerated in this predominantly normotensive population. The incidence of serious adverse events was 5.2% in the 2 groups. Thus, omapatrilat, an investigational vasopeptidase inhibitor, is effective in prolonging exercise duration and parameters of demand-induced myocardial ischemia in patients who have chronic angina at peak concentrations. The data confirm the proof of principle that broader vasopeptidase inhibition beyond angiotensin-converting enzyme inhibition is required to alleviate symptoms of chronic angina.
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