fibrinopeptide-a and Angina-Pectoris

Topics: Angina Pectoris; Blood Coagulation; Coronary Thrombosis; Fibrinolysis; Fibrinopeptide A; Humans; Myocardial Infarction; Plasminogen Inactivators

Topics: Angina Pectoris; Blood Coagulation Disorders; Blood Platelet Disorders; Coronary Disease; Coronary Vasospasm; Fibrinopeptide A; Humans; Myocardial Infarction; Prostaglandins; Thromboxanes

Tranexamic acid (TA) reduces blood loss in coronary artery surgery with cardiopulmonary bypass. The present prospective study was designed to investigate its hemostatic effect in off-pump coronary artery bypass (OPCAB).. Seventy-six patients undergoing elective OPCAB were randomized into two groups, received TA (0.75 g loading dose before surgery and 250 mg/h during surgery, gross dose: 1.5 g, n=36) and saline solution (control, n=40), respectively. Perioperative blood samples were collected. Hematochemical parameters including platelet adhesion rate, D-dimer and fibrinopeptide-A (FPA) were analysis. Volume of blood loss, blood transfusion and other clinical data were recorded throughout the perioperative period.. Cumulative blood loss was significantly reduced in the TA group as compared to the controls postoperatively (6 hrs (median [25th-75th]): TA: 200.0 [140.0-230.0] ml,. 225.0 [200.0-347.5.0] ml, p=0.009; 24 hrs: TA: 440.0 [270.0-605.0] ml,. 655.0 [500.0-920.0] ml, p<0.001). Number of patients received blood transfusion in each group was similar. Levels of D-dimer rose significantly after surgery, and were significantly lower in the TA group than that in controls. Platelet adhesion rate and FPA levels remained at baseline levels after the operation in two groups. Early clinical outcomes were similar between groups.. The results indicated that tranexamic acid limits fibrinolysis and reduces blood loss after off-pump coronary artery bypass surgery.

Topics: Aged; Angina Pectoris; Antifibrinolytic Agents; Chemoprevention; Coronary Artery Bypass, Off-Pump; Female; Fibrin Fibrinogen Degradation Products; Fibrinopeptide A; Humans; Male; Middle Aged; Perioperative Care; Platelet Adhesiveness; Postoperative Care; Postoperative Hemorrhage; Tranexamic Acid; Treatment Outcome

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

Increased thrombin generation is frequently associated with an increase in anginal activity. A cross-over, single-blind, completely randomized study was planned in order to evaluate whether the control of thrombin generation affected the increase in anginal activity. After discharge from the hospital, 24 patients (18 men and 6 women, aged 40 to 69 years) suffering from spontaneous angina were followed up to 12 months and were alternatively treated during two consecutive 6-month periods with calcium heparin, 12,500 IU by the subcutaneous route, or with placebo by the intramuscular route, in addition to the usual antianginal medications. Thrombin generation and clinical activity of angina were assessed every 15 days by measuring fibrinopeptide A (FPA) plasma levels and by grading in three classes (symptomless, mildly symptomatic, and severely symptomatic) the anginal activity on the basis of the number and the time concentration of the ischemic attacks and ECG changes. Low-dose heparin treatment significantly reduced both the FPA plasma level (from 4.1 +/- 3.7 to 2.3 +/- 1.8 ng/ml, p less than 0.001) and the clinical activity of angina. During heparin treatment, the frequency of the observations in the severely and mildly symptomatic classes decreased, respectively, by 53% and by 30%, whereas that in the symptomless class increased by 23% (p less than 0.001) in comparison with the period on placebo. Present results indicate that the control of thrombin generation obtained by low-dose heparin treatment favorably affects the degree of anginal activity in patients with spontaneous angina.

