6-ketoprostaglandin-f1-alpha and Angina-Pectoris

Mechanisms responsible for anti-ischemic benefits of enhanced external counterpulsation (EECP) remain unknown. This was the first randomized sham-controlled study to investigate the extracardiac effects of EECP on peripheral artery flow-mediated dilation.. Forty-two symptomatic patients with coronary artery disease were randomized (2:1 ratio) to thirty-five 1-hour sessions of either EECP (n=28) or sham EECP (n=14). Flow-mediated dilation of the brachial and femoral arteries was performed with the use of ultrasound. Plasma levels of nitrate and nitrite, 6-keto-prostaglandin F(1α), endothelin-1, asymmetrical dimethylarginine, tumor necrosis factor-α, monocyte chemoattractant protein-1, soluble vascular cell adhesion molecule, high-sensitivity C-reactive protein, and 8-isoprostane were measured. EECP increased brachial (+51% versus +2%) and femoral (+30% versus +3%) artery flow-mediated dilation, the nitric oxide turnover/production markers nitrate and nitrite (+36% versus +2%), and 6-keto-prostaglandin F(1α) (+71% versus +1%), whereas it decreased endothelin-1 (-25% versus +5%) and the nitric oxide synthase inhibitor asymmetrical dimethylarginine (-28% versus +0.2%) in treatment versus sham groups, respectively (all P<0.05). EECP decreased the proinflammatory cytokines tumor necrosis factor-α (-16% versus +12%), monocyte chemoattractant protein-1 (-13% versus +0.2%), soluble vascular cell adhesion molecule-1 (-6% versus +1%), high-sensitivity C-reactive protein (-32% versus +5%), and the lipid peroxidation marker 8-isoprostane (-21% versus +1.3%) in treatment versus sham groups, respectively (all P<0.05). EECP reduced angina classification (-62% versus 0%; P<0.001) in treatment versus sham groups, respectively.. Our findings provide novel mechanistic evidence that EECP has a beneficial effect on peripheral artery flow-mediated dilation and endothelial-derived vasoactive agents in patients with symptomatic coronary artery disease.

Topics: 6-Ketoprostaglandin F1 alpha; Aged; Angina Pectoris; Blood Pressure; Brachial Artery; C-Reactive Protein; Chronic Disease; Counterpulsation; Cytokines; Endothelin-1; Exercise Tolerance; Femoral Artery; Humans; Middle Aged; Nitric Oxide; Oxygen Consumption; Regional Blood Flow; Tumor Necrosis Factor-alpha; Vasodilation

We assessed the production of eicosanoids and the effects of very low dose aspirin in patients with stable angina under basal conditions and during rapid atrial pacing.. Platelet activation occurs in acute ischemic syndromes but is still controversial in stable angina. Very low dose aspirin is known to be platelet selective and can be used to test the hypothesis of the platelet origin of increased thromboxane production in stable angina.. Urinary excretion of eicosanoids was measured in 42 patients, including 24 patients with and 18 patients without coronary artery disease. The effects of 50 mg/day of aspirin were measured at rest and during pacing-induced ischemia in 10 patients with stable angina and were compared with a similar group of patients not treated by aspirin.. Excretion of 11-dehydro-thromboxane B2 was 2.6 times higher in patients with stable angina than in healthy subjects (mean [+/- SEM] 74.8 +/- 13.0 [24 patients] vs. 29.0 +/- 5.4 [18 patients] ng/mmol of creatinine, p < 0.01). Urinary prostacyclin metabolite levels did not differ between the two groups. Treatment for 8 days with 50 mg/day of aspirin inhibited platelet cyclooxygenase, as reflected by the 97% reduction of in vitro serum thromboxane production. This aspirin regimen normalized the level of urinary thromboxane metabolites in patients with angina (17.3 +/- 3.4 ng/mmol of creatinine [10 patients], p < 0.001 from baseline level before treatment) and did not change prostacyclin metabolite levels. Atrial pacing in patients with angina not treated with aspirin caused lactate and thromboxane release into the coronary sinus. In patients with very low dose aspirin therapy, pacing did not cause thromboxane release despite inducing myocardial ischemia. However, fractional lactate extraction decreased less sharply in patients with than without aspirin therapy.. Thromboxane production is greatly increased in patients with stable angina. Very low dose aspirin administered to these patients reduces thromboxane synthesis to normal levels, preserves prostacyclin biosynthesis and prevents acute thromboxane release into the coronary circulation during pacing-induced ischemia. Our data suggest that platelets (not monocytes/macrophages) are activated in stable angina to produce thromboxane.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Analysis of Variance; Angina Pectoris; Aspirin; Cardiac Pacing, Artificial; Dose-Response Relationship, Drug; Humans; Lactates; Middle Aged; Physical Exertion; Thromboxanes

To investigate the effects of bepridil on silent myocardial ischemia and on eicosanoid metabolism, 10 patients with chronic stable angina underwent exercise treadmill testing and 48-hour ambulatory electrocardiographic monitoring both before and after 4 weeks of bepridil administration (150 mg/day). Fasting venous levels of thromboxane B2, 6-keto-prostaglandin F1 alpha, and leukotriene C4 were measured by radioimmunoassay. Bepridil decreased heart rate responses to daily activities during ambulatory monitoring, and significantly (p < 0.05) reduced the median frequency and duration of silent myocardial ischemic episodes (from 5.5 to 0 events/48 hours and from 86 to 0 minutes/48 hours respectively). Bepridil significantly decreased the blood pressure heart rate product at peak exercise and significantly prolonged the mean exercise tolerance time (from 456.6 to 527.0 second). Bepridil also significantly decreased the plasma levels of thromboxane B2 and leukotriene C4 at rest. These results suggest that bepridil may reduce silent myocardial ischemic episodes either by the reduction of cardiac oxygen demand during daily activities and exercise stress, or by controlling coronary and systemic vasomotor tone. The drug also has a salutary effect on eicosanoid metabolism, to which its efficacy on silent myocardial ischemic episodes may be related.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; Angina Pectoris; Arachidonic Acids; Bepridil; Chronic Disease; Electrocardiography, Ambulatory; Exercise Test; Female; Heart Rate; Humans; Leukotriene C4; Male; Middle Aged; Myocardial Infarction; Myocardial Ischemia; Radioimmunoassay; Single-Blind Method; Thromboxane B2

