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)

The effect of the thymus polypeptide factor-thymidin on the lipid spectrum of the blood, thymic factor content in the blood and clinical course of the disease were studied in 156 patients with exertion stenocardia (II-IV functional class). Results indicate that patients with exertion stenocardia show with advance of the disease a reduction of the blood thymic factor and 85.6% develop hyperlipidemia. Complex treatment with inclusion of thymalin resulted in an increase of the thymic factor, normalization of the lipid metabolism increase of the contractile function of the myocardium and, thus, increases the treatment efficacy.
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PMID:[The effect of thymalin on lipid metabolism and the clinical course of ischemic heart disease]. 148 12

We investigated the relationship between plasma atrial natriuretic polypeptide (ANP) levels and hemodynamic indices during dynamic exercise testing in 15 patients with effort angina pectoris. Patients exercised on an angina-limited, supine, multistage bicycle ergometer, and plasma ANP levels and hemodynamic indices were measured at rest, at peak exercise, and 6 minutes after exercise. Plasma ANP levels increased significantly at peak exercise. Pulmonary artery wedge pressure (PAWP) and coronary sinus blood flow (CSBF) were significantly correlated with plasma ANP levels before and at peak exercise (PAWP: r = 0.69, p less than 0.001; CSBF; r = 0.45, p less than 0.05). In six of eight patients whose PAWP exceeded 20 mm Hg at peak exercise, plasma ANP levels were increased at 6 minutes after exercise, whereas PAWP had decreased relative to the values obtained at peak exercise. Plasma ANP concentrations at 6 minutes after exercise were not correlated with PAWP at the same time. However, PAWP at peak exercise was correlated with the plasma ANP levels at 6 minutes after exercise (r = 0.80, p less than 0.001). These results suggest that in patients with effort angina pectoris left ventricular dysfunction resulting from exercise-induced myocardial ischemia may increase preload excessively and may contribute to the excess secretion of ANP after dynamic exercise.
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PMID:Dynamic exercise-induced elevation in plasma levels of atrial natriuretic peptide in patients with effort angina pectoris. 214 50

In a prospective study, 22 patients with prolonged chest pain were monitored by serial serum tumour necrosis factor-alpha (TNF; cachectin) measurements. In five patients serum TNF markedly increased, peaking at greater than 145 ng l-1; all these patients had large infarcts complicated by hypotension, pulmonary oedema and/or arrhythmia. Two of these patients died. In contrast, TNF levels were either normal or only slightly raised in patients with small or uncomplicated infarcts and in patients with prolonged angina without evidence of infarction. The results show that extensive myocardial infarction induces the release of the monocyte/macrophage-derived polypeptide hormone TNF into circulation. This finding may be clinically relevant with respect to systemic metabolic consequences of myocardial infarction.
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PMID:Circulating tumour necrosis factor-alpha (cachectin) in myocardial infarction. 273 71

Correlations between plasma atrial natriuretic polypeptide (ANP) levels and hemodynamic parameters were studied in the central circulation of 12 patients with angina pectoris. The average plasma ANP level determined in the aorta was found to be 619 +/- 140 pg/ml. The plasma ANP levels showed a significant positive correlation with mean pulmonary arterial (PA) pressure, right ventricular pressure, and with cardiac index. In contrast, there was no significant correlation between plasma ANP levels and other hemodynamic variables including atrial pressure. These results suggest that hemodynamics other than the atrial pressure may have some role in modulating ANP secretion in certain pathological states.
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PMID:Atrial natriuretic peptide correlates with pulmonary arterial pressure and cardiac output. 295 33