Topics: Aged; Angina Pectoris; Clinical Trials as Topic; Drug Administration Schedule; Female; Fibrinogen; Fibrinopeptide A; Heparin; Humans; Male; Patient Compliance; Random Allocation; Thrombosis

In 19 patients with unstable angina pectoris at rest, plasma levels of the platelet-derived proteins beta-thromboglobulin and platelet factor 4 were significantly elevated in blood samples obtained during or within 4 hours after episodes of angina, but were usually normal during quiescent intervals. Plasma levels of the arachidonic acid metabolite thromboxane B2 were less clearly related to angina, and there was no association of angina with levels of the coagulation product fibrinopeptide A. This demonstration of an association of platelet activation and secretion with unstable angina pectoris by radioimmunoassay of circulating platelet constituents offers a new approach to assessment of therapy in ischemic heart disease and suggests that agents that alter platelet function should be evaluated in patients with unstable angina.

Topics: Adult; Aged; Angina Pectoris; beta-Thromboglobulin; Blood Platelets; Electrocardiography; Female; Fibrinopeptide A; Heparin; Humans; Male; Middle Aged; Myocardial Infarction; Platelet Factor 4; Thromboembolism; Thromboxane B2

Tissue factor pathway inhibitor (TFPI) is the endogenous inhibitor of the extrinsic coagulation pathway; however, its involvement during thrombus formation in patients with acute coronary syndromes (ACS) is still unknown.. Transcardiac (aorta/coronary sinus) free and total TFPI (free + lipoprotein-bound form) levels, as well as TFPI/factor Xa (FXa) complex levels, were measured in plasma samples obtained from patients with acute myocardial infarction undergoing primary PTCA and patients with unstable angina undergoing urgent PTCA. Patients with stable angina undergoing elective PTCA served as controls. In addition, prothrombin fragment 1+2 and fibrinopeptide A plasma levels were measured. Samples were collected at baseline, after PTCA, and after stent deployment. In patients with ACS, both total and free TFPI plasma levels in the coronary sinus were significantly lower than the corresponding levels measured in the aorta at any time point of the study; conversely, a significant increase in TFPI/FXa complex plasma levels was observed in the coronary sinus as compared with the aorta. In contrast, in patients with stable angina, no differences were observed in TFPI and TFPI/FXa levels at baseline in the coronary sinus as compared with the aorta.. TFPI is involved in the process of thrombus formation in vivo in patients with ACS, which suggests a potential role for TFPI in modulating coronary thrombosis.

Topics: Aged; Angina Pectoris; Angina, Unstable; Angioplasty, Balloon, Coronary; Anticoagulants; Aorta; Coronary Circulation; Coronary Thrombosis; Coronary Vessels; Factor Xa; Female; Fibrinolysis; Fibrinopeptide A; Heparin; Humans; Lipoproteins; Male; Middle Aged; Myocardial Infarction; Peptide Fragments; Prothrombin; Stents; Thrombin; Thrombophilia

The molecular markers of platelet activation, coagulation and fibrinolysis were detected in 60 cases of coronary heart disease (CHD), including 15 cases of stable angina (SA), 21 cases of unstable angina (UA) and 24 cases of acute myocardial infarction (AMI). The results showed that the platelet granule membrane protein 140 (GMP-140) level increased obviously in CHD groups compared with normal control, suggesting that platelet activation existed in CHD. Prothrombin fragment F1 + 2 and fibrinopeptide A (FPA) were examined to observe the activation of coagulation. No difference was found between SA group and normal controls, while their levels in both UA group and AMI group were significantly higher than in normal control and SA group (both P < 0.05). D-D dimer and alpha 2-plasma inhibitor (alpha 2-PI) were detected to observe fibrinolytic state. The results showed that no difference existed between SA group and normal controls, while both D-D dimer and alpha 2-PI in UA group and AMI group were significantly elevated than those in SA group and normal controls (P < 0.05).

