Nodal re-entry tachycardia with angina treated with adenosine.
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Adenosine↗
Biomedical subjects
P Eriksson
Publications and source records attributed to P Eriksson.
Ischaemia detected by continuous on-line vectorcardiographic monitoring predicts unfavourable outcome in patients admitted with probable unstable coronary disease.
BACKGROUND: Several methods have been suggested for risk stratification of patients with unstable coronary syndromes. However, most of these are applied several days after hospital admission. METHODS: In this study we investigated the prognostic value of continuous ST-segment and QRS vector monitoring with computerized vectorcardiography (VCG), serial measurements of creatine kinase isoenzyme MB (CK-MB), predischarge stress testing and baseline data in patients with unstable angina pectoris or non-Q-wave infarction. RESULTS: During the 24 h VCG monitoring, 56 (29%) of the 195 patients had ST-vector magnitude (ST-VM) episodes of ischaemia. Seventy-four (38%) patients had a peak CK-MB value of 6 micrograms/l or higher during the 48 h sampling period. Several discrete variables were associated with death or non-fatal infarction at 1 year of follow-up in an univariate analysis. Among these were age > or = 65 years, female sex, St depression on the admission ECG or VCG monitoring, and elevated CK-MB levels, but neither the occurrence, duration nor intensity of chest pain. With Cox's proportional hazards regression analysis, ST-VM episodes on VCG monitoring were identified as independent markers of the risk of death (P = 0.013), death or non-fatal infarction (P = 0.035) and death, non-fatal infarction, unstable angina during the first year, or revascularization before hospital discharge (P = 0.005). CONCLUSIONS: VCG monitoring of ischaemia provides independent prognostic information in unstable angina. High-risk patients can easily be identified within 24 h of hospital admission. Whether early intervention based on these criteria will result in improved prognosis remains to be shown in future studies.
Adult↗
Long term follow up of patients with anterior myocardial infarction complicated by left ventricular thrombus in the thrombolytic era.
OBJECTIVES: To examine the appearance and resolution of left ventricular thrombi and to study the relation between thrombus and mortality during long term follow up after anterior myocardial infarction. DESIGN: Ninety nine consecutive patients were prospectively studied until the last included patient had been followed for one year. Streptokinase and aspirin were used routinely, anticoagulants only after a decision by the attending physician. Echocardiography was performed within 3 d of admission, before discharge, and after one, three, and 12 months. SETTING: Umeå University Hospital, a teaching hospital in Northern Sweden. MAIN OUTCOME MEASURES: Left ventricular thrombus, segmental myocardial function, and mortality during follow up. RESULTS: Thirty patients (30%) had a thrombus on discharge. One month, three months, and 12 months after hospital discharge, the thrombus had resolved in 81%, 84%, and 90% of the patients, respectively. The proportion of resolved thrombi at one month was high irrespective of whether anticoagulants were given (10/11, 91%) or not (12/16, 75%), P = 0.4. New thrombi appeared in 12 patients after discharge and resolution and reapperance of thrombi continued during the follow up period. Patients who developed a thrombus during the hospital stay (n = 44, 44%) had more extensive myocardial dysfunction on discharge (P < 0.001) and significantly higher mortality during the follow up period than those without a thrombus (23% v 7%, P < 0.01). CONCLUSIONS: With routine thrombolytic and aspirin treatment of anterior myocardial infarction, left ventricular thrombi usually resolve during the first month after hospital discharge. Appearance and resolution of thrombi continue, however, in a significant proportion of the patients during long term follow up. A left ventricular thrombus during the initial hospital stay is associated with high long term mortality.
Adult↗
Sleep-disordered breathing in men with coronary artery disease.
