Tumour necrosis factor-alpha (TNF-alpha) polymorphisms-857C/A and -863C/A are associated with TNF-alpha secretion from human adipose tissue.
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Adipose Tissue↗
Biomedical subjects
P Eriksson
Publications and source records attributed to P Eriksson.
Fatty acid binding protein expression in different adipose tissue depots from lean and obese individuals.
AIMS/HYPOTHESIS: This study investigated the expression of adipose tissue fatty acid binding proteins (FABPs) in subcutaneous and visceral human adipose tissue depots from lean and obese individuals. METHODS: Adipocyte lipid binding protein (ALBP) and keratinocyte lipid binding protein (KLBP) expression was quantified by western blot in subcutaneous and omental adipose tissue from 20 obese and 9 lean individuals. RNA expression was quantified by Northern blot in the obese subjects. RESULTS: In the obese subjects, ALBP protein and RNA expression was higher in subcutaneous compared with omental adipose tissue (increases of 31 +/- 14 % and 40 +/- 13 % respectively, both p < 0.05), whereas in the lean group, KLBP protein levels were 32 +/- 9 % lower in subcutaneous fat (p < 0.03). However, the ALBP/KLBP ratio was greater in subcutaneous compared to omental adipose tissue from both lean and obese subjects: increases of 187 +/- 71 % (p = 0.01) and 52 +/- 23 % (p = 0.17) respectively for the protein ratio, and 21 +/- 6 % for RNA (p = 0.01, obese individuals). In lean subjects, insulin concentrations correlated positively with the ALBP/KLBP protein ratio in both depots (both p < or = 0.03). CONCLUSION/INTERPRETATION: There are regional differences in adipose tissue FABP expression, which could be influenced by obesity. However, the ALBP/KLBP ratio is greater in subcutaneous than visceral adipose tissue in lean as well as in obese subjects. Investigation of adipose tissue FABPs could further our understanding of the role of fatty acids in the insulin resistance syndrome.
Actins↗
Expression of interleukin-15 in mouse and human atherosclerotic lesions.
Atherosclerotic lesions are characterized by prominent macrophage and T-cell infiltration and atherosclerosis is widely recognized as an inflammatory disease. The cytokine interleukin-15 (IL-15) has T-cell chemotactic and pro-inflammatory properties and promotes the recruitment of T cells to sites of inflammation. We have therefore examined IL-15 expression in the atherosclerotic ApoE-deficient mouse model as well as in human atherosclerotic lesions. In gene expression arrays, a transcript corresponding to IL-15 mRNA was elevated in atherosclerotic aortas of ApoE-deficient mice fed a Western diet for 10 and 20 weeks, corresponding to lesions of the fatty streak and fibrofatty plaque stage, respectively. Immunostaining for IL-15 localized to aortic smooth muscle cells in nonatherosclerotic C57BL/6 mice, whereas both macrophages and smooth muscle cells stained positive for IL-15 in atherosclerotic lesions of ApoE-deficient mice. Finally, advanced atherosclerotic lesions of human carotid arteries were immunostained to determine whether IL-15 is involved in human disease. IL-15 protein was present also in the human lesions with a distribution primarily overlapping that of macrophages. In conclusion, IL-15 is up-regulated in both human and animal atherosclerotic lesions and may contribute to the recruitment of T cells and their activation during atherogenesis.
Aging↗
ECG criteria in diagnosis of acute myocardial infarction in the presence of left bundle branch block.