Topics: Angina Pectoris; Angina, Unstable; Blood Coagulation; Female; Fibrinopeptide A; Humans; Male; Middle Aged; Myocardial Infarction; P-Selectin; Prothrombin; Thrombophilia

To analyse whether lipoprotein(a) is a risk factor for myocardial infarction, stroke and acute peripheral arterial occlusion in coronary heart disease and whether this risk can be assessed by clotting activation markers.. A partly prospective, partly retrospective study of data on 237 consecutive patients (201 men, 36 women; mean age 55 [24-76] years) who had undergone coronary arteriography because of severe angina. Concentrations were measured for: beta-thromboglobulin, platelet factor 4, fibrinopeptide A, D-dimers, thrombin-antithrombin III factor (TAT), prothrombin fragments 1 + 2, lipoprotein(a), apolipoprotein A-I (apoA-I), cholesterol and triglycerides. Analysis of any relationship between the findings on coronary arteriography (degree of stenosis) and the occurrence of myocardial infarction, stroke and acute peripheral arterial occlusion before and during the 2 years after the arteriography.. There was no correlation between lipid parameters and clotting or platelet activation markers. Patients with a history of acute peripheral arterial occlusion had raised values for lipoprotein(a) and TAT. In the prospective part of the study (i.e. during the first 2 years after blood samples had been taken), there was no correlation.. In patients with coronary artery disease and angina pectoris no correlation was found between lipoprotein(a) and haemostasis activation markers. None of these parameters--prospectively evaluated--could predict risk of thromboembolism.

Topics: Adult; Age Factors; Aged; Angina Pectoris; Antithrombin III; beta-Thromboglobulin; Blood Coagulation Factors; Cholesterol; Coronary Angiography; Data Interpretation, Statistical; Female; Fibrinopeptide A; Follow-Up Studies; Humans; Lipoprotein(a); Male; Middle Aged; Peptide Hydrolases; Platelet Factor 4; Prospective Studies; Retrospective Studies; Risk Factors; Time Factors; Triglycerides

The current study was designed to investigate the number and affinity of platelet thromboxane A2/prostaglandin H2 (TxA2/PGH2) receptors in patients with unstable angina and, if any, the role played by the increased thrombin formation that is a common finding in these patients. Measurements taken during active unstable angina but not those taken during inactive angina showed an increase number (p < 0.001), without changes in affinity, of platelet TxA2/PGH2 receptors, evaluated as the binding capacity of iodine 125-PTA-OH, a stable TxA2 analogue. Moreover patients with active angina had higher plasma concentrations of fibrinopeptide A (FPA) (p < 0.0001), which were significantly related to the number of platelet TxA2/PGH2 receptors (r = 0.76; p < 0.01). Heparin infusion but not aspirin treatment promptly normalized the number of TxA2/PGH2 receptors and significantly reduced plasma FPA concentrations. In an in-vitro study thrombin in a concentration similar to that found in vivo significantly increased the number of platelet TxA2/PGH2 receptors (p < 0.01), whereas heparin did not affect TxA2/PGH2 receptors. These results have important therapeutic implications and indicate the preferential use of heparin rather than aspirin during the acute phase of unstable angina.

Topics: Aged; Angina Pectoris; Angina, Unstable; Aspirin; Blood Platelets; Dose-Response Relationship, Drug; Fibrinopeptide A; Heparin; Humans; Middle Aged; Physical Exertion; Platelet Activation; Prostaglandins H; Radioligand Assay; Receptors, Prostaglandin; Receptors, Thromboxane; Receptors, Thromboxane A2, Prostaglandin H2; Thrombin; Thromboxane A2

Fibrin generation and lysis were studied in 28 patients with angina pectoris (14 with active disease and 14 with inactive disease) and in 14 normal controls. The fibrinolytic response was evaluated by comparing the ratio between the plasma levels of fibrinopeptide A and fibrin degradation products. Levels of both were higher in patients than in controls (P < 0.001), with higher levels in active than in inactive disease (P < 0.001). The fibrinopeptide A/fibrin degradation products ratio was much higher (P < 0.001) in the active group than in other groups. Thus, in patients with angina pectoris, especially in the active state, the increased thrombin generation is not paralleled by an equivalent increase in fibrinolytic activity.

