Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pentane and isoprene concentrations were analyzed in single end-expiratory breath samples using gas chromatography. Breath analysis was performed in 15 patients with acute myocardial infarction, 15 patients with stable angina, and 15 healthy control subjects. The two patient groups were well matched for age, sex, smoking habits, hypertension and serum cholesterol levels. There was no significant difference in breath pentane concentration in the acute myocardial infarction group (0.29 +/- 0.03 nmol/l) (mean +/- SEM) compared to the group with stable angina (0.31 +/- 0.03 nmol/l) or the control group (0.36 +/- 0.04 nmol/l). However, breath isoprene concentration was higher (p < 0.01) in the acute myocardial infarction group (11.4 +/- 1.2 nmol/l), compared to both the stable angina group (7.7 +/- 0.5 nmol/l) and the control group (7.1 +/- 1.0 nmol/l). There was no difference in either the pentane or isoprene concentrations between the control group and the group with stable angina. Since pentane is thought to be an index of lipid peroxidation, the results do not support the presence of enhanced lipid peroxidation in acute myocardial infarction in the absence of thrombolytic therapy or primary angioplasty. The mechanism responsible for isoprene elevation in acute myocardial infarction is unknown.
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PMID:Expired hydrocarbons in patients with acute myocardial infarction. 758 9

The murine monoclonal antibody mAb-1H11 raised against malondialdehyde (MDA)-modified LDL, was used to detect cross-reacting material in human atheromatous tissue and in plasma. MDA-modified LDL levels in plasma were 0.19 +/- 0.02 mg/dl (mean +/- SEM) in 44 control subjects, 0.24 +/- 0.02 mg/dl in 15 patients with chronic stable angina pectoris (P = NS vs LDL cholesterol matched controls), 1.4 +/- 0.1 mg/dl in 60 patients with acute myocardial infarction (P < 0.001 vs controls), and 0.86 +/- 0.11 mg/dl in 22 patients with carotid atherosclerosis (P < 0.001 vs controls). Modified LDL, isolated from pooled LDL of 10 patients, showed a higher electrophoretic mobility on agarose gels, a higher content of thiobarbituric acid reactive substances, and a higher cholesterol/protein ratio than native LDL and had a similar reactivity (antigen/protein ratio) in the assay as the in vitro MDA-modified LDL used for calibration. Its apo B-100 moiety was not fragmented. Uptake of this modified LDL by macrophages resulted in foam cell generation. In conclusion, elevated plasma levels of atherogenic MDA-modified LDL may be a marker for unstable atherosclerotic cardiovascular disease.
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PMID:Malondialdehyde-modified low density lipoproteins in patients with atherosclerotic disease. 776 3

Streptokinase and staphylokinase, the presently available thrombolytic agents of bacterial origin, are immunogenic in man; their use may cause allergic reactions and/or refractoriness to renewed administration. Infusion of 2 to 10 mg of recombinant staphylokinase (STAR) in 20 patients with acute myocardial infarction or peripheral arterial occlusion induced IgG-related neutralizing activity in plasma with a lag phase of 10 to 12 days, from a baseline of 0.2 +/- 0.06 microgram STAR neutralized per ml plasma (mean +/- SEM) to a maximum of 30 +/- 6.2 micrograms/ml after 3 to 9 weeks, which persisted at a level of 14 +/- 5.8 micrograms/ml after 18 months (n = 4). In 4 baboons with a 125I-fibrin labeled clot in an extracorporeal arteriovenous loop, i.v. administration of 63 micrograms/kg STAR over 1 h, repeated at weekly intervals, induced a progressive increase of STAR-neutralizing activity (from 0.05 +/- 0.1 microgram/ml at baseline to 4.8 +/- 1.5 micrograms/ml at week 6), which was paralleled by a reduction of in vivo clot lysis (from 60 +/- 7% to 8 +/- 3%). After temporary discontinuation of STAR-administration, neutralizing activity reverted to baseline within 7 weeks, whereafter the sensitivity of in vivo clot lysis to STAR was restored. In rabbits, i.v. administration of 250 micrograms/kg STAR over 1 h, repeated at weekly intervals, also induced a progressive increase of STAR-neutralizing activity (from 0.5 +/- 0.2 microgram/ml at baseline to 6.4 +/- 1.1 micrograms/ml at week 6), which was paralleled by a reduction of in vivo clot lysis (from 68 +/- 3% to 31 +/- 7%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:On the immunogenicity of recombinant staphylokinase in patients and in animal models. 783 68