55 cases of Qi-deficiency and Blood-Stasis syndrome of coronary heart disease (CHD) and angina pectoris (AP) were divided randomly into two groups. Qi Xue granule (QXG) was administered to 30 cases of treated group, while compound Salvia tablet (CST) was administered to 25 cases of control group. Besides, both group were also given one placebo tablet or granule so as to eliminate the patient's psychological effects.. (1) Effects on clinical symptoms: Total effective rate for AP: 90% in QXG group, marked effective rate and effective rate for ischemic ECG changes were 30% and 46.6% respectively. All of these were better than that of CST group significantly (P < 0.05). Besides, QXG group could alleviate symptoms including asthenia. (2) Effects on submaximal paddle work load test: QXG group could prolong the capacity of exercise (from 336.2 +/- 34.7 to 437.5 +/- 43.8 seconds, P < 0.05), magnify the work load (from 73 +/- 7.18 to 94 +/- 8.5 W, P < 0.05) and elevate the ST segment (from 0.218 +/- 0.03 to 0.176 +/- 0.03 mV) significantly in comparison with CST group, which had little change only. (3) Effects on plasma TXB2, 6-keto-PGF1 alpha (6 Kp) level and ration of TXB2/6Kp in 10 normal subjects were 165 +/- 12.1 pg/ml, 142.6 +/- 17.4 pg/ml and 1.16 +/- 0.19 pg/ml respectively, while in 36 cases AP were 390.6 +/- 14.3, 106.0 +/- 7.9 and 3.67 +/- 0.85 pg/ml respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: 6-Ketoprostaglandin F1 alpha; Aged; Angina Pectoris; Drugs, Chinese Herbal; Exercise Tolerance; Female; Humans; Male; Medicine, Chinese Traditional; Middle Aged; Panax; Phytotherapy; Plants, Medicinal; Syndrome; Thromboxane B2; Yang Deficiency

Plasma bradykinin and prostaglandin metabolism are related to the anginal pain modulating system in patients with ischemic heart disease. We carried out a placebo controlled single blind test of diltiazem (30 mg three times a day) in 15 patients with chronic stable angina. The effect of diltiazem was evaluated by exercise treadmill testing and 48-h ambulatory electrocardiographic monitoring. Plasma bradykinin, thromboxane B2, and 6-keto-prostaglandin F1 alpha levels were determined by radioimmunoassay prior to and during diltiazem therapy. Diltiazem significantly increased the exercise time and reduced episodes of angina. Diltiazem, however, did not appreciably improve either the frequency of silent myocardial ischemic episodes or the total duration of the silent myocardial ischemic episodes. Diltiazem also tended to decrease plasma bradykinin, thromboxane B2, and 6-keto-prostaglandin F1 alpha levels. When ischemic episodes on ambulatory electrocardiographic monitoring are categorized according to heart rate change at the onset of episode (type A, preceded by heart rate increase > or = 5 beats/min; type B, no preceding heart rate increase), diltiazem was only effective on type A ischemic episodes as well as on symptomatic ischemia. Further, bradykinin was significantly decreased by diltiazem only in patients with exercise-induced silent ischemia or no exercise-induced ischemia, while the thromboxane B2/6-keto-prostaglandin F1 alpha ratio was unaffected by the administration of diltiazem. Thus, silent and symptomatic ischemia may be associated with different bradykinin and prostaglandin responses.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; Angina Pectoris; Bradykinin; Diltiazem; Electrocardiography, Ambulatory; Exercise Test; Female; Humans; Male; Middle Aged; Myocardial Ischemia; Single-Blind Method; Thromboxane B2

The hemodynamic and platelet effects of prostacyclin (PGI2) were investigated in 27 patients with unstable angina (14 treated patients; 13 control subjects) given a 72-hour infusion (5 ng/kg/min) or placebo. This randomized study was double-blind and conducted as a substudy of a multicenter trial testing the clinical efficacy of PGI2. The clinical and angiographic features were identical in the 2 groups. Blood pressure and heart rate were not modified significantly by PGI2. A recurrence of angina during infusion occurred in 8 treated patients (57.1%) and in 8 control subjects (61.5%). Two patients receiving PGI2 and none in the control group developed a myocardial infarction. Levels of 6-keto-prostaglandin F1 alpha, a stable metabolite of PGI2, increased from baseline values (less than 20 pg/ml) to 605 +/- 41 pg/ml during infusion. Levels of fibrinopeptide A, beta-thromboglobulin, platelet factor 4, thromboxane B2 and the platelet aggregates ratio in blood were similar between the 2 groups before, during and after PGI2 infusion. Prostacyclin reduced ex vivo platelet aggregation to adenosine diphosphate and thromboxane B2 generation by approximately 50% during the infusion period with return of aggregation to baseline and platelet thromboxane B2 production to above baseline after the discontinuation of PGI2. Thus, despite favorable effects of PGI2 upon platelet aggregation and systemic hemodynamics, the prostanoid failed to improve the clinical evolution of unstable angina.

Topics: 6-Ketoprostaglandin F1 alpha; Aged; Angina Pectoris; Angina, Unstable; Blood Platelets; Double-Blind Method; Epoprostenol; Female; Fibrinopeptide A; Hemodynamics; Humans; Male; Middle Aged; Multicenter Studies as Topic; Platelet Aggregation; Platelet Aggregation Inhibitors; Platelet Factor 4; Randomized Controlled Trials as Topic; Recurrence; Thromboxane B2

The effect of a chemically stable prostacyclin analogue (Iloprost) on platelet function was investigated in a controlled study in patients with angiographically confirmed stable angina pectoris after ischaemic exercise. In placebo experiments, ADP platelet aggregation was increased after exercise only when measured in whole blood and not in PRP. While plasma thromboxane B2 levels were unchanged, those of 6-keto PGF1 alpha were significantly although transiently increased after exercise. Iloprost displayed a potent antiaggregating activity in PRP and also reversed platelet hyperaggregation occurring in whole blood determinations after exercise. Plasma thromboxane B2 levels were significantly reduced but occasionally a rebound increase occurred 30 min. after end of the infusion. In contrast plasma level of 6-keto PGF1 alpha did not change after Iloprost and its recorded post-exercise increase was counteracted, thus suggesting a negative feed-back mechanism between Iloprost and natural prostacyclin. The data also suggest that degradation of the analogue is probably accomplished through pathways different from those of PGI2.