Topics: Adult; Angina Pectoris; Blood Coagulation; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinolysis; Fibrinopeptide A; Humans; Middle Aged; Thrombin

To determine whether, in patients undergoing percutaneous transluminal coronary angioplasty (PTCA), there are prothrombotic markers indicating those with a predisposition to restenosis.. Venous blood samples were obtained from patients undergoing PTCA for chronic stable angina. Patients with restenotic lesions, conduit stenoses or occlusive lesions were not included in the study. Samples were assayed for coagulation factors (fibrinopeptide A, antithrombin III, protein C), fibrinolytic factors [tissue-type plasminogen activator (t-PA), alpha 2 antiplasmin, plasminogen activator inhibitor (PAI-1)] and markers of platelet activation (platelet factor 4, beta thromboglobulin).. Of 46 patients who underwent successful PTCA, restenosis, defined as loss in absolute gain of more than 50%, occurred in 16 (35%). The minimal luminal diameter (mean +/- SD) at follow-up in those who had suffered restenosis was 1.07 +/- 0.7 mm compared with 1.73 +/- 0.5 mm in the non-restenotic patients. However, no significant differences in the levels of markers of platelet activation, coagulation factors, or fibrinolytic factors were observed between the two groups. The only significant difference between the groups was a higher platelet count in the restenotic patients [median (interquartile range): 263 (247-278) versus 224 (175-263), P < 0.05].. Our results suggest that patients who suffer restenosis following PTCA appear to have no clearly detectable pre-existing imbalance in their prothrombotic/antithrombotic status. Although the platelet count was higher in restenotic patients, the levels of markers of platelet activation were no different in the two groups. Thus, it is at present unlikely that simple blood assays before PTCA assessing an individual's 'thrombotic state' can help to predict which of the 30-40% of patients undergoing PTCA will suffer restenosis.

Topics: alpha-2-Antiplasmin; Angina Pectoris; Angioplasty, Balloon, Coronary; Antithrombin III; beta-Thromboglobulin; Biomarkers; Coronary Angiography; Coronary Disease; Female; Fibrinopeptide A; Follow-Up Studies; Humans; Male; Middle Aged; Plasminogen; Plasminogen Activator Inhibitor 1; Platelet Factor 4; Protein C; Recurrence; Risk Factors; Thrombosis; Tissue Plasminogen Activator

The blood coagulation system is activated in the acute phase of unstable angina and acute myocardial infarction. However, it remains unclear whether augmented function of the hemostatic mechanism serves only as a marker of the acute thrombotic episode or whether a hypercoagulable state persists for a prolonged period after clinical stabilization.. We prospectively measured the plasma concentrations of prothrombin fragment 1 + 2 (F1 + 2) and fibrinopeptide A (FPA) in consecutive patients presenting with unstable angina (n = 81) or acute myocardial infarction (n = 32), respectively. At 6 months, plasma determinations were repeated in patients experiencing an uneventful clinical course (unstable angina, n = 57; myocardial infarction, n = 23). We quantitated the plasma levels of F1 + 2 and FPA in control patients with stable angina (n = 37) or healthy individuals (n = 32) who were matched for age and sex. The median plasma concentrations of F1 + 2 and FPA are significantly higher in patients presenting with unstable angina (F1 + 2, 1.08 nmol/L; FPA, 2.4 nmol/L) or acute myocardial infarction (F1 + 2, 1.27 nmol/L; FPA, 3.55 nmol/L) compared with patients with stable angina (F1 + 2, 0.74 nmol/L; FPA, 1.3 nmol/L; P < .0001) or healthy individuals (F1 + 2, 0.71 nmol/L; FPA, 0.80 nmol/L; P < .0001). At 6 months, the median plasma levels of F1 + 2 in patients exhibiting an uneventful clinical course did not differ from values obtained at admission (unstable angina, 1.26 versus 1.07 nmol/L, P = NS; myocardial infarction, 1.22 versus 1.29 nmol/L, P = NS), whereas the median plasma levels of FPA in the same two subpopulations were significantly reduced (unstable angina, 1.1 versus 2.9 nmol/L, P = .0003; myocardial infarction, 1.1 versus 3.0 nmol/L; P = .0028).. During the acute phase of unstable angina and myocardial infarction, patients exhibit increased coagulation system activity. Over the next 6 months, patients with unstable angina or myocardial infarction experiencing an uneventful clinical course manifest a persistent hypercoagulable state with minimal generation of fibrin.

