fibrin and Angina-Pectoris

Topics: Angina Pectoris; Coronary Artery Bypass; Coronary Circulation; Coronary Vessels; Fibrin; Humans; Myocardium; Necrosis; Postoperative Complications; Saphenous Vein; Thrombosis; Transplantation, Autologous

Web-like (W) and membrane-like (M) structures have been observed on coronary stent edges on angioscopy but their incidence and mechanisms remain obscure.. First, 26 patients [acute coronary syndromes (ACS) in 10 and stable angina (SA) in 16] underwent angioscopy of the stented coronary artery immediately after, and 32 patients (ACS in 18 and SA in 14) 6 months after insertion of bare-metal stents. Second, angioscopy of the stented coronary artery was performed in 4 beagles 5 h after, and in 9 beagles 1 month after stenting. W and M were observed in patients with ACS and those with SA (80.0% vs 18.7%; P<0.05) immediately after and 6 months after stenting (55.5% vs 28.5%; NS). They were stained with Evans blue that selectively stains fibrin immediately after stent insertion, but not 6 months later. In beagles, W and M were observed in 75.0% at 5 h and in 66.6% 1 month later. Histologically, W and M were composed of fibrin at 5 h, whereas they were composed of collagen fibers at 1 month.. W and M were frequently formed on the edges of coronary stents. They were formed with fibrin in the acute phase, whereas this fibrin was replaced by collagen fibers in the chronic phase.

Topics: Acute Coronary Syndrome; Angina Pectoris; Angioscopy; Animals; Collagen; Coronary Vessels; Dogs; Fibrin; Humans; Stents; Time Factors

The long-term safety of drug-eluting stents (DES) for acute myocardial infarction (AMI) remains uncertain. Using autopsy data, we evaluated the pathological responses of the stented segment in patients treated with DES for AMI and compared with patients with stable angina.. From the CVPath Registry of 138 DES autopsies, we identified 25 patients who presented with AMI and had an underlying necrotic core with a ruptured fibrous cap. Twenty-six patients who had stable angina with thick-cap fibroatheroma treated by DES were selected as controls. Histomorphometric analysis was performed in patients with >30-day stent duration. We compared the response to stenting at the culprit site in these 2 groups and to nonculprit sites within each stent. Late stent thrombosis was significantly less frequent in stable (11%) than in AMI (41%; P=0.04) patients. Although neointimal thickness in the AMI culprit site was significantly less (median, 0.04 mm; interquartile range [IQR], 0.02 to 0.09 mm), the prevalence of uncovered struts (49%; IQR, 16% to 96%), fibrin deposition (63+/-28%), and inflammation (35%; IQR, 27% to 49%) were significantly greater compared with the culprit site in stable patients (neointimal thickness: 0.11 mm [IQR, 0.07 to 0.21 mm], P=0.008; uncovered struts: 9% [IQR, 0% to 39%], P=0.01; fibrin: 36+/-27%, P=0.008; inflammation, 17% [IQR, 7% to 25%], P=0.003) and the nonculprit site within each stent.. Vessel healing at the culprit site in AMI patients treated with DES is substantially delayed compared with the culprit site in patients receiving DES for stable angina, emphasizing the importance of underlying plaque morphology in the arterial response to DES. Our data suggest an increased risk of thrombotic complications in patients treated with DES for AMI.

Topics: Adult; Aged; Angina Pectoris; Autopsy; Coronary Vessels; Drug-Eluting Stents; Female; Fibrin; Humans; Inflammation; Male; Middle Aged; Myocardial Infarction; Prosthesis Implantation; Retrospective Studies; Thrombosis; Time Factors; Treatment Outcome