Topics: 6-Ketoprostaglandin F1 alpha; Aged; Angina Pectoris; Blood Platelets; Cardiovascular Agents; Coronary Disease; Epoprostenol; Humans; Iloprost; Male; Middle Aged; Physical Exertion; Platelet Aggregation; Platelet Function Tests; Random Allocation; Thromboxane B2

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; Angina Pectoris; beta-Thromboglobulin; Clinical Trials as Topic; Coronary Disease; Drugs, Chinese Herbal; Female; Humans; Male; Middle Aged; Platelet Aggregation

Platelet activation and coagulation abnormality have been observed during coronary spasm. It is crucial whether platelet activation occurs even during a nonischemic period.. This study was designed to determine whether platelets might be activated across the coronary bed during a nonischemic interval in patients with vasospastic angina.. Plasma levels of serotonin, 6-keto-prostaglandin F1 alpha, and catecholamines in the aorta and the coronary sinus were simultaneously measured in 16 patients with vasospastic angina and 13 control patients with nonischemic heart disease.. None of these patients showed myocardial ischemia during sampling. The difference in transcardiac plasma levels of serotonin in patients with vasospastic angina was significantly higher than that in controls (1.48 +/- 1.08 ng/ml vs. 0.07 +/- 0.12 ng/ml, respectively, p < 0.001). Coronary sinus plasma norepinephrine levels in these two groups were almost the same (204.8 +/- 110.8 pg/ml vs. 190.4 +/- 131.6 pg/ml, respectively). The ratio of 6-keto-prostaglandin F1 alpha in the coronary sinus and the aorta was not different between the two groups (1.17 +/- 0.96 in patients with vasospastic angina vs. 1.15 +/- 0.68 in controls).. These data suggest that platelet activation across the coronary bed should be ascribed to endothelial dysfunction. Lack of compensatory enhancement of prostacyclin production might be concerned with dysfunction of coronary endothelial cells in these patients.

Topics: 6-Ketoprostaglandin F1 alpha; Angina Pectoris; Aorta; Cardiac Catheterization; Catecholamines; Chromatography, High Pressure Liquid; Coronary Vasospasm; Coronary Vessels; Electrocardiography, Ambulatory; Female; Humans; Male; Middle Aged; Pilot Projects; Platelet Activation; Radioimmunoassay; Risk Factors; Serotonin

Caffeine significantly (p < 0.05) increased the output of prostacyclin (PGI2) from the perfused rat mesenteric vascular bed. The outputs of PGE2 and PGF2 alpha were also increased by caffeine. This stimulatory response to caffeine did not show rapid desensitization. Ryanodine also increased PG output, suggesting that caffeine may be acting via the stimulation of a ryanodine receptor. The increased production of a vasodilator such as PGI2 from blood vessels following exposure to caffeine may explain why caffeine has a beneficial effect in angina.

Topics: 6-Ketoprostaglandin F1 alpha; Angina Pectoris; Animals; Caffeine; Dinoprost; Dinoprostone; Endothelium, Vascular; Epoprostenol; Male; Mesenteric Arteries; Mesenteric Veins; Muscle, Smooth, Vascular; Perfusion; Prostaglandins; Rats; Ryanodine; Stimulation, Chemical

The effects of oral atenolol on coronary hemodynamics and prostaglandin metabolism have been investigated in 8 chronic stable angina pectoris patients who underwent the supine bicycle ergometer. At rest, atenolol taken orally reduced the pressure-rate product significantly (P < 0.05) but did not significantly affect the coronary sinus blood flow or the coronary sinus pressure. During exercise, atenolol also reduced the pressure-rate product significantly (P < 0.05) but did not significantly affect the coronary sinus blood flow, the coronary sinus pressure, or the coronary vascular resistance. Atenolol also did not significantly affect the thromboxane B2/6-keto prostaglandin F1 alpha ratio in the arterial blood before and after exercise but did reduce this ratio in the coronary sinus blood by 15% from 1.9 +/- 1.1 to 1.5 +/- 0.46 (P < 0.10) after exercise. These results indicate that atenolol taken orally does not significantly depress the coronary hemodynamics. However, the effects of atenolol on the prostaglandin metabolism could not be clearly determined.

Topics: 6-Ketoprostaglandin F1 alpha; Administration, Oral; Adult; Aged; Angina Pectoris; Atenolol; Blood Pressure; Exercise Test; Heart; Heart Rate; Hemodynamics; Humans; Lactates; Male; Middle Aged; Prostaglandins; Regional Blood Flow; Thromboxane B2; Vascular Resistance

We tested whether alteration of platelet sensitivity to prostacyclin (PGI2) is involved in the activation of platelets induced by exercise in patients with stable angina. Twenty patients and 20 control subjects underwent treadmill testing. Blood samples were obtained before and immediately after exercise for plasma thromboxane B2 (TXB2) and 6-keto-PGF1 alpha (6kP) assays and platelet aggregation studies. Dose-response curves for platelet aggregation to collagen were obtained in the presence and absence of 1 nmol/L PGI2 to quantify the antiaggregation effects of PGI2. At rest, platelet aggregation by collagen was enhanced in the patients. However, platelets were more sensitive to exogenous PGI2, apparently associated with lower plasma 6kP levels in the patients. After exercise, plasma TXB2 levels increased in the patients but not in the control subjects. Plasma 6kP levels remained unchanged and platelet sensitivity to PGI2 decreased in the patients whereas these values increased in the control subjects. The exercise-induced changes in platelet sensitivity to PGI2 correlated with those of platelet adenylate cyclase activity in response to 1 nmol/L PGI2 (r = 0.787, p less than 0.01). Thus impaired sensitivity of platelets to PGI2, in addition to the reduced response of prostanoid secretion, might be relevant to the platelet activation associated with exercise in patients with stable angina.