Topics: Adult; Aged; Angina Pectoris; Angina, Unstable; Blood Coagulation; Female; Fibrinopeptide A; Humans; Male; Middle Aged; Myocardial Infarction; Osmolar Concentration; Peptide Fragments; Prospective Studies; Prothrombin; Reference Values

Fibrinopeptide A was determined in 75 middle aged male patients, five control subjects and a control group of young medical students, divided into nine subsets. The FPA levels were significantly elevated in the patient group, particularly among the diabetics, when compared with the medical students and also age matched controls. Diabetic patients who smoked and had vascular pathology had high FPA levels even after they stopped smoking.

Topics: Angina Pectoris; Biomarkers; Coronary Artery Disease; Diabetic Angiopathies; Fibrinopeptide A; Humans; Male; Middle Aged; Smoking; Thrombosis

Plasma levels and 24-hour urine excretion of fibrinopeptide A were measured in a consecutive series of 179 patients with angina pectoris. Sixty-four patients had stable angina and 115 patients had unstable angina. Urine was collected over 24 hours the day before coronary arteriography, and blood samples were taken at the end of urine collection. When the values of fibrinopeptide A in plasma and in the 24-hour urine specimens were compared, no significant correlation was found in patients with either stable (rs = 0.16, difference not significant) and unstable (rs = 0.07, difference not significant) angina. The concentrations of fibrinopeptide A in the plasma did not differ significantly when patients with stable angina (range 0.1 to 82.6, median 7.4 ng/mL) were compared with patients with unstable angina (range 0.2 to 61.7, median 14 ng/mL, p = 0.055), whereas fibrinopeptide A 24-hour urinary excretion was significantly higher in patients with unstable angina (range 0.3 to 38.1, median 11.8 micrograms/24 hr) than in patients with stable angina (range 0.4 to 38.1, median 3.8 micrograms/24 hr, p less than 0.001). Twenty-four-hour urine excretion of fibrinopeptide A in patients with unstable angina and angiographically documented intracoronary thrombi were higher than the corresponding values in patients with unstable angina without such angiographic characteristic (p less than 0.001). The largest increase in plasma and urine concentration of fibrinopeptide A was observed in patients whose first episode of angina at rest occurred within the previous 48 hours. We conclude that the cumulative thrombin activity, assessed by 24-hour urinary excretion of fibrinopeptide A, is a more useful index, compared with single fibrinopeptide A measurement in plasma, for discriminating between patients with stable and with unstable angina pectoris.

Topics: Angina Pectoris; Angina Pectoris, Variant; Angina, Unstable; Coronary Angiography; Coronary Thrombosis; Female; Fibrinogen; Fibrinopeptide A; Humans; Male; Middle Aged; Prevalence; Prospective Studies; Thrombin

To examine whether acute myocardial ischemia activates the coagulation system and platelet activation in the coronary circulation, we measured plasma levels of fibrinopeptide A and beta-thromboglobulin in the coronary sinus and the aortic root simultaneously in 15 patients with coronary spastic angina before and after the left coronary spasm induced by intracoronary injection of acetylcholine and in 15 patients with stable exertional angina before and after acute myocardial ischemia induced by rapid atrial pacing. Fifteen patients with chest pain but normal coronary arteries and no coronary spasm served as controls. The coronary sinus-arterial difference of fibrinopeptide A increased markedly (p less than 0.001) from 0.1 +/- 0.2 to 4.3 +/- 0.7 ng/ml after the anginal attacks in the coronary spastic angina group. However, fibrinopeptide A levels remained unchanged after the attacks in the stable exertional angina group and after intracoronary injection of acetylcholine in the control group. Plasma beta-thromboglobulin levels remained unchanged after the attacks in both patient groups and after acetylcholine in the control group. Our data indicate that coronary spasm induces thrombin generation and may lead to thrombus formation in the coronary artery involved, but pacing-induced ischemia does not activate the coagulation system.