We have previously shown that plasma vasoactive intestinal polypeptide (VIP) is increased in normal subjects by low-frequency transcutaneous nerve stimulation. The latter may also increase short-term physical performance in athletes (running, swimming and ergometer cycling). The present study examines whether the plasma VIP level is similarly increased in short-term ergometer exercise in seven healthy volunteers. A group of four patients with angina pectoris were included, since a lowered concentration of VIP is found in diseased heart tissue. In the group of healthy subjects, ergometer exercises with progressive increases in workload until exhaustion, lasting from 16 to 32 min (mean 26 min) and with a corresponding maximum energy output of 1500 to 5100 W (mean 3560 W), resulted in an increase in plasma VIP concentration from a pre-stimulatory level of 3.3 pmol . l-1 to 5.3, 5.2 and 5.6 pmol . l-1, measured 3, 10 and 20 min respectively, following termination of the exercise, i.e. a maximal 70% increase. In the patients with angina pectoris there was no significant VIP increase (cycling time 7-15 min, work performed 400-1350 W). Possible triggering mechanisms for VIP release and its source are discussed.
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PMID:Increase in plasma vasoactive intestinal polypeptide (VIP) in muscular exercise in humans. 372 Nov 87

Ten patients with coronary artery disease and stable angina (mean age fifty-seven) were included in the study. Five of the patients had normal left ventricular function, 5 had local hypokinesia or akinesia; 8 had one-stem and 2 had two-stem disease, but all had left anterior descending (LAD) lesions ranging from 75% to 100%. Ejection fraction varied between 35% and 75% (mean 59%). Immunoreactive atrial natriuretic polypeptide (ANP) levels in the femoral vein (FV) and the coronary sinus (CS) were measured before, immediately after, and up to twenty-four hours after percutaneous transluminal coronary angioplasty (PTCA) of the LAD. ANP secretion increased by 83% (FV) and 11% (CS) within minutes after PTCA and reached control levels after thirty to sixty minutes. In patients with hypokinesia of the anterior wall, ANP secretion was significantly lower, 48% (FV) and 11% (CS) respectively. ANP secretion during PTCA was higher in patients with concomitant increase in pulmonary capillary pressure (PCP) but was also observed without an increase of PCP, suggesting ventricular ANP secretion. IN conclusion, transient myocardial ischemia leads to immediate ANP secretion even in the absence of significant pressure elevation in the left atrium. As a part of the continuous medical education program of the American College of Angiology the second part of the paper reviews the mechanisms that allow the ischemic heart to counteract the ischemic condition and thus to escape from myocardial infarction. A review of this subject is presently not available in the literature.
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PMID:Observations on plasma ANP levels during short-term transient myocardial ischemia produced by PTCA in patients with LAD stenosis. 845 78

Ninety cases of angina pectoris patients with the Deficiency of Heart Qi Syndrome (DHQS), Deficiency of Heart-Yin Syndrome (DHYS) and blood stasis in Heart vessels Syndrome (BSHVS) were studied. The number of patients were 30 for each group. Their regulatory polypeptides:atrial natri-uretic polypeptide (ANP), beta-Endorphine (beta-EP), Endothelin (ET), Angiotensin (A-II) were tested. Results showed that in comparing with normal level, P < 0.05 or < 0.01, ANP and beta-EP of them: DHQS > BSHVS > normal group > DHYS. ET and A-II of them: DHYS > BSHVS > normal group > DHQS. And the comparison between groups revealed that P < 0.05 or < 0.01. So ANP, beta-EP, ET and A-II were the principal material basis, and they could be the specific objective parameters of the Syndrome Differentiation.
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PMID:[Relations of regulatory polypeptide and syndrome differentiation of traditional Chinese medicine of angina pectoris patients]. 938 48