Topics: 6-Ketoprostaglandin F1 alpha; Adenylyl Cyclases; Angina Pectoris; Blood Platelets; Epoprostenol; Exercise; Exercise Test; Female; Humans; Male; Middle Aged; Platelet Aggregation; Thromboxane B2

The relationship between 68 cases of thromboxane B2(TXB2), 6-keto-prostaglandin F1 alpha (6-K-PGF1 alpha), beta-thromboglobulin (beta TG), platelet factor 4 (PF4), protein C antigen (PC:Ag), total-proteins (T-Ps) with coronary heart disease (CHD) based on TCM syndrome differentiation were studied. 45 cases of male, 23 cases of female, they were divided into 30 cases of blood stasis group and 38 cases of Qi syndrome group. 39 healthy subjects of same age and sex were chosen as the control group. The results were as follows: The TXB2, beta TG, PF4 in CHD were higher than those of control. 6-K-PGF1 alpha was lower (P less than 0.05, P less than 0.01) respectively. The TXB2 in blood stasis was significantly higher than that of Qi syndrome while the 6-K-PGF1 alpha in Qi Syndrome was significantly lower than that of blood stasis syndrome (P less than 0.01). The PC:Ag, T-Ps in CHD were higher than those of the control. The PC:Ag in blood stasis was lower and was higher in Qi syndrome (P less than 0.01). It showed that microthrombosis formed in blood stasis group caused blood flow slowly, while coronary-pathy and/or coronary spasm were the major pathologic change in Qi syndrome. Elevated PC:Ag, T-Ps in Qi syndrome showed that there were complementary action to hypercoagulation in Qi syndrome to eliminate coagulation factor to prevent coagulation happening and stimulation of fibrinolysin activator, promoting fibrinogenolysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; Angina Pectoris; Antigens; beta-Thromboglobulin; Blood Platelets; Coronary Disease; Female; Humans; Male; Medicine, Chinese Traditional; Middle Aged; Platelet Factor 4; Protein C

To investigate the prostaglandin I2 (PGI2) half-life regulated by high density lipoprotein (HDL) in patients with coronary artery disease (CAD), we determined the stability of PGI2 and serum apolipoprotein A-I (Apo A-I) and apolipoprotein A-II (Apo A-II) levels in four age-matched groups of patients: controls (n = 17), angina pectoris (n = 18), unstable angina pectoris (n = 17), myocardial infarction (n = 19) (acute phase, 3.6 +/- 1.7 hours from onset; subacute phase, 75 +/- 15 hours from onset in the same patients). Serum PGI2 half-life and total serum Apo A-I levels were lower in the CAD group than in the control group. PGI2 was least stable in patients with unstable angina and the acute phase of myocardial infarction. In these patients, the molar ratio of Apo A-I to Apo A-II and HDL-associated Apo A-I levels were decreased, and free Apo A-I levels were increased. After in vitro incubation of HDL with increasing amounts of Apo A-II, Apo A-I in HDL was displaced by Apo A-II, with the parallel decrease in stability of PGI2. Free Apo A-I cannot stabilize PGI2. HDL-associated Apo A-I, whose amount is affected by Apo A-II, stabilized PGI2 and correlated well with stability of PGI2 in patients with CAD and control patients. Decreased PGI2 half-life may play an important role in the pathogenesis of atherosclerosis and thrombus formation in the coronary arteries, especially thrombus formation during an acute coronary event.

Topics: 6-Ketoprostaglandin F1 alpha; Aged; Angina Pectoris; Angina, Unstable; Apolipoprotein A-I; Apolipoproteins A; Cholesterol, HDL; Epoprostenol; Half-Life; Humans; Lipoproteins, HDL; Middle Aged; Myocardial Infarction; Platelet Aggregation

24 angina pectoris patients were treated with Codonopsis pilosulae (CP) oral solution 20 ml (containing crude CP 20 g) thrice daily for 7 days, other 10 cases were treated by aspirin 0.5 g per day for a week as the control group. After treatment, in the CP group, the plasma level of TXB2 was obviously reduced from 156.76 +/- 11.87 pg/ml to 125.01 +/- 8.85 pg/ml (means +/- S means), the inhibitory rates was 15. 67% (P less than 0.05), and of 6-keto-PGF1 alpha (6-K) was not markedly changed (P greater than 0.05). In the aspirin group, TXB2 was also reduced significantly (P less than 0.05); 6-K was reduced more than that of CP group, the inhibitory rate was 24.33 +/- 9.40% (P less than 0.05). To reveal the mechanism of CP action on the synthesis of TXA2 and PGI2, the porcine lung microsome was used as the donor of cyclooxygenase, thromboxane synthase and prostacyclin synthase, the effects of CP on the formation of TXB2 and 6-K from arachidonic acid (AA) or endoperoxides were measured by RIA respectively. The results showed that both the levels of the formation of TXB2 from AA or endoperoxides were markedly reduced by CP in a dose-dependent (at doses of 3-300 mg/ml). The synthesis of TXB2 was distinctly inhibited alone with a dose of 100 mg/ml CP, which suggested that CP might be an inhibitor of TXB2 synthase at that dose; while at a dose of 300 mg/ml CP, the synthesis of TXB2 and 6-K were inhibited simultaneously (P less than 0.001). It showed that a larger dosage of CP, which could inhibited the synthesis of both TXA2 and PGI2, its mechanism of action needs further study.

Topics: 6-Ketoprostaglandin F1 alpha; Angina Pectoris; Animals; Drugs, Chinese Herbal; Epoprostenol; Female; Humans; Male; Microsomes; Swine; Thromboxane B2

Plasma concentrations of thromboxane B2 (TXB2) and 6-keto-prostaglandin Fl alpha(6-K-PGFl alpha), the stable nonenzymatic metabolites of TXA2 and prostacyclin were assayed in 30 patients suffering from angina pectoris before and after administration of puerarin. In addition, serum lipids and HDL were also measured at the same time. 20 healthy subjects were chosen as the control group. Two weeks before and during administration of puerarin, aspirin, calcium-antagonists, all kinds of hypotensors and drugs relieving chest pain of angina pectoris were strictly prohibited. Puerarin was intravenously given, 500 mg daily for 7 days, which was considered as a therapeutic course. Besides relieving of chest pain, decreasing of heart rate and reduction of blood pressure clinically, it was also found that plasma 6-K-PGFl alpha concentrations were significantly elevated from 38.32 +/- 15.40 to 158. 79 +/- 98.62 pg (P less than 0.01) after administration of puerarin, but there was no significantly difference between plasma TXB2 concentrations before and after administering the drug. In addition, serum HDL was apparently enhanced as compared with that before the administration of puerarin (P less than 0.01). The results indicated that puerarin has the function of anti-angina, reducing both systolic and diastolic blood pressure and diminishing myocardial oxygen consumption.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Angina Pectoris; Female; Flavonoids; Humans; Isoflavones; Male; Oxygen Consumption; Radioimmunoassay; Thromboxane B2; Vasodilator Agents