Topics: Angina Pectoris; beta-Thromboglobulin; Cardiac Pacing, Artificial; Coronary Circulation; Coronary Vasospasm; Fibrinopeptide A; Humans; Lactates; Lactic Acid; Physical Exertion

Plasma levels of fibrinopeptide A (FPA), beta-thromboglobulin (BTG), and platelet factor 4 (PF4) were examined on venous plasma samples taken every 4 hours for 24 hours in 20 patients with variant angina and 20 patients with stable exertional angina together with 24-hour Holter recordings. The mean plasma FPA levels (ng/ml) at 2:00 PM, 6:00 PM, 10:00 PM, 2:00 AM, 6:00 AM, and 10:00 AM were 4.6 +/- 1.0, 3.1 +/- 0.5, 6.1 +/- 1.6, 9.9 +/- 2.4, 8.7 +/- 1.4, and 4.2 +/- 0.8 in patients with variant angina (p less than 0.01) and 1.8 +/- 0.2, 2.3 +/- 0.3, 1.9 +/- 0.3, and 2.3 +/- 0.2 in those with stable exertional angina. In seven patients with variant angina, we also examined the effects of heparin (3,000 units), given subcutaneously at 6:00 PM, 10:00 PM, and 2:00 AM, on the plasma FPA levels and the anginal attacks. Although heparin suppressed the elevation and circadian variation of plasma FPA levels, it did not suppress the attacks and their circadian variation in these patients. Plasma FPA levels increased significantly from 3.7 +/- 0.5 to 12.5 +/- 2.7 ng/ml during or immediately after an attack in the seven patients with no heparin. On the other hand, the plasma levels of BTG and PF4 were increased in patients with variant angina as compared with those with stable exertional angina but did not show a significant circadian variation in both groups. We conclude that 1) plasma levels of FPA, BTG, and PF4 were increased in patients with variant angina as compared with those with stable exertional angina; 2) there was a significant circadian variation in the plasma levels of FPA in parallel with that of the frequency of the attacks with the peak level occurring from midnight to early morning in patients with variant angina; and 3) elevated levels of plasma FPA are the result and not the cause of coronary spasm.

Topics: Angina Pectoris; Angina Pectoris, Variant; beta-Thromboglobulin; Circadian Rhythm; Electrocardiography, Ambulatory; Female; Fibrinogen; Fibrinopeptide A; Heparin; Humans; Male; Middle Aged; Physical Exertion; Platelet Factor 4

Fibrinopeptide A (FPA) levels were determined in 40 consecutive patients admitted to the coronary care unit with a typical history of chest pain: in 24 of them a diagnosis of acute myocardial infarction (AMI) and in 16 a diagnosis of angina was made. Seven of the patients with AMI suffered from recurrent episodes of early post-infarctional angina. FPA levels were determined in each patient on admission and every 4 h for 48 h. On admission in patients with both angina and AMI the FPA levels were significantly higher than in normal controls; these levels were higher in patients with AMI than in those with angina, but this difference was not significant. In patients with angina the values decreased progressively after 12 h to baseline values, while in those with AMI the high levels of FPA persisted throughout the 48-hour observation period. In many instances, particularly after 24 h, the differences between the two groups were statistically significant. In patients with early post-infarctional angina the episode of angor was preceded by or corresponded to a new great elevation of FPA levels. These data suggest that the thrombin generation is higher and more prolonged in patients with AMI than in those with angina; the determination of FPA levels, which are an index of 'in vivo' thrombin generation, can be useful to follow the clinical course of ischaemic heart disease.

