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

Recent evidence suggests that an inflammatory process has a significant role in the evolution of atherosclerosis. A chronic inflammatory response in the blood vessel's wall causes the formation of a lesion that narrows the artery's lumen and may cause such conditions as stable angina (SA). Destabilization of the atheromatous lesion, blood clot formation and rapid narrowing of the artery lumen may appear as part of an acute process, superimposed on the chronic inflammation. Such an acute process may be the mechanism underlying acute conditions such as unstable angina (UA) or myocardial infarction. Recent studies are trying to shed light on the process which causes destabilization of the atheromatous lesion. These studies implicate T lymphocytes and, especially, T helper 1 (Th1) cells (a sub-population of T lymphocytes) as having an important role in the destabilization of the lesion. Interferon gamma, an important cytokine secreted by Th1 cells, diminishes the production of collagen by smooth muscle cells and activates macrophages which destroy collagen and elastin. Furthermore, interferon gamma encourages clot formation and disrupts production of nitric oxide by endothelial cells. These qualities of interferon gamma support the hypothesis by which Th1 cells play a significant role in the evolution of UA. Unlike Th1 cells, Th2 cells, another sub-population of T lymphocytes, may help protect the atheromatous lesion from destabilization. This hypothesis is supported by the qualities of interleukin 10, one of the important cytokine secreted by Th2 cells. Interleukin 10 diminishes the secretion of interferon-gamma, inhibits the secretion of enzymes which destroy connective tissue in the atheromatous lesion and interferes with clot formation on the unstable lesion.
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PMID:[The role of cytokines secreted by T cells in the pathogenesis of angina pectoris]. 1451 65

Atherosclerotic plaques develop as a consequence of the accumulation of circulating lipid and the subsequent migration of inflammatory cells (macrophages and T-lymphocytes) and VSMCs (vascular smooth muscle cells). Advanced plaques consist of a lipid-rich core, separated from the lumen by a fibrous cap composed of VSMCs, collagen and extracellular matrix. Plaque enlargement ultimately narrows the lumen (stenosis) causing angina. However, recent studies have emphasized that acute coronary syndromes (unstable angina/myocardial infarction) are caused by lesion erosion/rupture with superimposed thrombus formation on often small non-stenotic plaques. Thus current therapies work predominantly on stabilization of plaques rather than plaque regression. Apoptosis (programmed cell death) is increasingly observed as plaques develop, although the exact mechanisms and consequences of apoptosis in the development and progression of atherosclerosis are still controversial. Increased endothelial cell apoptosis may initiate atherosclerosis, whereas apoptosis of VSMCs and macrophages localizes in 'vulnerable' lesions, i.e. those most likely to rupture, and at sites of rupture. This review will focus on the regulation of apoptosis of cells within the vasculature, concentrating on the relevance of apoptosis to plaque progression and clinical consequences of vascular cell apoptosis.
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PMID:Role of apoptosis in atherosclerosis and its therapeutic implications. 1523 Jun 90

Despite major advancements in the technology used for the percutaneous treatment of coronary artery disease, chronic total occlusions (CTOs) persist as a major challenge to the interventional cardiologist with relatively low success rates. CTOs are evident in 20% of patients undergoing cardiac catheterization and are responsible for the majority of cases that are referred to bypass surgery. There is growing evidence that patients may benefit from recanalization of a CTO by alleviation of angina, improving left ventricular function, and potentially long-term survival. The major obstacle to percutaneous recanalization of CTOs is the inability to cross the occlusion with coronary guidewires. Even when crossed, the operator has to deal with the exact location of the distal wire (e.g., dissection or true lumen) and the existence of relatively long lesion requiring multiple stents with high restenosis rates. New technologies for CTO revascularization have been focused mainly on a mechanical approach including specialized guidewires and more recently, specific devices using highly sophisticated technology such as laser guidewire, optical coherence reflectometry, and a blunt microdissection catheter. An alternate biological approach involves the local administration of enzymes such as plasminogen activators (urokinase) or collagenase, which can act locally to specifically degrade the collagen content of the CTO, thereby "softening" the occlusion and allowing easier guidewire crossing. In conclusion, CTOs emerge as a great technical challenge and are the focus of novel series of mechanical and biological approaches.
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PMID:Novel approaches for the treatment of chronic total coronary occlusions. 1554 94

