Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A group of patients with athero-arteriosclerotic vascular disease (coronary heart disease and atherosclerosis of the extremities) have been subjected to platelet antiaggregating-antidyslipidaemic treatment with a chlofibrate-dipyridamol association; a control series was treated with chlofibrate alone. Frequency of angina pectoris, pain intensity and trinitrine consumption ware evaluated in patients with coronary heart disease, claudicometry, oscillometry and thermometry in patients with atherosclerosis of the extremities. The following laboratory parameters were also analysed: cholesterolaemia, triglyceridaemia, prothrombin activity, fibrinogenaemia, uricaemia and tolerance of oral glucose loading. Analysis of the results has shown that the association improved the parameters considered in statistically significant fashion; chlofibrate alone led to significant modifications of coronaropathic group parameters (with the exception of pain intensity) whereas it did not lead to significant changes in parameters evaluated for atherosclerosis of the extremities. All laboratory parameters were modified favourably by the association to a statistically greater extent than by chlofibrate alone. Both the association and chlofibrate were well tolerated.
 ...
PMID:[The clofibrate-dipyridamole combination in the treatment of athero-arteriosclerotic vasculopathy]. 43 77

Twenty-seven patients underwent reoperation because of thrombotic obstruction of a disc-type cardiac valve prosthesis. Preoperative clinical features included effort dyspnea in 81%, new-onset angina in 44%, a new murmur in 89%, and an abnormal opening or closing sound associated with the prosthetic valve in 56%. Symptoms were present for 1 week or more before reoperation in 86%, although many patients were referred only after acute exacerbation of heart failure and development of pulmonary edema. Noninvasive studies confirmed prosthetic valve malfunction in only 33%, but cardiac catheterization documented thrombotic obstruction in all 15 patients in whom it was performed. In 14 of the 27 patients, prothrombin time was in the therapeutic range at the time of admission. Prompt reoperation for valve replacement or thrombectomy was performed with an operative mortality of 11%, and long-term outcome was satisfactory in all but 1 hospital survivor. These findings emphasize the importance of considering the diagnosis of thrombosed heart valves in patients with mechanical heart valves who are seen with nonspecific symptoms.
 ...
PMID:Thrombotic obstruction of disc valves: clinical recognition and surgical management. 276 2

The use and type of antithrombotic therapy for patients with cardiac disease are described based on an understanding of the pathophysiologic mechanisms involved, the risk of thromboembolism, and the evidence from prospective and, if necessary, retrospective clinical trials. The indications and intensity of anticoagulant therapy in patients with valvular heart disease and prosthetic valves are first discussed. We recommend that the prothrombin time be reported as a ratio and standardized using the International Normalized Ratio. The pivotal role of platelets and the clotting system in the initiation and progression of atherosclerosis and the acute coronary syndromes is described. There is no evidence to date that antiplatelet therapy is of value in primary prevention or in patients with stable angina, but the value of aspirin in patients with unstable angina was clearly shown in two well-designed studies. Adequate prophylactic therapy to prevent the thrombotic complications of acute myocardial infarction (i.e., venous thrombosis and intracardiac thrombosis) is described, and the available data on the prevention of coronary reocclusion after thrombolysis reviewed. There is now convincing evidence from studies in animals and in patients that vascular injury during aortocoronary vein bypass graft surgery requires antitihrombotic therapy starting before the procedure to minimize acute platelet thrombus deposition and prevent occlusion. Restenosis after arterial angioplasty appears to be related to acute platelet thrombus deposition on the site of deep arterial injury. Therapeutic interventions should probably involve both anticoagulants and platelet inhibitor therapy. Implications derived from recent animal studies are discussed.
 ...
PMID:Antithrombotic therapy for patients with cardiac disease. 307 28

To determine the influence of adjunctive treatment with coumadin or aspirin on recurrence rate after percutaneous transluminal coronary angioplasty (PTCA), 248 patients in whom PTCA was assessed to be a primary success were randomized to either 325 mm aspirin daily or to coumadin treatment sufficient to maintain a prothrombin time 2 to 2.5 times the control value. The follow-up protocol included stress testing and coronary angiographic examinations 3 to 6 months after PTCA. All patients were followed for at least 9 months. Of the 122 patients randomized to coumadin 44 (36%) had recurrent stenoses as opposed to 34/126 (27%) of patients on aspirin, a difference that did not reach statistical significance at the .05 level. However, patients with at least a 6 month history of angina demonstrated a significantly different response to adjunctive treatment in that 19/43 (44%) of coumadin patients as compared with 10/48 (21%) of aspirin patients had recurrent stenoses (p less than .05). Thus, coumadin was not shown to be more effective than aspirin as adjunctive treatment after PTCA, while aspirin was shown to be superior to coumadin in patients with a longer history of angina.
 ...
PMID:Coumadin and aspirin in prevention of recurrence after transluminal coronary angioplasty: a randomized study. 623 Jan 74