OBJECTIVE: To examine the occurrence of sleep apnea and nocturnal hypoxemia in men with symptomatic coronary artery disease (CAD) and to evaluate the relationship between disordered breathing and coronary artery disease. DESIGN: Case-control study. Cases were randomly selected from men undergoing coronary angiography because of angina pectoris. Controls were age matched and selected from the population registry. Pulse oximetry, oronasal thermistors, body position indicator, and recording of body and respiratory movements were used to quantify desaturations and apneas. SETTING: Norrland University Hospital, a referral center for northern Sweden. SUBJECTS: One hundred forty-two men with angina pectoris and angiographically verified CAD and 50 controls without known heart disease. MAIN OUTCOME MEASURES: The number of arterial oxygen desaturations of 4% or more per hour of sleep, oxygen desaturation index (ODI), and the number of apneas or hypopneas per hour of sleep, apnea-hypopnea index (AHI). RESULTS: Men with CAD had a high occurrence of sleep-disordered breathing measured as ODI of 5 or more, 39% (n=55), or AHI of 10 or more, 37% (n=50), while, the same proportions in controls were 22% (n=11, p<0.05) and 20% (n=10, p<0.05). Mean values of ODI in cases and controls were 6.4 and 2.7, respectively (p<0.001). Multiple logistic regression analysis identified ODI, AHI, body mass index, and hypertension as significant predictors of CAD (p<0.05). CONCLUSION: Sleep- disordered breathing is common in men with CAD. A significant association between sleep apnea with nocturnal hypoxemia and CAD remains after adjustment for age, hypertension, body mass index, diabetes, and smoking.
Adult↗
Glomerular filtration rate in primary Sjögren's syndrome with renal disease.
Renal disease in Primary Sjögren's syndrome (SS) is often overlooked, because of a paucity of symptoms. Distal renal tubular acidosis (dRTA) and tubulointerstitial nephritis (TIN) might be present. Only a few cases of SS with decreased glomerular filtration rate (GFR) have been reported. We have studied GFR in 27 female SS-patients, mean age 62 years (37-78). GFR was measured as the single injection 51Cr-EDTA plasma clearance. Eighteen women had normal GFR (group 1), and nine (33%) had values below the lower normal limit (group 2). In group 2, dRTA was present in 8/9 urolithiasis in 6/9, previous upper urinary tract infection (UTI) in 2/9 and TIN in 5/6 patients who were kidney biopsied. Among patients with dRTA 8/18 (44%) had decreased GFR. We conclude that decreased GFR is not unusual in SS-patients with dRTA, and decreased GFR is mostly associated with TIN. Urolithiasis and UTI may contribute to decreased GFR in some individuals.
Acidosis, Renal Tubular↗
[Effects of alcohol intoxication].
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Alcoholic Intoxication↗
Sleep-disordered breathing: a novel predictor of atrial fibrillation after coronary artery bypass surgery.
BACKGROUND: Sleep-disordered breathing is a common condition associated with nocturnal hypoxaemia, sympathetic activation and haemodynamic stress that can trigger arrhythmias. We examined whether preoperatively diagnosed disordered breathing was associated with an increased incidence of atrial fibrillation after coronary artery bypass surgery. METHODS: A sleep study was performed in 121 consecutive patients, who were monitored prospectively until discharge from hospital after surgery. Disordered breathing was defined as an apnoea-hypopnoea index (AHI) > or = 5 or an oxygen desaturation index (ODI) > or = 5. All episodes of atrial fibrillation requiring pharmacological intervention or cardioversion were included in the analysis. RESULTS: Atrial fibrillation was diagnosed in 32% of patient with AHI > or = 5 (25 of 78) and in 18% patients with AHI < 5 (7 of 39, P = 0.11). Similarly, atrial fibrillation was diagnosed in 39% of patients with ODI > or = 5 (19 of 49) and in 18% of patients with ODI < 5 (13 of 72, P = 0.02). In a multiple-logistic regression model including age, left ventricular function, aortic cross clamp time, maximum postoperative level of lactate dehydrogenase and disordered breathing (ODI > or = 5), greater age and disordered breathing were independent predictors of postoperative atrial fibrillation. The relative risk of atrial fibrillation was 2.0 (95% confidence interval 1.1-3.8) for a 10-year increase in age and 2.8 (95% confidence interval 1.2-6.8) for disordered breathing (ODI > or = 5). CONCLUSIONS: Pre-operatively diagnosed sleep-disordered breathing with nocturnal hypoxaemia is an independent predictor of atrial fibrillation after coronary bypass surgery.