Platelet aggregation is an important in vitro test to assess platelet aggregation response in IHD. The present prospective case control study was undertaken to evaluate the platelet aggregation response in IHD and the effects of aspirin therapy on it. Platelet aggregation was conducted on whole blood by the Chrono- Log whole blood Aggrometer model 540-VS. Various agonists used for platelet aggregation were collagen, ADP, Epinephrine and Thrombin. High platelet aggregation was observed in-patients of IHD as compared to controls by few or all of the reagents used. Platelet aggregation was high in both MI and angina as compared to control cases. However, cases of MI showed higher response than those of angina. Aspirin intake was associated with a decrease in platelet aggregation in patients of IHD. The platelet aggregation response was higher in PRP as compared to whole blood with similar concentration of reagents, however whole blood was equally effective as PRP in detecting hyper-responsive platelets in--patients of IHD.
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PMID:Platelet aggregometric study on whole blood of patients with ischaemic heart disease. 1640 37

Ten patients with chronic stable angina pectoris and ten aged-matched healthy controls were investigated. Aspirin was given as 160 mg/day and clopidogrel as 300 mg loading dose followed by 75 mg/day. Whole blood aggregometry was performed at baseline and after 10 days with collagen or ADP as stimulator. ADP as well as collagen-induced platelet aggregation was each reduced (P<0.02) both in healthy volunteers and in patients with stable angina pectoris with combination therapy compared with aspirin only. In conclusion, treatment with clopidogrel and aspirin provides significantly greater inhibition of platelet activity than aspirin alone in patients with stable angina pectoris and in healthy control subjects.
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PMID:Clopidogrel inhibits platelet aggregation in patients on aspirin with stable chronic angina pectoris. 1732 Feb 8

This study used a small-sized collagen bead column system to investigate platelet functions under high shear stress in 28 patients with effort angina and 15 healthy controls. Soluble P-selectin and soluble L-selectin were also evaluated. Patients underwent stent insertion, followed by treatment with aspirin (100 mg/day) and ticlopidine (200 mg/day). High-shear-dependent platelet function was measured using small-sized collagen beads. The retention rate of platelets from patients with angina was higher than that in healthy controls (10.9% +/- 3.9% versus 5.6% +/- 1.7%, P < .01). Soluble P-selectin and soluble L-selectin levels of patients with angina significantly increased after passage through the columns. Levels of soluble P-selectin and L-selectin in healthy controls did not exhibit significant changes with passage through the columns. These results suggested that high shear stress caused abnormal activation of leukocytes or adhesive proteins in patients with effort angina, and ticlopidine failed to suppress hyperaggregability of platelets in these patients.
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PMID:Evaluation of platelet and leukocyte functions in effort angina patients using high shear conditions in small-sized collagen bead columns. 1791 Nov 96

Radix Salviae miltiorrhiza (RSM, 'Dansham' in Korea, 'Danshen' in Chinese), the root of Salviae miltiorrhiza Bunge (Labiate) has been used as Chinese fork medicine for the treatment of cardiovascular diseases such as angina pectoris, coronary heart disease, myocardial infarction, and hypertension. In the present study, we evaluated the inhibitory effects of 15,16-Dihydrotanshinone I, one of the major ingredients of Salvia miltiorrhiza Bunge, on platelet aggregation, with elucidation of its mechanisms of action. 15,16-Dihydrotanshinone I concentration-dependently inhibited collagen-induced aggregation of rabbit washed platelets with IC50 of 8.7+/-5.6 microM, the potency being about seven-fold greater than EGCG, an active Green tea catechin component (IC50: 56.6+/-48.7 microM). 15,16-Dihydrotanshinone I significantly inhibited the intracellular calcium ([Ca2+]i) mobilization in a concentration-dependent manner. 15,16-dihdydrotanshinone I also significantly suppressed collagen (50 microg/mL)-induced liberation of [3H]Arachidonic acid from [3H]Arachidonic acid-incorporated rabbit platelet. In addition, 15,16-Dihydrotanshinone I at 50 microM slightly but significantly inhibited collagen-induced production of thromboxane B2. These results indicate that 15,16-Dihydrotanshinone I exert potent anti-platelet activity via suppression of [Ca2+]i mobilization and arachidonic acid liberation.
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PMID:15,16-dihydrotanshinone I, a major component from Salvia miltiorrhiza Bunge (Dansham), inhibits rabbit platelet aggregation by suppressing intracellular calcium mobilization. 1827 7

