Disease relevance of Angina, Unstable

• 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 [1].
• Among the patients admitted with a diagnosis of acute myocardial infarction, unstable angina preceded infarction in 14 of the 22 patients (64 percent) with levels of C-reactive protein and serum amyloid A protein > or = 0.3 mg per deciliter but in none of the 7 patients with levels < 0.3 mg per deciliter [2].
• METHODS: In a double-blind, placebo-controlled study, we randomly assigned 3171 patients with angina at rest or non-Q-wave myocardial infarction to receive either 1 mg of enoxaparin (low-molecular-weight heparin) per kilogram of body weight, administered subcutaneously twice daily, or continuous intravenous unfractionated heparin [3].
• Silent ischemia in unstable angina: altered cardiac norepinephrine handling [4].
• CONCLUSIONS: Our data indicate that in patients with unstable angina pectoris, intracoronary thrombus formation is associated with a hypercoagulative state, including activation of the contact phase and of the kallikrein system and increased bradykinin generation [5].

Psychiatry related information on Angina, Unstable

• Accordingly, combined treatment with aspirin and heparin has proved more efficacious than either treatment alone in the risk reduction of serious cardiac events in patients with unstable angina or non-Q-wave infarction [6].

High impact information on Angina, Unstable

• CONCLUSIONS: In patients with unstable angina and myocardial infarction without ST-segment elevation who were treated with the glycoprotein IIb/IIIa inhibitor tirofiban, the use of an early invasive strategy significantly reduced the incidence of major cardiac events [7].
• CONCLUSIONS: Pravastatin has a moderate effect in reducing the risk of stroke from any cause and the risk of nonhemorrhagic stroke in patients with previous myocardial infarction or unstable angina [8].
• METHODS: Among 1265 patients with unstable angina who were enrolled in the c7E3 Fab Antiplatelet Therapy in Unstable Refractory Angina (CAPTURE) trial, serum samples drawn at the time of randomization to abciximab or placebo were available from 890 patients; we used these samples for the determination of troponin T and creatine kinase MB levels [9].
• C-reactive protein and serum amyloid A protein in unstable angina [10].
• The prognostic value of C-reactive protein and serum amyloid a protein in severe unstable angina [2].

Chemical compound and disease context of Angina, Unstable

• Reactivation of unstable angina after the discontinuation of heparin [11].
• BACKGROUND: In patients with refractory unstable angina, the platelet glycoprotein IIb/IIIa-receptor antibody abciximab reduces the incidence of cardiac events before and during coronary angioplasty [9].
• Cardiac troponin T in serum appears to be a more sensitive indicator of myocardial-cell injury than serum creatine kinase MB activity, and its detection in the circulation may be a useful prognostic indicator in patients with unstable angina [12].
• If so, biochemically selective inhibition of the synthesis or action of thromboxane A2 would be desirable in the treatment of unstable angina [1].
• Prostacyclin for unstable angina [13].

Biological context of Angina, Unstable

• METHODS AND RESULTS: Platelet P-selectin (CD62) and activated GP IIb/IIIa (PAC-1) expression on platelet membrane was quantified in whole blood as well as platelet aggregation in platelet-rich plasma in 43 patients with unstable angina before and during treatment with UFH or enoxaparin [14].
• BACKGROUND: We have previously reported aspirin failure in suppressing enhanced thromboxane (TX) biosynthesis in a subset of episodes of platelet activation during the acute phase of unstable angina [15].
• Left ventricular ejection fraction averaged 65 +/- 11% (mean +/- standard deviation) at control, decreased in all patients during angina at rest to 49 +/- 14% (p less than 0.01) and increased in all patients after isosorbide dinitrate to 66 +/- 12% [16].
• The natural history of medically treated patients with pure coronary spasm is characterized by recurrent angina at rest, frequent spontaneous remission, a poor response to long-acting nitrate therapy and a good response to calcium antagonists [17].
• Platelet activation in unstable angina: role of thromboxane A2 and other mediators of vasoconstriction [18].

Anatomical context of Angina, Unstable

• In patients with unstable angina, monocyte TF expression (both stimulated and unstimulated, assessed by biological activity and by antigen techniques) and fibrinogen levels were correlated with the time elapsed from the beginning of the most recent episode of pain (.61 < r < .72, .02 < P < .0001) [19].
• Lymphocytes in patients with stable and unstable angina showed a similar percent expression of CD2/CD19 and CD3/HLA-DR antigens, with no difference between aortic and coronary sinus blood [20].
• Intracellular neutrophil myeloperoxidase is reduced in unstable angina and acute myocardial infarction, but its reduction is not related to ischemia [21].
• Seventy-two patients with stable or unstable angina treated since 1983 by multivessel-PTCA(MVP) were retrospectively compared with 44 similar patients that were suitable for MVP, but who had undergone bilateral mammary artery (BIMA) surgery (and additional vein grafts in 60.5% of the patients) since 1986 [22].
• Stem cells in unstable angina: the dynamic duo [23].

Gene context of Angina, Unstable

• In protocol B, CRP, SAA, and IL-6 did not change in stable angina patients after angiography but increased in unstable angina patients (all P<0.05) [24].
• Elevated basic fibroblast growth factor in pericardial fluid of patients with unstable angina [25].
• CONCLUSIONS: Similar to CRP, baseline elevation of SAA identifies patients hospitalized with unstable angina and NQMI at higher risk for early mortality, even among those with a negative rapid assay for cTnT [26].
• 2) T cells, and particularly monocytes, seem to contribute to the raised IL-8, MCP-1 and MIP-1-alpha levels in unstable angina [27].
• Serum levels of soluble TRAIL but not TNF-alpha or Fas-ligand were reduced significantly in patients with unstable angina as compared with patients with stable atherosclerotic disease and healthy subjects [28].

Analytical, diagnostic and therapeutic context of Angina, Unstable

• Adding heparin to aspirin reduces the incidence of myocardial infarction and death in patients with unstable angina. A meta-analysis [29].
• These pilot study results support the concept that effective blockade of the platelet GPIIb/IIIa receptors can reduce myocardial infarction and facilitate PTCA in patients with refractory unstable angina [30].
• The influence of captopril on recurrent MI, cardiac revascularization procedures, and hospitalization with unstable angina was examined [31].
• Significantly fewer patients were rehospitalized for unstable angina in the warfarin group than in the control group (7.1% and 17.2%, respectively; RR, 0.42; 95% CI, 0.18 to 0.96; P=0.03) [32].
• CONCLUSIONS: Our results add to previous evidence suggesting that the low-molecular-weight heparin dalteparin administered by twice-daily subcutaneous injection may be an alternative to unfractionated heparin in the acute treatment of unstable angina or non-Q-wave myocardial infarction [33].

References