Aged↗
Neurotoxicity of cysteine: interaction with glutamate.
L-Cysteine produces excitotoxic brain damage but its chemical structure differs from that of other excitotoxins. Although it is an NMDAmimetic, its mode of action is complex and may encompass antiexcitotoxic components. The purpose of the present study was to investigate whether cysteine kills neurons by potentiating the effects of glutamate and/or by releasing glutamate. In primary cultures of cortical neurons, 24 h of exposure to glutamate caused a concentration-dependent, dizocilpine-sensitive cell death as measured by release of lactate dehydrogenase. Cysteine was also toxic but higher concentrations were required. In addition, N-acetylcysteine produced mild toxicity at 1 mM. There was no general potentiation between either glutamate and cysteine or glutamate and N-acetylcysteine although some combinations acted synergistically. In no case did the thiols inhibit glutamate toxicity. The interaction between glutamate and cysteine toxicity was also assessed in the immature rat arcuate nucleus in vivo. When given at a dose (0.5 mg/g) that did not cause any toxicity per se, cysteine enhanced the toxicity of glutamate (0.3-0.8 mg/g). Cortical microdialysis was carried out in anesthetized rats (8-10 days old) administered a toxic dose of cysteine (1 mg/g). The levels of taurine were elevated 15-fold, phosphoethanolamine 3-fold and alanine 2-fold. Despite the observation that glutamine decreased markedly and rapidly, there was only a delayed doubling of glutamate concentrations. It is therefore unlikely that cysteine induces neurotoxicity by releasing glutamate. Taken together, the results suggest that there is a synergistic effect between cysteine and glutamate. Speculatively, this potentiation may be produced by reduction by cysteine of the redox site of the glutamate-activated NMDA receptor-ionophore complex.
Animals↗
Bioallethrin causes permanent changes in behavioural and muscarinic acetylcholine receptor variables in adult mice exposed neonatally to DDT.
We recently reported changes in the density of muscarinic acetylcholine receptors in cerebral cortex of mice treated neonatally with DDT (1,1,1-trichloro-2,2-bis(p-chlorophenyl)-ethane) and receiving bioallethrin as adults. We also found behavioural aberrations in adult mice treated with bioallethrin, whether neonatally treated with DDT or the vehicle. To ascertain whether these changes were permanent, 10-day-old mice received an oral dose of DDT (0.5 mg/kg body weight) and at the age of 5 months they received bioallethrin orally (0.7 mg/kg body weight/day; 7 days). The animals were investigated at the age of 7 months. Here we report muscarinic acetylcholine receptor changes, additional behavioural disturbances and learning disabilities in mice receiving DDT as neonates and bioallethrin as adults, whereas the behavioural disturbances in mice receiving vehicle as neonates and bioallethrin as adults had diminished and changes in proportions of high- and low-affinity binding sites had developed. No changes in the density of nicotinic acetylcholine receptors were noted for any of the treated groups. In conclusion, exposure of neonates to DDT leads to increased susceptibility in adults to a short-acting pesticide with similar neurotoxic action. An adult exposure to this short-acting pesticide to mice neonatally exposed to DDT leads to irreversible muscarinic acetylcholine receptor changes and behavioural disturbances with additional changes 2 months after the exposure.
Allethrins↗
Exposure to an organophosphate (DFP) during a defined period in neonatal life induces permanent changes in brain muscarinic receptors and behaviour in adult mice.