The objectives of this study were to investigate whether the systemic inflammatory response differs, in patients undergoing coronary angiography, among the arterial closure devices FemoStop, AngioSeal, and Perclose. The study is a prospective and randomized study. We measured pre- and postprocedural C-reactive protein (CRP), fibrinogen, and interleukin-6 (IL-6) plasma levels and collected clinical and procedural data on 77 patients who underwent coronary angiography because of stable angina pectoris. Patients were randomized to the following device: FemoStop (mechanical compression), AngioSeal (anchor and collagen sponge), or Perclose (nonabsorbable suture). No patient group experienced an increased incidence of vascular complications. There were no differences among the three groups regarding CRP, fibrinogen, or IL-6 values before or after coronary angiography. IL-6 levels increased 6 h after the procedure in all groups (p < 0.01), however, the increase did not differ among the groups. After 30 days there were no increased values of CRP or fibrinogen. We conclude that the femoral arterial closure devices AngioSeal and Perclose do not enhance an inflammatory response after a diagnostic coronary angiography, measured by CRP, fibrinogen, and IL-6, compared to femoral arterial closure using a mechanical compression device.
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PMID:The inflammatory response to femoral arterial closure devices: a randomized comparison among FemoStop, AngioSeal, and Perclose. 1839 39

Combined antiplatelet therapy reduces recurrent atherothrombotic events in stable coronary disease patients; however, high residual platelet reactivity measured ex vivo still raises concerns as a condition related to treatment failure. Alpha-2 adrenoceptor enhances platelet reactivity and might contribute to this phenomenon. For the present study, 121 stable angina patients on standard dual antiplatelet therapy (75 mg clopidogrel and 100 mg acetylsalicylic acid) were recruited. Born aggregometry was performed with adenosine diphosphate (ADP), collagen and epinephrine. To verify platelet adrenergic activity, potentiation by low-dose epinephrine and inhibition by selective alpha-2 receptor blocker atipamezole were determined. To assess the P2Y(12)-specific residual activity, cangrelor was used. Plasma norepinephrine, soluble CD40-ligand, high-sensitivity-C-reactive protein (hsCRP) - and in 24 subjects platelet P-selectin positivity were measured. Epinephrine - at very low concentration (10(-9)g/ml) - significantly potentiates (1.25 microM ADP: 26.5% vs. 43%; 5 microM ADP: 53% vs. 64.5%; collagen: 17% vs 42%, p < 0.001) while atipamezole inhibits ADP- and collagen-induced platelet aggregations (1.25 microM ADP: 26.5% vs. 23%; 5 microM ADP: 53% vs. 47%; collagen: 17% vs. 11%, p < 0.001). Patients with high adrenergic activity have significantly increased baseline ADP- and collagen-induced platelet aggregation. Based on cangrelor's efficacy, these patients have significantly more residual P2Y(12) activity as well. HsCRP and soluble CD40-ligand levels were similar. In conclusion, stable coronary heart disease patients with prominent adrenoceptor activity in vitro have significantly increased platelet aggregability and more functional P2Y(12) receptor, indicating poor inhibitory response to thienopyridines. Therefore, platelet adrenergic receptor represents a considerable, dynamic factor of high residual platelet reactivity and might contribute to cardiovascular events indicating failure of antiplatelet therapy.
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PMID:Analysis of platelet alpha2-adrenergic receptor activity in stable coronary artery disease patients on dual antiplatelet therapy. 1898 8

Coronary artery disease (CAD) is a major cause of mortality and morbidity. Noninvasive proteome analysis could guide clinical evaluation and early/preventive treatment. Under routine clinical conditions, urine of 67 patients presenting with symptoms suspicious for CAD were analyzed by capillary electrophoresis directly coupled with mass spectrometry (CE-MS). All patients were subjected to coronary angiography and either assigned to a CAD or non-CAD group. A training set of 29 patients was used to establish CAD and non-CAD-associated proteome patterns of plasma as well as urine. Significant discriminatory power was achieved in urine but not in plasma. Therefore, urine proteomic analysis of further 38 patients was performed in a blinded study. A combination of 17 urinary polypeptides allowed separation of both groups in the test set with a sensitivity of 81%, a specificity of 92%, and an accuracy of 84%. Sequencing of urinary marker peptides identified fragments of collagen alpha1 (I and III), which we furthermore demonstrated to be expressed in atherosclerotic plaques of human aorta. In conclusion, specific CE-MS polypeptide patterns in urine were associated with significant CAD in patients with angina-typical symptoms. These promising findings need to be further evaluated in regard to reliability of a urine-based screening method with the potential of improving the diagnostic approaches for CAD.
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PMID:Evaluation of urine proteome pattern analysis for its potential to reflect coronary artery atherosclerosis in symptomatic patients. 1905 29


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