Bradykinin, alone or in combination with prostaglandin, is thought to produce pain in patients with coronary heart disease. To elucidate this further, we have investigated and compared serum bradykinin, TXB2 and 6 KPGF1 alpha levels in patients with silent myocardial ischemia (SMI, n = 18), painful myocardial ischemia (PMI, n = 8) and normal subjects (NL, n = 18). In addition, SMI and PMI subjects were given exercise testing and the results then compared. After Holter monitoring for 48 hours, exercise testing was performed. Blood was sampled in the morning between the Holter and exercise regimen. Maximal heart rate, systolic blood pressure and the double products were not significantly different between the SMI and PMI groups. The duration of exercise for the SMI group was 7.08 +/- 2.1 min vs 5.9 +/- 1.9 in the PMI group (p less than 0.10). Plasma bradykinin was 14 +/- 3 pg/ml in the SMI group and 15 +/- 3 in the PMI group (N.S), whereas it was 7 +/- 4 in the NL (p less than 0.05). The TXB2/6KPGF1 alpha for the SMI group was 1.3 +/- 0.3, which was significantly higher than that for the NL group (0.8 +/- 0.3, p less than 0.01), though this did not greatly differ from the PMI group (1.2 +/- 0.3). These results suggest that SMI patients under Holter monitoring who manifest no symptoms but show significant ST segment depressions must receive the same careful attention given to PMI patients. In both group of patients bradykinin and prostaglandin metabolism is similarly changed, as was demonstrated by exercise stress testing.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; Angina Pectoris; Bradykinin; Coronary Disease; Electrocardiography, Ambulatory; Exercise Test; Humans; Male; Middle Aged; Thromboxane B2

An effect of the electrocardiographic exercise on serum 6-keto-PGF1 alpha was investigated in healthy individuals and patients with exercise-induced stable angina pectoris. It was found that serum 6-keto-PGF1 alpha concentration was higher in healthy individuals following single exercise and at rest than that in the patients with exercise-induced stable angina pectoris. Single exercise increased serum 6-keto-PGF1 alpha concentration only in healthy individuals.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Angina Pectoris; Humans; Male; Middle Aged; Physical Exertion; Reference Values

The changes of platelet functions including platelet membrane microviscosity (PMMV), plasma 5-HT, plasma TXB2 and 6-K-PGF1a were studied in 30 cases of AMI and 13 cases of unstable angina (UA), 20 normal subjects as control. After onset of AMI, PMMV, plasma 5-HT, 6-k-PGF1a all increased quickly, especially on the 1st day (P less than 0.001-0.01). During 3 weeks observation, only 6-K-PGF1a decreased to the normal level on 14th day. There were no obvious decrease of plasma TXB2, 5-HT and PMMV. It showed that in acute phase of AMI without intervention of any antiplatelet drugs the platelets were activated continuously. Plasma 5-HT was the most sensitive predictor for the severity of AMI as observed by the comparison between the cases with complications and serum peak CK greater than 1000 U/L, and those without complications and peak CK less than 1000 U/L (P less than 0.001-0.05). The great change of PMMV was a bad prognosis. In patients with UA, during acute myocardial ischemia, the platelets were also activated significantly, but the extent was not as high as that in AMI.

Topics: 6-Ketoprostaglandin F1 alpha; Aged; Aged, 80 and over; Angina Pectoris; Angina, Unstable; Blood Platelets; Female; Humans; Male; Middle Aged; Myocardial Infarction; Platelet Function Tests; Serotonin; Thromboxane B2

Platelet function (aggregation, circulating platelet aggregates, platelet factor 4, beta-thromboglobulin, thromboxane B2, 6-keto-PGF1 alpha, platelet count) was evaluated in patients with angina of new onset, as compared to individuals without coronary heart disease, and patients with angina of long standing (28 +/- 4.6 months). Some of the patients with angina of new onset were examined repeatedly 6 to 12 months after the onset of angina. Platelet activity was shown to be significantly higher in patients with stable angina of new onset, as compared to patients with lasting angina, where ADP and serotonin were used as inductors. Platelet aggregation, induced by platelet activation factor and collagen, was similar in all groups. Repeated investigation 6 to 12 months after the first anginal attacks demonstrated that most of platelet functional parameters declined or tended to decline.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Angina Pectoris; Angina, Unstable; beta-Thromboglobulin; Female; Humans; Male; Middle Aged; Platelet Aggregation; Platelet Factor 4; Thromboxane B2; Time Factors

Topics: 6-Ketoprostaglandin F1 alpha; Adolescent; Adult; Aged; Angina Pectoris; Animals; Diabetes Mellitus; Female; Humans; Hypercholesterolemia; Male; Middle Aged; Pre-Eclampsia; Pregnancy; Rabbits; Radioimmunoassay; Rats; Rats, Inbred Strains; Thromboxane B2

Topics: 6-Ketoprostaglandin F1 alpha; Aged; Angina Pectoris; Humans; Male; Middle Aged; Physical Exertion; Thromboxane B2

Fibrinopeptide A, platelet factor 4, beta-thromboglobulin, thromboxane B2, and 6-keto-prostaglandin F1 alpha were estimated by radioimmunoassay on venous plasma samples taken within 48 hr of admission from 16 consecutive patients with unstable angina and 15 patients with stable angina matched for clinical variables. The ratio of circulating platelet aggregates, platelet aggregation to increasing concentrations of ADP (0.455 to 1.82 micrograms/ml), and platelet thromboxane B2 production in vitro were also tested. The two groups of patients were statistically similar in terms of sex distribution, age, presence of risk factors, use of medication, extent of coronary artery disease and history of previous myocardial infarction. Mean plasma levels of fibrinopeptide A were 2.7 +/- 0.4 ng/ml (geometric means +/- SEM, range 1.5 to 5.5) in patients with stable angina vs 5.5 +/- 1.8 ng/ml (range 2.4 to 32; p less than .001) in those with unstable angina. In the latter group, after 6 to 8 days, fibrinopeptide A levels decreased to 3.6 +/- 0.5 ng/ml (range 1.5 to 9.3; p less than .04 vs admission). All other variables measured were statistically identical in the two groups. We conclude that plasma fibrinopeptide A levels, as opposed to platelet factors, discriminate between patients with unstable and stable angina, indicating an activation of the coagulation system in unstable angina.