Plaque rupture with the exposure of a tissue factor-rich procoagulant surface is considered the common pathogenetic mechanism of unstable angina and myocardial infarction. Activated factor VII, the key enzyme for initiating blood coagulation under resting conditions, is increased in pathological situations associated with tissue factor exposure. We measured the plasma levels of activated factor VII and studied their relation with signs of coagulation enzyme activity in patients with acute coronary syndromes. The plasma levels of activated factor VII, prothrombin fragment 1 + 2, and fibrinopeptide A were measured on admission in consecutive patients presenting with acute myocardial infarction (n = 28), unstable angina (n = 32), and stable angina (n = 17) and in age- and sex-matched healthy individuals (n = 33). Plasma determinations of the same markers were also repeated at 15 days and 3 and 6 months. On admission, the patients with unstable angina or myocardial infarction had significantly higher plasma levels of prothrombin fragment 1 + 2 (P < .0001) and fibrinopeptide A (P < .0001) than those with stable angina or healthy individuals, whereas no differences were detected in the plasma levels of activated factor VII. During follow-up there was a significant decrease in the plasma levels of fibrinopeptide A both in patients with unstable angina (P < .001) and in those with myocardial infarction (P < .001), whereas no changes in plasma prothrombin fragment 1 + 2 or activated factor VII levels were observed. Hence, in the acute and chronic phases of myocardial infarction and unstable angina, heightened coagulation enzyme activity is not accompanied by an increase in activated factor VII.
 ...
PMID:Heightened thrombin formation but normal plasma levels of activated factor VII in patients with acute coronary syndromes. 758 43

Ischemic electrocardiographic changes were recorded within 2 hours of admission using a 12-lead electrocardiographic continuous monitor with a 20-second scanning interval and an alarm mode for asymptomatic events. Blood samples were obtained at admission and at the moment of asymptomatic events (group A). In the other patients who did not develop ischemia, a second blood sample was taken 12 hours later (group B). We determined prothrombin time, activated partial thromboplastin time, clotting factor VIII activity, tissue plasminogen activator activity, tissue plasminogen activator inhibitor-1, cross-linked fibrin degradation product, and thrombin-antithrombin III complexes. There was a statistically significant difference between group A and B patients when the basal samples were analyzed for thrombin-antithrombin III (p = 0.046) and d-Dimer (p = 0.005). Prothrombin fragment 1 + 2 were significantly reduced, and d-Dimer was elevated when basal blood samples were compared with the second sample in patients who developed silent events (p = 0.008 and 0.055, respectively). A plasma concentration of thrombin-antithrombin III complex was also significantly decreased when sample 2 was compared with the basal blood sample (p = 0.039). Five recurrent episodes of angina and 2 nonfatal infarctions occurred, and 4 urgent revascularization procedures were performed in group A. In group B, there was only 1 nonfatal infarction (p = 0.01). The results of the present study suggest that a time-dependent thrombotic process is detectable in the blood stream as a cyclic movement. Further studies are needed to determine if some other factors, such as intensive shear stress in the vessel wall, may activate plaque instability during asymptomatic episodes.
 ...
PMID:Time significance of acute thrombotic reactant markers in patients with and without silent myocardial ischemia and overt unstable angina pectoris. 761 Nov 44

To characterize the extent of early activation of the hemostatic system following angioplasty, we obtained blood samples from the involved coronary artery of 11 stable angina patients during the procedure and measured sensitive markers of thrombin formation (fibrinopeptide A, prothrombin fragment 1.2, and soluble fibrin) and of platelet activation (beta-thromboglobulin). Levels of hemostatic markers in venous blood obtained from 14 young individuals with low pretest probability for coronary artery disease were not significantly different from levels in venous blood or intracoronary samples obtained prior to angioplasty. Also, there was no translesional (proximal and distal to the lesion) gradient in any of the hemostatic markers before or after angioplasty in samples obtained between 18 and 21 min from the onset of the first balloon inflation. Furthermore, no significant difference was noted between angioplasty and postangioplasty intracoronary concentrations. We conclude that intracoronary hemostatic activation does not occur in the majority of patients during and immediately following coronary angioplasty when high doses of heparin and aspirin are administered.
 ...
PMID:Markers of hemostatic activation in affected coronary arteries during angioplasty. 790 72