The organophosphate Diisopropylfluorophosphate (DFP) is a well-known inhibitor of cholinesterases. We have recently observed that neonatal exposure to a single subsymptomal dose of DFP induces permanent alterations in muscarinic cholinergic receptors (MAChRs) and in spontaneous behaviour, in the mice as adults. In order to determine if there is a critical period for these effects, neonatal mice were given a single oral dose of 1.5 mg/kg DFP b.wt. on postnatal day 3, 10 or 19, causing equal inhibition of AChE. At the adult age of 4 months the mice were tested for spontaneous motor behaviour, and were subsequently sacrificed for measurement of density of MAChRs and subpopulations of MAChRs in the cerebral cortex by using the antagonist quinuclidinyl benzilate ([3H]QNB), and agonist carbachol, respectively. At adult age, mice exposed to DFP on postnatal day (PND) 3 or 10 showed significant (P < or = 0.01) alterations in spontaneous motor behaviour and a significant (P < or = 0.01) decrease in muscarinic receptor density. There were no alterations mice exposed on PND 19. The proportions and affinity-constants of high- and low-affinity MAChR binding sites were not affected in mice showing altered MAChR density. The lack of effect on mice exposed on PND 19 was not due to differences in AChE activity.
Animals↗
Allele-specific increase in basal transcription of the plasminogen-activator inhibitor 1 gene is associated with myocardial infarction.
Increased plasminogen-activator inhibitor 1 (PAI-1) activity is a common finding in patients with coronary heart disease. Here we provide evidence for an independent, etiological role of PAI-1 in myocardial infarction. The 4G allele of a recently described common 4/5-guanine-tract (4G/5G) polymorphism in the PAI-1 promoter is associated with higher plasma PAI-1 activity. The prevalence of the 4G allele is significantly higher in patients with myocardial infarction before the age of 45 than in population-based controls (allele frequencies of 0.63 vs. 0.53). Both alleles bind a transcriptional activator, whereas the 5G allele also binds a repressor protein to an overlapping binding site. In the absence of bound repressor, the basal level of PAI-1 transcription is increased.
Adult↗
Fibrinolysis and atherosclerosis.
The link between impaired fibrinolytic function and CHD has been reinforced considerably in the past couple of years. This has been achieved by a combination of epidemiological, clinical, cell biological and molecular biological studies. The molecular mechanisms for the identified associations between more established risk factors for atherosclerotic disease and impaired fibrinolytic function now need to be disentangled to promote the design of specific drugs that may pave the way for intervention. The possibility that some of the observed relations are epiphenomena should also not be disregarded. The concept of genotype-specific differences in the susceptibility of the individual to common metabolic disturbances needs to be examined in greater detail. Basic research on the role of fibrinolysis in atherosclerosis and its thrombotic complications should be given high priority, because the modulation of fibrinolytic function is likely to become an important approach to prevention.
Animals↗
Left ventricular thrombosis after anterior myocardial infarction with and without thrombolytic treatment.
OBJECTIVES: To examine the incidence of left ventricular thrombus in patients with anterior myocardial infarction, with and without streptokinase treatment. To identify predictors of thrombus development. DESIGN: Consecutive patients prospectively studied during the hospitalized period. Echocardiography was performed within 3 days of admission and before discharge. SETTING: Umeå University Hospital, a teaching hospital in Northern Sweden. SUBJECTS: Ninety-nine patients with anterior myocardial infarction of whom 74 were treated with streptokinase. MAIN OUTCOME MEASURES: Left ventricular thrombus and left ventricular segmental myocardial function. RESULTS: During the hospital stay, a thrombus developed in 46% (95% confidence interval [CI], 35-57%) of the patients in the thrombolysis group and in 40% (95% CI, 21-59%) of the patients in the non-thrombolysis group. No difference in left ventricular segmental myocardial function was found between the thrombolysis and non-thrombolysis groups at hospital discharge. No embolic events were observed. The occurrence of a left ventricular thrombus at hospital discharge was significantly associated with previous myocardial infarction, peak enzyme levels, left ventricular global and segmental dysfunction and an increased dose of peroral diuretics or use of parenteral diuretics. In a multiple logistic regression model, left ventricular segmental dysfunction was the most important predictor of left ventricular thrombus. CONCLUSION: Thrombolytic treatment with streptokinase does not prevent the development of a left ventricular thrombus but the risk of embolic complications is low. The left ventricular segmental myocardial score can be used to assess the risk of thrombus development, also, after thrombolysis.