Topics: Adult; Aged; Angina Pectoris; Coronary Disease; Fibrinogen; Fibrinopeptide A; Humans; Middle Aged; Myocardial Infarction

Because acute coronary thrombosis can cause unstable coronary artery disease, fibrinopeptide A, a reliable marker of coagulation activity, may play a role in the evaluation of unstable ischemic syndromes. A new method of fibrinopeptide A sampling, spot urine normalized to urinary creatinine, was evaluated in patients with stable and unstable angina pectoris and acute myocardial infarction. Serial samples were obtained to characterize the changes in urinary fibrinopeptide A levels over time in patients with ischemic heart disease. Admission values (mean +/- SD) were similar in the control group (3.3 +/- 1.4 ng/mg creatinine) and the stable angina group (3.2 +/- 1.1 ng/mg creatinine) (p = NS). Values in the unstable angina group (5.7 +/- 2.6 ng/mg creatinine) were higher than those in the control (p = 0.008) and stable angina (p less than 0.001) groups. Myocardial infarction admission values (8.4 +/- 10.0 ng/mg creatinine) were higher than those in the control (p = 0.005) and stable angina (p less than 0.001) groups, but not higher than those in the unstable angina group. Peak values (the highest of multiple samples) were higher in the unstable angina group (7.6 +/- 5.9 ng/mg creatinine) than in the stable angina group (4.0 +/- 1.0 ng/mg creatinine) (p = 0.04), but not in the control group (4.5 +/- 1.9 ng/mg creatinine) (p = 0.056). The two patients with unstable angina with the highest peak values subsequently exhibited infarction. Peak values in patients with infarction (44.5 +/- 60.0 ng/mg creatinine) were significantly higher than those in patients with unstable (p = 0.03) or stable (p = 0.002) angina and control patients (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Angina Pectoris; Angina, Unstable; Coronary Disease; Female; Fibrinogen; Fibrinopeptide A; Humans; Male; Middle Aged; Myocardial Infarction; Prospective Studies

Topics: Adult; Angina Pectoris; Angina, Unstable; beta-Thromboglobulin; Diltiazem; Drug Evaluation; Female; Fibrinogen; Fibrinopeptide A; Humans; Male; Middle Aged

Protein C and fibrinopeptide A (FpA) levels in plasma were measured in 30 controls and in two groups of patients with angina. The first group was formed by 27 patients suffering from spontaneous ischemic attacks (active angina). The second one was formed by patients who had previously suffered from angina, but were free from myocardial ischemic attacks for at least one month (inactive angina). Protein C (measured by electroimmunoassay) and FpA (radioimmunoassay) were higher than controls in both groups but were significantly higher in patients with active angina than in patients with inactive angina. A clear trend toward a linear correlation existed between protein C and FpA levels, though it did not reach the statistical significance. These results confirm a significant involvement of blood clotting system in ischemic heart disease and specially in active angina.

Topics: Adult; Aged; Aged, 80 and over; Angina Pectoris; Fibrinogen; Fibrinopeptide A; Humans; Middle Aged; Protein C

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

In this study, betathromboglobulin (BTG) and fibrinopeptide A (FPA) in peripheral venous blood were measured in 20 patients with stable angina pectoris before and immediately after exercise-induced myocardial ischaemia; in 5 of the 20 patients stable angina was associated with typical peripheral artery disease. A total of 10 patients with angiographically documented peripheral artery disease without angina and 10 normal volunteers were taken as control groups. BTG and FPA in the 15 patients with stable angina before exercise were 41 +/- 14 ng ml-1 and 2.3 +/- 0.9 ng ml-1 and were not statistically different from the values in normal controls; after exercise-induced myocardial ischaemia no significant increase occurred in these patients. Conversely, in the 5 patients with stable angina associated with peripheral artery disease BTG and FPA before exercise were 61 +/- 10 ng ml-1 and 3.5 +/- 0.8 ng ml-1 and increased to 114 +/- 14 ng ml-1 (P less than 0.001) and 4.1 +/- 0.5 ng ml-1 (P less than 0.01): These results were similar to those found in the 10 patients with isolated peripheral artery disease. We conclude that BTG and FPA in peripheral venous blood in patients with stable angina are not elevated either at rest or after exercise-induced myocardial ischaemia. Elevated values of BTG and FPA in patients with stable angina may reflect a major interaction between blood and atherosclerotic vessel wall, suggesting the presence of associated atherosclerotic lesions in peripheral artery disease.