Topics: 6-Ketoprostaglandin F1 alpha; Adenosine Diphosphate; Angina Pectoris; Angina, Unstable; beta-Thromboglobulin; Coronary Angiography; Fibrinogen; Fibrinopeptide A; Heart Ventricles; Humans; Physical Exertion; Platelet Aggregation; Platelet Factor 4; Thromboxane B2; Time Factors

We studied the levels of thromboxane B2 (TXB2), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), platelet aggregability, beta-thromboglobulin and platelet factor 4 in 30 coronary artery disease (CAD) patients and 21 normal subjects during exercise. During treadmill exercise, 13 of 30 CAD patients reported chest pain. We administered a selective thromboxane synthetase inhibitor (OKY-046) for 2 weeks to 10 CAD patients with exercise-induced chest pain and studied its effects. At rest, the plasma TXB2 levels and platelet aggregation were significantly lower in normal subjects than in CAD patients, and there was no difference between CAD patients with and without exercise-induced chest pain. On treadmill testing, plasma TXB2 levels and platelet aggregation increased significantly only in the CAD patients with exercise-induced chest pain. Plasma 6-keto-PGF1 alpha levels in normal subjects were significantly higher than those in CAD patients both at rest and during exercise. After administration of OKY-046, mean exercise time increased significantly from 7.5 to 8.6 min (p less than 0.001). Plasma TXB2 level and platelet aggregation decreased significantly after OKY-046 administration both at rest and during exercise. These results suggest that a marked increase in TXA2, with only a minimal change in PGI2, during exercise may contribute to exercise-induced myocardial ischemia, and that OKY-046 is useful in the treatment of CAD patients.

Topics: 6-Ketoprostaglandin F1 alpha; Acrylates; Angina Pectoris; Coronary Disease; Epoprostenol; Female; Humans; Male; Methacrylates; Physical Exertion; Platelet Aggregation; Thromboxane B2; Thromboxane-A Synthase; Vasoconstriction

Thromboxane released from activated platelets and prostacyclin of the vessel wall may act as potent antagonistic modulators of platelet aggregability and coronary vascular tone. Therefore, urinary excretion of their major metabolites, 2,3-dinor-thromboxane B2 and 2,3-dinor-6-ketoprostaglandin F1 alpha, was studied in 16 patients presenting with prolonged angina at rest. The 10 patients whose condition did not improve under vigorous antianginal treatment within 48 hours exhibited higher thromboxane metabolite excretion than did the 6 patients who responded to therapy (2,208 +/- 1,542 versus 609 +/- 312 ng/g creatinine; p less than 0.001). Elevated values were also found in four of eight patients with sustained postinfarction angina. Enhanced thromboxane metabolite excretion was frequently associated with angiographic evidence of thrombus formation. When nine patients were restudied in a stable phase after 11 +/- 5 months, thromboxane metabolite excretion was consistently normal or high normal. Excretion of prostacyclin metabolites was not depressed in any patient but correlated weakly with thromboxane (r = 0.41). Thus, enhanced thromboxane production as an index of platelet activation may identify patients with active thrombus formation who could benefit most from platelet inhibitory treatment.

Topics: 6-Ketoprostaglandin F1 alpha; Aged; Angina Pectoris; Angina, Unstable; Electrocardiography; Exercise Test; Female; Follow-Up Studies; Humans; Male; Middle Aged; Monitoring, Physiologic; Platelet Aggregation; Thromboxane B2

Topics: 6-Ketoprostaglandin F1 alpha; Angina Pectoris; Drugs, Chinese Herbal; Female; Humans; Male; Thromboxane B2

Platelet function was studied in patients with diverse clinical patterns of unstable angina. In vasospastic angina, anginal attacks coincide with the highest increment in Ca2+ of platelets, and their high sensitivity to aggregation inductors, which declines as the condition stabilizes. Unstable angina without the vasospastic component is associated with reduced platelet sensitivity to aggregation inductors, particularly so in patients showing signs of intracoronary thrombosis. Spontaneous anginal attacks are accompanied with a rise of thromboxane B2 and a drop in the stable prostacyclin metabolite level.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Angina Pectoris; Angina, Unstable; Blood Platelets; Calcium; Cytoplasm; Female; Humans; Male; Middle Aged; Platelet Aggregation; Thromboxane B2

The mechanism of action by which nitrates produce vasodilation has not been fully clarified so far. Experimental studies indicate a possible relationship to the prostaglandin system. This study describes the consequences of acute prostaglandin synthesis inhibition on the hemodynamic effects of nitroglycerin in patients with stable angina pectoris. Intravenous application of 1 g acetylsalicylic acid was associated with a small but significant blunting of the pressure decline in the pulmonary and systemic circulation following the sublingual administration of 0.8 mg nitroglycerin. Premedication with 75 mg indomethacin i.m. was followed by a decrease in pressure decline in the pulmonary artery during intravenous nitroglycerin infusion. Significant inhibition of prostaglandin synthesis was shown by a substantial decline in plasma levels of circulating prostaglandin metabolites in both experiments. These results indicate that the mechanism of action of nitroglycerin may be partially mediated by vasodilatory prostaglandins.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Angina Pectoris; Aspirin; Cyclooxygenase Inhibitors; Dinoprostone; Epoprostenol; Exercise Test; Female; Hemodynamics; Humans; Indomethacin; Male; Middle Aged; Nitroglycerin; Prostaglandins; Prostaglandins E

Thirty-four patients with unstable angina and 14 patients with stable effort angina were investigated for cardiac prostacyclin and prostaglandin E2 (PGE2) biosynthesis, under resting conditions and after cold pressor testing. Twenty-seven patients undergoing cardiac catheterization and coronary angiography for congenital or acquired heart diseases other than coronary artery disease were studied as a control group. Prostacyclin (as 6-keto-PGF1 alpha) and PGE2 were measured by specific radioimmunoassay of blood from the coronary sinus and aorta. During resting conditions no significant differences in plasma 6-keto-PGF1 alpha and PGE2 concentrations were found between coronary sinus and aortic blood, and no transcardiac gradient existed either in control subjects or in patients with stable and unstable angina, respectively. In control subjects cold pressor testing induced a significant increase in 6-keto-PGF1 alpha and PGE2 levels in blood from the different sampling sites, and a significant transcardiac gradient occurred (+11.2 +/- 6.4 pg/ml for 6-keto-PGF1 alpha and +5.1 +/- 3.4 pg/ml for PGE2). However, in angina patients no significant increase in 6-keto-PGF1 alpha and PGE2 plasma levels was found and no transcardiac gradient was formed after cold pressor testing. These results indicate impaired cardiac prostacyclin and PGE2 biosynthesis both in patients with stable and unstable effort angina.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; Angina Pectoris; Angina, Unstable; Dinoprostone; Epoprostenol; Female; Humans; Male; Middle Aged; Physical Exertion; Prostaglandins E; Radioimmunoassay