Adult↗
Cloning and characterization of GPD2, a second gene encoding sn-glycerol 3-phosphate dehydrogenase (NAD+) in Saccharomyces cerevisiae, and its comparison with GPD1.
We have cloned and characterized a homologue of the previously isolated GPD1 gene, encoding sn-glycerol 3-phosphate dehydrogenase (NAD+) in Saccharomyces cerevisiae. This second gene, called GPD2, encodes a protein of 384 amino acids that shares 69% sequence identity with GPD1. Like GPD1 it has an amino-terminal extension of unknown function. GPD2 is located on chromosome VII and cross-hybridizes with GPD1 at chromosome IV as well as with an unknown homologue at chromosome XV. Disruption of the GPD2 gene did not reveal any observable phenotypic effects, whereas overexpression resulted in a slight, but significant, increase of GPD enzyme activity in wild-type cells. Analysis of gene transcription by a CAT-reporter gene fused to the GPD promoters revealed decreased transcriptional activity of the GPD2 promoter in cells grown on nonfermentable as opposed to fermentable carbon sources, and no induction in cells exposed to high osmolarity or heat shock. Similar analysis of GPD1 demonstrated an 8-17-fold higher basal level of transcription compared to GPD2. Furthermore, such analysis revealed that the GPD1 promoter was induced by increased osmolarity essentially independent of the type of stress solute used, the level of GPD1 transcription being increased about sevenfold in cells growing at 1.4 M NaCl.
Amino Acid Sequence↗
Pulmonary venous systolic flow fraction in patients with mitral regurgitation: transoesophageal echocardiographic findings in relation to haemodynamic and angiographic evaluation.
In patients with mitral regurgitation (MR), pulmonary venous systolic flow fraction (PVSFfr) recorded using pulsed Doppler transoesophageal echocardiography (TEE) was compared with PVSFfr in normal subjects, to angiographic grading and to haemodynamic parameters. PVSfr was calculated as the systolic flow velocity integral divided by total inflow integral. PVSfr is negative when systolic flow is reversed. Forty patients with MR were studied. PVSFfr < 0 was 100% sensitive for angiographic severe MR (specificity 83%). In 35 patents heart rate differed by 10 bpm or less between TEE and cath, either at rest or during stress. PVSFfr was correlated with angiographic grade (r = -0.69, P < 0.0001), with mean PCW (r = -0.61, P < 0.0001), with the v-wave (r = -0.72, P < 0.0001), with systolic blood pressure (r = 0.48, P < 0.005) and with left atrial diameter (r = -0.52, P < 0.005). Stepwise forward multiple linear regression analysis revealed the v-wave, angiographic grading and systolic blood pressure to be independent predictors of PVSFfr. PVSFfr differed in normal subjects, patients with 0-2+ and patients with 3-4+ regurgitation. PVSFfr is a valuable index in assessing mitral regurgitation. This index may be less dependent on equipment and operator than colour flow imaging.
Adult↗
Physiological correlates of simulated wheelchair racing in trained quadriplegics.
This study examined the physiological responses during a 7.5-km simulated wheelchair race (SR) performed on rollers by 8 male quadriplegic marathon racers and analyzed the factors associated with SR time. Cardiac output (Q) was estimated during the SR using carbon dioxide rebreathing, from which stroke volume (SV) and (alpha-v)O2 diff were calculated. Subjects raced at 90 and 93% of peak oxygen uptake (VO2) and peak heart rate, respectively. SR time was inversely related (p < 0.05) to peak VO2, and VO2, Q, and SV during the SR, but not (alpha-v)O2 diff, age, and lesion level. Multiple regression analysis included only absolute SR VO2 in the equation to predict SR time: Y = -29.7X + 65.9; SE = 5.8. SR VO2 was significantly (p < 0.05) related to Q and SV but not to (alpha-v)O2 diff. These descriptive data suggest that SR performance in trained male quadriplegics might be limited by central, as opposed to peripheral, factors that determine VO2.