Topics: Angina Pectoris; beta-Thromboglobulin; Coronary Disease; Fibrin; Fibrinopeptide A; Humans; Male; Physical Exertion; Platelet Aggregation

Thirty-seven patients affected by spontaneous angina and 15 comparable control subjects were enrolled in a 12-month prospective study to evaluate the relationship between blood clotting activation (assessed by fibrinopeptide A [FPA] plasma concentration) and the occurrence of myocardial ischemic attacks. FPA measurements and clinical examinations in patients were performed every 2 weeks. In control subjects blood sampling was performed every 4 weeks. Data from 28 patients who completed the study and from the 15 control subjects were analyzed. The clinical activity of angina was divided into three classes (asymptomatic, mildly symptomatic, and severely symptomatic) on the basis of the number and time-concentration of the ischemic attacks and ECG changes during the 15 days preceding each clinical examination. In all but one patient, a cyclic pattern of activity of coronary artery disease was observed. During follow-up studies, 624 FPA measurements were performed in patients and 173 in control subjects. Mean values were 4.68 +/- 4.53 and 1.32 +/- 0.60 ng/ml, respectively (p less than 0.001). FPA levels differed markedly in relation to the activity of angina. A relationship between FPA levels and activity of disease (r = 0.54, p less than 0.01) was found in time course. Bolus heparin administration (100 IU/kg) during the active phase of angina sharply but incompletely lowered FPA plasma levels, indicating thrombin formation both intravascularly and extravascularly. Present results indicate that a marked blood clotting activation occurs simultaneously with the outbursts of clinical activity of spontaneous angina.

Topics: Adult; Aged; Angina Pectoris; Female; Fibrinogen; Fibrinopeptide A; Humans; Male; Middle Aged; Prospective Studies; Time Factors

Fibrinopeptide A (FpA) concentrations in plasma and in 24 hr urine specimens as well as beta-thromboglobulin (BTG) in plasma were measured in 17 patients with severe angina pectoris, including both stable and unstable angina, and in 19 patients with acute myocardial infarction. Patients with unstable angina had plasma FpA and BTG levels of 5.2 +/- 1.7 ng/ml and 91 +/- 23 ng/ml, respectively. The corresponding concentrations of FpA in the 24 hr urine specimens were 8.2 +/- 1.4 micrograms/24 hr. These values were similar to those measured in patients with acute myocardial infarction and higher than the corresponding levels in patients with stable angina (p less than .05) and in normal control subjects (p less than .01). The similarity of the platelet and coagulation findings in patients with unstable angina and in those with myocardial infarction favors the hypothesis that coronary thrombosis may play a major role in the pathogenesis of acute myocardial infarction.

Topics: Angina Pectoris; Beta-Globulins; beta-Thromboglobulin; Blood Coagulation; Fibrinogen; Fibrinopeptide A; Humans; Myocardial Infarction

The purpose of this study was to investigate the degree of platelet activation and thrombin generation in 40 patients with stable angina pectoris and in 20 patients with acute myocardial infarction (AMI) by determining the plasma beta thromboglobulin (BTG) and fibrinopeptide A (FPA) concentrations. In patients with angina pectoris increased platelet activation correlated with extensive coronary pathology; the activation, however, was not influenced by a previous myocardial infarction, use of oral anticoagulants, beta-blocking agents, or hyperlipidemia. The plasma beta thromboglobulin concentration predicted more accurately the extent of the coronary artery disease than the functional angina pectoris classification. Thrombin generation was within the normal range. In patients with acute myocardial infarction increased platelet activation and enhanced thrombin generation were found, which were not related to the infarct localization, infarct size, or the presence of complications. Consequently, in these patients determination of plasma beta thromboglobulin and fibrinopeptide A concentrations is useless for the diagnosis of venous thromboembolism.

Topics: Adult; Aged; Angina Pectoris; Beta-Globulins; beta-Thromboglobulin; Blood Platelets; Coronary Disease; Fibrinogen; Fibrinopeptide A; Humans; Middle Aged; Myocardial Infarction; Myocardium; Thrombin; Thrombophlebitis