The purpose of the study was to measure the blood level of thrombus precursor protein (TpP), a soluble fibrin monomer, in patients with stable exertional angina (SEA) and healthy people. The study included the examination of 33 patients with SEA (functional class II and III) and 29 practically healthy volunteers (control group). The detection of TpP in blood plasma was performed by solid-phase immune-enzyme analysis ("sandwich" type) using commercial diagnosticum "Kit" ("ABS", USA) and a microplate reader "IEMS Analyzer\\Dispenser, with automatic result calculation in "Logistic fif" mode. TpP level in patients with SEA on the average was slightly higher than in control group, but the difference was not significant. TpP blood level was independent of the patients' gender, age, angina functional class and an old myocardial infarction. TpP blood level in patients with SEA depended on the duration of the illness, and proved to be significantly higher (compared with that in control group) in patients with SEA during the first 5 years of the illness, i.e. at early stages of CHD. Solid-phase immune-enzyme analysis ("sandwich" type) is a highly informative and affordable clinical method. TpP level in patients with SEA on the average was slightly higher than in healthy people (1.21 +/- 0.06 mkg/ml and 1.01 +/- 0.12 mkg/ml, respectively), but the difference was significant only in patients during the first 5 years of having SEA (1.41 +/- 0.11 mkg/ml).

Topics: Adult; Aged; Aged, 80 and over; Angina Pectoris; Biomarkers; Disease Progression; Female; Fibrin; Humans; Immunoenzyme Techniques; Male; Middle Aged; Severity of Illness Index; Time Factors

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

The in vitro effect of acetylsalicylic acid (ASA) on fibrin gel lysis by exogenous t-PA was studied in 13 patients with angina pectoris. Six patients received 75 mg, and seven patients 160 mg of ASA. Plasma clots were formed and lysed in microtiter plate wells and turbidity monitored spectrophotometrically. Mean lysis times in the 75 mg group were 8.7, 11.4 and 11.2 min during ASA treatment, and after 1 and 2 weeks ASA withdrawal respectively. Reduced changes were observed in the 160 mg group. Additionally, a relationship was found between the fibrin fiber mass/length ratio, i.e. fiber thickness in mature clots and lysis times after ASA administration (P = 0.0015). Importantly, fibers are thicker during treatment with ASA. It was subsequently demonstrated that the potential to produce thicker fibers by varying the thrombin concentration has a noticeable effect on turbidimetric profiles in the presence of exogenous t-PA. This effect was similar to the changes observed during and after ASA treatment. Thus, these results suggest that the enhancement of fibrin gel lysis during ASA treatment may be due to alterations in gel structure. In addition, a reduction in the fibrin mass in lower turbidity clots, suggests an added mechanism by which ASA may enhance lysis.

Topics: Angina Pectoris; Aspirin; Fibrin; Humans; Time Factors; Tissue Plasminogen Activator

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

Two groups of male patients with CHD were examined. The first group (30 persons) was treated with a 30-day therapeutic course of physical training on a bicycle ergometer, the second group received nitrates of prolonged action and beta-blocking agents. Eleven healthy men receiving a course of physical training were entered into the control group. The content of fibrinogen, soluble fibrin and fibrinogen degradation products in the blood plasma was investigated prior to and after a therapeutic course. An analysis of the blood plasma protein spectrum was performed using gel-filtration on a chromatographic column as well as separate disk-electrophoresis of the blood plasma proteins and isolated fractions in polyacrylamide gel. Regular physical training of the CHD patients resulted in a significant decrease in the content of fibrinogen, soluble fibrin and fibrin degradation products in the blood that might be conducive to the improvement of microcirculation and hence to lessening the number of angina attacks in these patients.

Topics: Adult; Angina Pectoris; Blood Protein Electrophoresis; Chromatography, Gel; Coronary Artery Disease; Coronary Disease; Exercise Therapy; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Humans; Male; Middle Aged; Myocardial Infarction; Physical Exertion

Topics: Adolescent; Adult; Angina Pectoris; Chronic Disease; Diabetes Mellitus; Female; Fibrin; Fibrinogen; Hematologic Diseases; Humans; Kidney Diseases; Liver Diseases; Male; Middle Aged; Myocardial Infarction; Neoplasms

Topics: Adult; Aged; Angina Pectoris; Aorta; Arteriosclerosis; Coronary Disease; Female; Fibrin; Fluorescent Antibody Technique; Humans; Immune Sera; Male; Microtomy; Middle Aged; Myocardial Infarction