Pathological and clinical studies have suggested that platelets have a role in the pathogenesis of unstable angina and myocardial infarction. However, the relation of platelet activation to episodic ischemia in patients with unstable angina is unknown. We assessed the biosynthesis of thromboxane and prostacyclin as indexes of platelet activation in patients with stable and unstable coronary disease by physicochemical analysis of metabolites in plasma and urine. Prostacyclin biosynthesis was markedly elevated in patients with acute myocardial infarction and correlated with plasma creatine kinase (r = 0.795; P less than 0.001). The largest rise in thromboxane synthesis was observed in patients with unstable angina, in whom 84 percent of the episodes of chest pain were associated with phasic increases in the excretion of thromboxane and prostacyclin metabolites. However, 50 percent of such increases were not associated with chest pain, possibly reflecting silent myocardial ischemia. These data indicate that platelet activation occurs during spontaneous ischemia in patients with unstable angina. The increment in prostacyclin biosynthesis during such episodes may be a compensatory response of vascular endothelium that limits the degree or effects of platelet activation. If so, biochemically selective inhibition of the synthesis or action of thromboxane A2 would be desirable in the treatment of unstable angina. In contrast, thromboxane inhibitors or antagonists would not be expected to be effective in patients with chronic stable angina, in whom there was no increase in the formation of thromboxane A2.

Topics: 6-Ketoprostaglandin F1 alpha; Angina Pectoris; Angina, Unstable; Blood Platelets; Epoprostenol; Humans; Myocardial Infarction; Thromboxane A2; Thromboxane B2

The levels of TxB2 and 6-keto-PGI alpha in the coronary sinus and thoracic aorta blood were determined in 14 patients with angina pectoris and signs of coronary atherosclerosis. 12 patients were involved in a dynamic study: before, during and 10 minutes after ischaemia-inducing atrial pacing. In all the patients atrial pacing resulted in a typical episode of angina, in 7 of them ST-segment depression of not less than 2 mm was seen on the ECG. In one patient arachidonic acid metabolites were evaluated during the control period and during a spontaneous episode of angina accompanied by ST-segment elevations. In 8 of 9 patients TxB2 was produced by the myocardium during atrial pacing. During monitored evaluation of arachidonic acid metabolites one patient with spontaneous angina demonstrated a gradual lowering of the 6-keto-PGI alpha, it being minimal by the beginning of the episode; TxB2 level increased more rapidly.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Angina Pectoris; Coronary Disease; Electric Stimulation; Heart Atria; Humans; Male; Middle Aged; Thromboxane B2

Topics: 6-Ketoprostaglandin F1 alpha; Acrylates; Angina Pectoris; Coronary Disease; Humans; Methacrylates; Oxidoreductases; Physical Exertion; Platelet Aggregation; Prostaglandins; Thromboxane B2; Thromboxane-A Synthase

Topics: 6-Ketoprostaglandin F1 alpha; Angina Pectoris; Coronary Disease; Dinoprostone; Humans; Myocardium; Prostaglandins; Prostaglandins E; Thromboxane B2

To elucidate the contribution of prostanoids in coronary spasm, plasma levels of thromboxane B2 (TXB2) and 6-keto PGF1 alpha at the coronary sinus and ascending aorta in 21 patients with variant angina were measured, as compared with findings in 20 with effort angina and 13 subjects with normal coronaries. In the coronary sinus blood, plasma TXB2 in patients with effort angina exhibited statistically significant high levels, as compared with data in the controls. On the contrary, the data obtained from patients with variant angina were not statistically significant. However, eight patients whose coronary angiogram revealed more than 50% of coronary stenoses had statistically significant high levels of TXB2 and other patients with normal coronaries or less than 50% of narrowing showed almost the same levels of TXB2 as the controls. In contrast to TXB2, the plasma levels of 6-keto PGF1 alpha in patients with variant angina were very low in both groups with variant angina. These data suggest that high levels of TXB2 observed in patients with atherosclerotic coronaries may be an accelerating factor while low levels of prostacyclin may be an essential factor leading to spasm. HLA analysis of 23 patients with variant angina was performed to search for genetic factors, under the hypothesis that such may contribute to the low levels in prostacyclin. This preliminary study revealed statistically significant high frequencies of Bw52 and B-40 in the patients, as compared with frequencies among 152 normal Japanese. Genetic studies are ongoing in our clinic.

Topics: 6-Ketoprostaglandin F1 alpha; Aged; Angina Pectoris; Angina Pectoris, Variant; Coronary Vasospasm; Electrocardiography; Female; Histocompatibility Antigens Class II; HLA Antigens; Humans; Male; Middle Aged; Thromboxane A2; Thromboxane B2; Thromboxanes

In order to diagnose patients in thrombotic state, it is quite important to detect increased concentration of plasma thromboxane B2 (TXB2), a stable catabolite of TXA2. To determine plasma TXB2 levels with high sensitivity and selectivity, we employed gas chromatography-mass spectrometry (GC/MS). The trimethylsilyl (TMS) ether derivatives conventionally employed in GC/MS analysis of prostanoids are not suitable for quantitation of plasma prostanoids, because the mass spectra are deficient in ions with high intensity in the high mass range and TMS ether derivatives are sensitive to moisture. To solve these problems we employed tert-butyldimethylsilyl (t-BDMS) ether derivatives, based on the observation that t-BDMS ether derivatives afforded abundant ions at [M-57]+ and showed good hydrolytic stability. The reaction conditions of tert-butyldimethylsilylation were also examined to optimize the selected ion monitoring response. The t-BDMS ether derivatives of prostanoids were successfully analyzed with a short capillary column with a relatively large diameter, with maintaining good separation. In conjunction with the use of reversed-phase high performance liquid chromatography as purification procedure, a sensitive and reproducible stable isotope dilution assay of plasma TXB2 was developed. The values obtained by this method correlated well with those obtained by the radioimmunoassay we have developed.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; Angina Pectoris; Coronary Vasospasm; Dinoprost; Dinoprostone; Female; Gas Chromatography-Mass Spectrometry; Humans; Male; Middle Aged; Myocardial Infarction; Organosilicon Compounds; Prostaglandin D2; Prostaglandins D; Prostaglandins E; Prostaglandins F; Silicon; Thromboxane B2; Thromboxanes