To investigate the clinical significance of plasma brain natriuretic peptide (BNP) measurement in patients with acute myocardial infarction (MI), circulating levels of BNP, atrial natriuretic peptide, creatine kinase (CK), and hemodynamic parameters were serially determined in 24 patients with a first episode of acute MI. Plasma BNP (mean +/- SEM) gradually increased and peaked 21 h after the onset (from 13.7 +/- 2.2 to 23.0 +/- 3.3 fmol/ml; p < 0.001). A significant correlation was found between the increase in plasma BNP level and both the peak CK level (r = 0.83; p < 0.05) and the MI size (r = 0.74; p < 0.05). The increase in plasma BNP in the acute phase was found to be a significant predictor of left ventricular (LV) function evaluated in the convalescent phase (LV ejection fraction, r = -0.63; p < 0.05, LV end-diastolic pressure, r = 0.56; p < 0.05). In conclusion, in patients with acute MI, increases in plasma BNP concentration during the early phase reflect MI size, and thereby may predict later LV function.
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PMID:Relationship between plasma level of brain natriuretic peptide and myocardial infarct size. 785 Aug 23

We investigated the pathophysiological and clinical significance of thyroid stimulating hormone (TSH) levels in patients within 4 days after onset of ischemic heart disease (IHD) or aggravation of congestive heart failure (CHF) due to myocardial infarction. We classified patients into 3 groups: 1) angina pectoris (AP) group [n = 66, 62 years (Mean)], 2) acute myocardial infarction (AMI) group (n = 58, 65 years) and 3) CHF group (n = 16, 68 years). Soon after admission, blood samples were obtained to measure TSH by the IRMA method. Blood samples for creatine phosphokinase (CPK) were obtained every 3 hours. All patients showed TSH levels that were normal or below normal. Those in whom TSH levels were below normal, were defined as "low TSH" patients. The incidence of low TSH patients in the CHF group (31.3%) was significantly higher (p < 0.05) than that in the AP group (4.5%). In the AMI group, plasma CPK activity of 5037 +/- 1102 U/l (Mean +/- SEM) in low TSH patients were significantly higher (p < 0.05) than that of 1931 +/- 255 U/l in patients with normal TSH levels. These results indicate that in patients with extensive myocardial cell damage, "low TSH" frequently develops during emergency.
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PMID:[Low serum TSH levels in patients with emergent conditions due to ischemic heart disease or congestive heart failure]. 786 44

Cardiovascular events were analyzed in the subset of 49 consecutive patients with vasospastic coronary artery disease who underwent diagnostic coronary arteriography from December, 1987 to March, 1991 to confirm coronary artery spasm during anginal attacks. During the follow-up period (30 +/- 14 months, mean +/- SEM), seven patients had cardiovascular accidents including acute myocardial infarction, unstable angina, and stroke (group A), while the remaining 42 patients were event-free (group B). Current smokers at the end of the follow-up period were more common in group A (71%) than in group B (12%) (p < 0.01). Serum total-cholesterol, low density lipoprotein cholesterol, and triglyceride levels were not significantly different between the two groups before or after the follow-up period. The baseline high-density lipoprotein cholesterol (HDL-C) level also did not differ between group A (32.5 +/- 8.3 mg/dl) and group B (41.0 +/- 12.9 mg/dl). However, the HDL-C level significantly increased during the follow-up period in group B (delta HDL-C 6.1 +/- 9.4 mg/dl) (p < 0.01), but not in group A (delta HDL-C -3.3 +/- 7.2 mg/dl). The HDL-C level at the end of the follow-up period in group A (29.2 +/- 9.0 mg/dl) was significantly lower than in group B (47.1 +/- 11.5 mg/dl) (p < 0.01). Cardiovascular accidents were significantly more common in current smokers (50%) (p < 0.01) than in current nonsmokers (5%) after the follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Increased HDL-cholesterol level improves the prognosis in patients with coronary vasospasm]. 793 71

Details of possible complement activation in acute myocardial infarction (AMI) and the in vivo effects of fibrinolytic agents on this activation are not yet known. We measured complement activation in 40 patients with AMI: 20 were treated with streptokinase, and 20 did not receive any fibrinolytic agent. Anaphylatoxin C4a, C3a and membrane attack complexes SC5b-9 increased about 10-fold (p < 0.0001) during streptokinase infusion. There were no increases in complement catabolic products in AMI patients not treated with streptokinase. Significant transient leukopenia (-29.5%, 7.0 SEM, p = 0.001) and a drop in systolic pressure (-29%, 3.4 SEM, p < 0.0001) occurred after 15 min of streptokinase infusion simultaneously with the peak of anaphylatoxins in plasma.
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PMID:Thrombolytic treatment and complement activation. 794 96