Antithrombotic and antiplatelet agents, particularly unfractionated heparin and aspirin, are longstanding therapeutic mainstays for acute coronary syndromes such as unstable angina and non-Q-wave myocardial infarction (MI). Early studies demonstrated that aspirin reduces the risk of mortality or nonfatal MI by 50-70% in patients presenting with unstable angina or non-Q-wave MI. Added to aspirin, heparin regimens further diminish the incidence of these myocardial ischemic events in the acute setting. Three major clinical studies demonstrated that such enhanced risk reductions can be achieved without significant increases in bleeding complications. The low-molecular-weight (LMW) heparin, dalteparin, proved superior to placebo but not unfractionated heparin in diminishing the incidence of (1) death or MI; (2) death, MI, or recurrence of angina; or (3) frequency of revascularization procedures. On the other hand, another LMW heparin, enoxaparin, did reduce these events at 14 and 30 days, as well as 1 year after treatment. The principal biophysical limitation of heparins, however, is that they cannot inactivate clot-bound thrombin, which probably contributes to morbidity and mortality in acute coronary syndromes. The natural leech-derived polypeptide hirudin and its derivatives (e.g., lepirudin) inactivate both fibrin-bound and free thrombin. Lepirudin has been approved in certain countries for the treatment of heparin-induced thrombocytopenia and is now being evaluated in the clinical management of acute myocardial ischemic syndromes. The well-documented pathophysiologic foundation for acute coronary syndromes is partial or intermittent thrombotic occlusion of a coronary artery as the result of atherosclerosis. Although a stable atherosclerotic plaque may not be clinically problematic, plaque rupture, which occurs under a variety of stimuli, touches off a cascade of enzymatic and cellular responses that frequently culminate in thrombotic occlusion. In the coronary circulation, such an occlusion may cause transmural MI, unstable angina, or non-Q-wave MI. Because the pathogenetic mechanisms of atherosclerosis with thrombotic complications have been elucidated, this knowledge can be translated into a rational clinical approach using antithrombotic therapies.
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PMID:Anticoagulants in acute coronary syndromes. 1050 36

Fibroblast growth factors (FGFs) are being investigated in human clinical trials as treatments for angina, claudication, and stroke. We designed a molecule structurally unrelated to all FGFs, which potently mimicked basic FGF activity, by combining domains that (1) bind FGF receptors (2) bind heparin, and (3) mediate dimerization. A 26-residue peptide identified by phage display specifically bound FGF receptor (FGFR) 1c extracellular domain but had no homology with FGFs. When fused with the c-jun leucine zipper domain, which binds heparin and forms homodimers, the polypeptide specifically reproduced the mitogenic and morphogenic activities of basic FGF with similar potency (EC50 = 240 pM). The polypeptide required interaction with heparin for activity, demonstrating the importance of heparin for FGFR activation even with designed ligands structurally unrelated to FGF. Our results demonstrate the feasibility of engineering potent artificial agonists for the receptor tyrosine kinases, and have important implications for the design of nonpeptidic ligands for FGF receptors. Furthermore, artificial FGFR agonists may be useful alternatives to FGF in the treatment of ischemic vascular disease.
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PMID:Semirational design of a potent, artificial agonist of fibroblast growth factor receptors. 1058 18

Adiponectin is a novel polypeptide that modulates endothelial function. Association between high serum adiponectin level and stimulation of new blood vessel formation have been reported in two experimental studies, however, data in humans are lacking. We sought to determine relationship between serum adiponectin and collateral vessel development in patients with coronary artery disease. We included 89 patients with stable angina pectoris and angiographically documented total occlusion in one of the major coronary arteries. Coronary collateral circulation was graded according to Rentrop scoring method in which collateralisation was graded between 0 and 3 from the poorest to the best. Adiponectin was determined by the ELISA method. High serum adiponectin level were significantly associated with increased new collateralisation (p = 0.001). With the increase of body mass index and waist circumference, the collateral development decreased (p = 0.001, p = 0.002; respectively). Presence of the diabetes mellitus (DM) was more frequent in those with poor collateral group than in those with good collateral group. DM was associated with poor collateral development (p = 0.002). In multiple stepwise logistic regression analysis, low level of serum adiponectin (p = 0.0001), waist circumference (p = 0.001), and presence of DM (p = 0.003) were found to be significant independent predictors of poor collateral formation. In conclusion, we have shown for the first time that elevated levels of serum adiponectin are associated with coronary collateral development in patients with coronary artery disease and additionally, the present study confirms many of the metabolic associations reported previously with adiponectin.
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PMID:High serum levels of adiponectin improve coronary collateral development in patients with coronary artery disease. 1740 74


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