The results of prior studies indicate that nitroglycerin stimulates prostacyclin release by cultured endothelium and by the coronary vasculature in vivo. However, the accuracy of these findings in coronary vasculature relies on plasma samples obtained from the circulation via cardiac catheters, a procedure we have shown to stimulate prostacyclin release, thereby confounding interpretation of drug action. We studied the effects of short-acting (nitroglycerin) and long-acting (isosorbide dinitrate) nitrates on a noninvasive index of prostacyclin synthesis, excretion of urinary 2,3-dinor-6-keto-PGF1 alpha. Nitroglycerin was infused into six subjects to either a maximum of 480 micrograms/min or until mean arterial pressure fell by 20 mm Hg. Urine was collected for negative ion chemical ionization gas chromatographic, mass spectrometric analysis before and during the nitroglycerin infusion and for two 2 hr periods after nitroglycerin. The peak nitroglycerin infusion rate was 387 +/- 67 micrograms/min, which caused a fall in supine blood pressure (systolic/diastolic) of 11 +/- 5/14 +/- 4 mm Hg and a 12 +/- 3 beats/min increase in heart rate. Excretion of 2,3-dinor-6-keto-PGF1 alpha (pg/mg creatinine) was unchanged from control infusion values (106 +/- 19.5) either during (123 +/- 21) or after (134 +/- 14.6; 139 +/- 36) nitroglycerin infusion. Platelet aggregation to arachidonic acid (0.33 to 1.33 microM) and epinephrine (1 to 10 microM) ex vivo was inhibited in only one subject in whom excretion of 2,3-dinor-6-keto-PGF1 alpha was unaltered. Serum thromboxane B2 was not changed by nitroglycerin infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Angina Pectoris; Arachidonic Acid; Arachidonic Acids; Blood Pressure; Epinephrine; Epoprostenol; Heart Rate; Humans; Isosorbide Dinitrate; Middle Aged; Nitroglycerin; Platelet Aggregation

Prostacyclin (PGI2) is a naturally occurring vasodilator and inhibitor of platelet aggregation that produces vasodilatation of the systemic, pulmonary and coronary vascular beds in animal models. Because the endogenous production of PGI2 is reduced in those with coronary arterial disease (CAD), it may have a therapeutic role in patients with ischemic heart disease. To assess its safety and efficacy in this clinical setting, 17 patients with stable angina and CAD received an incremental intravenous infusion of either PGI2 (n = 10) to a maximum dose of 10 ng/kg/min (average 9.8 +/- 0.8 [mean +/- standard deviation]), or diluent buffer solution (placebo) (n = 7). All patients who received PGI2 became flushed, but experienced no other adverse effects PGI2 caused an increase in heart rate (66 +/- 11 to 80 +/- 11 beats/min, p less than 0.001) and cardiac index (2.88 +/- 0.65 to 3.97 +/- 1.17 liters/min/m2, p less than 0.001) and a decrease in mean femoral arterial pressure (96 +/- 18 to 86 +/- 11 mm Hg, p less than 0.001), but no change in mean pulmonary arterial or capillary wedge pressure. Total systemic and pulmonary vascular resistance decreased significantly (p less than 0.001). In response to PGI2, mean coronary sinus blood flow did not change significantly (100 +/- 40 to 121 +/- 52 ml/min), but coronary vascular resistance decreased (1.07 +/- 0.40 to 0.83 +/- 0.36 U, p less than 0.001). No variable was altered by placebo infusion. PGI2 caused a marked increase in 6-keto PGF1 alpha (the stable metabolite of PGI2) concentrations in both arterial (42 +/- 29 to 567 +/- 216 pg/ml, p less than 0.001) and venous (46 +/- 31 to 604 +/- 229 pg/ml, p less than 0.001) blood but no demonstrable change in plasma renin activity. Thus, intravenous PGI2 to a dosage of 10 ng/kg/min is a safe and effective systemic, pulmonary and coronary arterial vasodilator in patients with CAD and stable angina pectoris.

Topics: 6-Ketoprostaglandin F1 alpha; Angina Pectoris; Blood Pressure; Cardiac Output; Coronary Circulation; Dose-Response Relationship, Drug; Epoprostenol; Female; Heart Rate; Hemodynamics; Humans; Infusions, Parenteral; Male; Middle Aged; Prostaglandins; Random Allocation; Vascular Resistance

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; Angina Pectoris; Epoprostenol; Humans; Middle Aged; Myocardial Infarction; Radioimmunoassay; Thromboxane A2; Thromboxane B2; Thromboxanes

Endogenous modulators of platelet aggregability and vascular tone may play a part in coronary-artery disease. We therefore measured the release of prostaglandins and thromboxane into the coronary circulation in patients with various kinds of cardiac disease. Simultaneous coronary-sinus (CS) and ascending-aortic (AO) blood samples were obtained from 60 patients for measurement of 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha, a prostaglandin I2 metabolite) and of thromboxane B2 (TxB2). Samples from 45 of these patients were also tested for prostaglandin E2 (PGE2) and lactate. Patients with unstable angina pectoris who reported chest pain within 24 hours of study had higher TxB2 CS/AO ratios (5.8 +/- 2.8, mean +/- S.D.) than patients whose most recent anginal pain was more than 96 hours before study (1.3 +/- 0.6; P less than 0.05), than those with nonischemic chest pain (1.2 +/- 0.4; P less than 0.05), or with valvular or congenital nonischemic heart disease (1.2 +/- 0.6; P less than 0.05). Those whose most recent anginal pain occurred 24 to 96 hours before study were distributed bimodally: the majority had low TxB2 CS/AO ratios (range, 0.5 to 2.1) like the patients in the three aforementioned groups, whereas a few had markedly elevated values (range, 10.5 to 46.6). The 6-keto-PGF1 alpha and PGE2 CS/AO ratios and myocardial lactate extraction were not significantly different among the five groups. These data suggest that local thromboxane release is associated with recent episodes of angina in patients with unstable angina pectoris, but whether this release is a cause or an effect is not yet known.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; Angina Pectoris; Coronary Circulation; Coronary Disease; Female; Humans; Lactates; Male; Middle Aged; Prostaglandins; Prostaglandins E; Prostaglandins F; Thromboxane B2; Thromboxanes