From January 1990 to February 1993, 88 patients (group 1) received an emergency stent implantation with threatening vascular occlusion within the framework of an elective PTCA or a second emergency PTCA after up to 5 days following a primary successful PTCA. In addition, 36 patients (group 2) received an intracoronary stent during emergency PTCA of instable angina pectoris or acute myocardial infarction. The attempted stent implantation was not successful in 6 other patients. All patients were anticoagulated with heparin, aspirin (100 to 500 mg), and phenprocoumon. Since October 1991, 3 x 75 mg dipyridamole was given and heparinization was stopped after measuring the anticoagulation factor II (prothrombin time < 40%). Main complications within the first 2 to 3 weeks were acute and subacute stent thrombosis (21.8%) and complications of the puncture site (bleeding 19.3%, a. spurium/av-fistula 1.6%). The risk of acute stent thrombosis was significantly higher in patients of group 2 (instable angina pectoris despite of drug therapy or acute myocardial infarction) compared with group 1 (42.4 versus 14.8%). Implantation of multiple stents to stabilize extended dissections had a lower occlusion rate (6.3%). Acute myocardial infarctions were registered in group 1 in 25% (11.4% following implantation, 13.6% following stent occlusion, CK 153 to 3380 U/I, average 826 U/I) and in 58.3% of the high risk patients in group 2 (50% just before or following implantation, 36.1% infarctions or re-infarctions caused by stent occlusion, CK 152 to 1950 U/I, average 657 U/I). The risk of infarction could be limited to approximately 58% of the patients of group 2.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Emergency intracoronary stent implantation: complications and experiences with 124 patients]. 805 40

Despite developments in percutaneous transluminal coronary angioplasty, the success of this treatment method remains clouded by early and late reocclusion. Increased experience, advances in technology, and the introduction of adjunctive devices have contributed to a higher procedural success rate (90% to 95%) and to a lower complication rate (4% to 5%), in spite of the expanded indications for angioplasty. Late renarrowing of the treated coronary artery, in combination with recurrence of angina pectoris, occurs in 15% to 40% of angioplasty patients. Several multicenter randomized trials of pharmaceutical agents have been conducted or are in progress, in an effort to diminish the rate of late reocclusion. No major breakthrough has been reported, although a clear progression has been made in the understanding of the restenosis phenomenon. It is evident that thrombin plays a detrimental role in the vascular wall injury resulting from angioplasty procedures. Current pharmacologic research concentrates on direct inhibition of prothrombin conversion and thrombus formation. Animal experimental work in this field is encouraging, and the results of clinical trials will elucidate important questions about the safety, efficacy, and immuno-allergic potential of modern antithrombotic medication.
 ...
PMID:Thrombin and antithrombotic therapy in interventional cardiology. 806 38

Plasma levels of the prothrombin activation fragment 1 + 2 (F 1 + 2) and of thrombin antithrombin III complexes (TAT) were determined in 225 patients with angina pectoris undergoing coronary angiography. Oral anticoagulant therapy was associated with a marked reduction in mean F1 + 2 (0.63 vs 1.62 nmol/l, p < 0.0001) and TAT levels (1.65 vs 2.23 micrograms/l, p < 0.0001). Omitting patients on oral anticoagulants, TAT values showed a positive association with patients' age (r = 0.18; p = 0.01) and were slightly higher in patients with a history of myocardial infarction than in those without (2.47 vs 2.11 micrograms/l; p = 0.06). Both F1 + 2 and TAT levels were increased in patients with angiographically verified coronary atherosclerosis as compared to patients with angina and angiographically normal coronaries (F1 + 2: 1.76 vs 1.36 nmol/l, TAT: 2.35 vs 2.00 micrograms/l; p-values after adjusting for age, sex and past history of myocardial infarction 0.06 and 0.11 respectively). However, no graded relationship between F1 + 2 or TAT values and severity of atherosclerosis was observed. This study provides suggestive evidence that a procoagulant state exists in patients with angina pectoris and coronary atherosclerosis. Its relevance in predicting coronary ischaemic events needs to be studied prospectively.
 ...
PMID:Prothrombin activation fragment 1 + 2 and thrombin antithrombin III complexes in patients with angina pectoris: relation to the presence and severity of coronary atherosclerosis. 811 78


1 2 3 4 5 Next >>