Adult↗
Oxidized LDL induces transcription factor activator protein-1 but inhibits activation of nuclear factor-kappa B in human vascular smooth muscle cells.
Oxidized LDL (Ox-LDL) has been implicated in the development of atherosclerotic lesions, mainly due to its enhanced uptake by macrophages and its ability to alter gene expression in arterial cells. In the present study we demonstrated that Ox-LDL activates activator protein-1 (AP-1), a transcription factor generally induced by mitogenic substances. Lysophosphatidylcholine, which is generated during oxidation of LDL, stimulated AP-1 in a dose-dependent manner. In contrast, the radical-dependent transcription factor nuclear factor-kappa B (NF-kappa B) was not activated by Ox-LDL, and at a concentration of 50 micrograms/mL, Ox-LDL inhibited lipopolysaccharide-induced activation of NF-kappa B. Oxysterols but not lysophosphatidylcholine inhibited lipopolysaccharide-induced NF-kappa B activation, suggesting that they may be responsible for the inhibitory effect of Ox-LDL. In conclusion, Ox-LDL has opposing effects on the activities of NF-kappa B and AP-1, suggesting involvement of mechanisms for transcriptional regulation that are strongly affected by lipid oxidation products.
Cells, Cultured↗
Coagulation factor VII mass and activity in young men with myocardial infarction at a young age. Role of plasma lipoproteins and factor VII genotype.
Factor VII (FVII) coagulant activity has been proven to be associated with the risk of future fatal coronary heart disease (CHD) in middle-aged men. Recent studies have emphasized the role of triglyceride-rich lipoproteins and FVII genotype in determining plasma levels of FVII protein and activity. The present study was undertaken to examine whether FVII activity state and protein concentration in fasting plasma are altered in young men with proven myocardial infarction (MI) and examined the relations of FVII to subfractions of apo B-containing lipoproteins and the Arg-->Gln polymorphism in the FVII gene. Activated FVII (FVIIa) was determined by a clotting assay using soluble, recombinant, truncated tissue factor. A total of 94 men with a first MI before the age of 45 (mean age +/- SD, 39.6 +/- 4.5 years) were included in the study along with 99 population-based, age-matched control subjects. In addition to FVIIa and FVII antigen (FVII:Ag), a panel of FVII activity assays were included for comparison with previous work in this field. The plasma level of FVII:Ag was higher in patients than in control subjects when the entire groups were compared (537 +/- 128 versus 479 +/- 93 ng/mL, P < .001), the differences being accounted for by patients with hypertriglyceridemic lipoprotein phenotypes. In contrast, FVIIa was similar in patients and control subjects (4.6 +/- 1.4 versus 4.3 +/- 1.3 ng/mL, NS), which means that the proportion of FVIIa molecules was unaltered or even lower in the patients. As expected, the Arg-->Gln polymorphism significantly influenced both FVII mass and activity levels. In addition, presence of the Gln allele appeared to be associated with a lower proportion of fully active FVII molecules. The polymorphism also affected the relation between the plasma concentration of VLDL and FVII:Ag. The triglyceride content and particle number of all VLDL subfractions, irrespective of particle size, correlated fairly strongly with FVII mass determinations but not at all with FVIIa. HDL cholesterol concentration, on the other hand, presumably reflecting the efficiency of lipoprotein lipase-mediated lipolysis of VLDL, related significantly to the FVIIa level. The Arg-->Gln polymorphism, independent of lipoprotein effects, explained 5% to 10% of the variation in FVII mass and activity. In conclusion, the present findings speak against a role of FVII as a risk factor for CHD, because a significantly increased potential for activation of coagulation (ie, raised basal concentration of FVIIa) was not observed among young postinfarction patients.(ABSTRACT TRUNCATED AT 400 WORDS)
Adult↗