Time delays to fibrinolytic treatment and outcome were assessed in 100 consecutive patients, with suggestive symptoms and electrocardiographic changes of acute myocardial infarction, admitted to the coronary care unit of this hospital. All patients admitted from out-of-hospital had access to a mobile coronary care unit. Initially, 40 patients called a general practitioner, 30 called the '999' operator, 12 called the mobile coronary care unit, 10 reported directly to the Accident and Emergency Department, seven were in-hospital and one spoke to the general practitioner's receptionist. Subsequently, 59 patients were attended by the mobile coronary care unit, 34 were admitted via the Accident and Emergency Department and seven had symptoms in-hospital. Thrombolytic therapy was initiated in 45/59 (76%) patients by the mobile coronary care unit staff and in 29/34 (85%) patients in the Accident and Emergency Department by cardiac staff. The remaining 26 patients received thrombolytic treatment in the hospital coronary care unit or cardiac department. The mean (+/- SEM) time from symptom onset to the initiation of thrombolytic therapy was 127 (+/- 11 min) for those patients treated by the mobile coronary care unit staff and for those treated in the Accident and Emergency Department was 187 (+/- 13 min) (P = 0.005). Multiple regression analysis showed significant reductions in total time delay if patients received thrombolytic therapy by the mobile coronary care unit staff out-of-hospital, when chest pain began in-hospital, or if patients had a previous myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Time delays to lytic therapy and outcome in 100 consecutive patients with a history suggestive of acute myocardial infarction in an area with access to a mobile coronary care unit. 805 97

The sympathetic nervous system is activated in acute myocardial infarction (MI). Scarce data exist, however, regarding the release of the sympathetic cotransmitter neuropeptide Y (NPY) during the acute and early convalescent phases after acute MI. Plasma NPY determination was obtained on days 1 and 3 after admission from 47 patients with acute MI and from eight control patients with acute chest pain without MI. Samples were also obtained on day 30 from the 39 survivors from the original MI cohort. Plasma NPY peaked on day 3 in the MI group (day 1: mean = 46.0 pmol/L, SEM = 6.4 pmol/L; day 3: mean = 60.8 pmol/L, SEM = 5.7 pmol/L; day 30: mean = 27.2 pmol/L, SEM = 4.1 pmol/L; days 1 to 3: p = 0.002; days 3 to 30: p < 0.001), whereas in the control group a nonsignificant decrease from day 1 (mean = 42.6 pmol/L, SEM = 12.3 pmol/L) to day 3 (mean = 34.0 pmol/L, SEM = 5.6 pmol/L) was observed. Plasma NPY levels were significantly increased in patients with MI on day 3 (p = 0.044), but not at baseline compared with the control group. No significant association between plasma NPY and plasma catecholamines, clinical heart failure, or 1-month survival was evident. These results suggest that increased plasma levels of the vasoconstrictory and cardiodepressant sympathetic neurotransmitter NPY are present in the recovery phase of MI, but with a plasma profile distinct from that of catecholamines.
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PMID:Plasma neuropeptide Y levels in the acute and early convalescent phase after myocardial infarction. 815 14

This randomized study compares the coronary perfusion rate in patients with acute myocardial infarction (AMI) treated with 2 different intravenous thrombolytic agents: streptokinase 1.5 million U given over 60 minutes and anisoylated human plasminogen streptokinase activator complex (anistreplase) administrated as a bolus of 30 U over 5 minutes. One hundred seventy-five patients (149 men and 26 women, mean age 54 years) have been included in this study. Eighty-nine patients were treated with anistreplase and 86 patients with streptokinase. AMI was inferior in 54 patients (61%) in the anistreplase group and in 54 patients (63%) in the streptokinase group. It was anterior in 35 (40%) and 32 (37%) patients, respectively. Coronary angiography and ventriculography were performed at a mean time (+/- SEM) of 207 +/- 11 minutes after the beginning of thrombolysis in 170 patients. A perfusion score grade of 2 or 3 according to the Thrombolysis in Myocardial Infarction trial was found in 63 patients (72%) in the anistreplase group and in 56 patients (68%) in the streptokinase group (p = NS). Severe bleeding occurred in 7 patients (8%) after anistreplase and in 6 patients (7%) after streptokinase. No cerebral hemorrhage occurred. Nine patients (5%) died during their hospital stay: 6 after anistreplase and 3 after streptokinase. It is concluded that intravenous administration of anistreplase or streptokinase is efficient and safe. Coronary patency 207 minutes after fibrinolysis, incidence of adverse events and mortality are similar in both groups.
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PMID:Comparison of results of intravenous infusion of anistreplase versus streptokinase in acute myocardial infarction. 842 67


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