BACKGROUND: The diagnosis of acute myocardial infarction in the presence of left bundle branch block is difficult. Recently a diagnostic ECG scoring system was suggested, showing good diagnostic abilities. This scoring system has never been tested in a prospective manner; we have done so and investigated if it might bear prognostic information. METHODS: A prospective multi-centre study. Consecutive patients with left bundle branch block and suspicion of acute myocardial infarction, admitted to 14 Swedish coronary care units. Recruitment from March 1996 to December 1997. ECG registered on admission and after 12-24 h. RESULTS: One hundred and fifty-eight patients were included, mean age 74.9 years. Seventy-six patients (48%) had an acute myocardial infarction. The proposed cut-off total score of > or = 3 of the ECG scoring system for the diagnosis of acute myocardial infarction had a sensitivity of 17.1% (95% CI 8.6-25.6%) and specificity of 94.0% (95% CI 88.9-99.1%). Clinical judgement of acute myocardial infarction resulted in a sensitivity of 15.8% (95% CI 7.6-24%) and specificity of 96.0% (CI 92.3-100%). No difference was seen in 3-month or 1-year survival between those with total ECG score > or = 3 versus total score < 3. CONCLUSION: The diagnostic abilities of the proposed ECG criteria are low and not better than the clinical judgement. The criteria are therefore not suitable for screening patients with suspicion of acute myocardial infarction in the presence of left bundle branch block, nor do they seem to identify high risk patients.
Aged↗
Neonatal iron potentiates adult MPTP-induced neurodegenerative and functional deficits.
The interactive effects of neonatal iron and adult MPTP treatment groups of C57 Bl/6 mice were studied through adminustration of iron (Fe(2+)) 7.5mg/kg b.w., p.o. or vehicle (saline) on days 10-12 post partum, followed at 3months of age by administration of either MPTP (2x20 or 2x40mg/kg, s.c.) or saline. Neonatal iron administration to mice-induced hypoactivity during the first 20-min period of testing and hyperactivity during the 3rd and final 20-min period for all three parameters of motor activity tested at 4months of age. MPTP treatment caused a dose-related hypokinesia throughout the 3x20-min test periods; in the mice that received both neonatal iron and MPTP severe deficits of motor activity (akinesia) were obtained. Iron treatment impaired the ability of mice to habituate to the novel testing environment and later administration of MPTP potentiated the impairment markedly. Neurochemical analyses of striatal and frontal cortical dopamine (DA) and DA metabolites demonstrated that the depletions were potentiated under conditions of combined neonatal iron and adult MPTP. The analysis of total iron content (µg/g) in brain regions indicated notably elevated levels in the basal ganglia, but not in the frontal cortex, of mice administered Fe(2+). Iron-overload combined with MPTP treatment induced functional and neurochemical deficits with interactive consequences beyond a mere additive effect that may have implications for the neurodegenerative process in parkinsonism.
Journal Article↗
The Arg 389 Gly beta1-adrenergic receptor gene polymorphism and human fat cell lipolysis.
BACKGROUND: The beta1-adrenoceptor is a candidate gene for obesity because of its role in catecholamine-induced energy homeostasis. A common Arg 389 Gly variant polymorphism has been shown in recombinant cells to influence its-coupling properties. OBJECTIVE: To investigate the effect of the Arg 389 Gly beta1-adrenoceptor polymorphism on catecholamine-induced lipolysis in native human fat cells obtained by subcutaneous biopsy. SUBJECTS: Two-hundred and ninety-eight apparently healthy male and female subjects with a wide variation in body mass index (BMI, 18-60 kg/m2). MEASURES: The lipolytic sensitivities and maximum lipolytic action of noradrenaline and the selective adrenoceptor agonists dobutamine (beta1), terbutaline (beta2) and CGP 12177 (beta3) were determined in isolated subcutaneous adipocytes and related to beta-adrenoceptor radioligand binding parameters. RESULTS: No differences in the sensitivity or maximum lipolytic capacity of the agonists were found between the genotypes. This was true both when all subjects were analyzed together and when subgroups (lean, obese, men, women) were analyzed separately. Radioligand binding to beta1- or beta2-adrenoceptors was also similar between genotypes. The polymorphism had no important influence on either BMI or the distribution of obese and non-obese subjects between the genotypes. CONCLUSION: The distribution of the Arg 389 Gly polymorphism is similar in lean and obese subjects and has no apparent effect on the lipolytic response to beta-adrenergic stimulation in native human adipocytes. This suggests, despite the altered coupling properties reported in recombinant cells, that the Arg 386 Gly polymorphism has no important influence on human obesity.
Adipocytes↗
Allele-specific regulation of matrix metalloproteinase-7 promoter activity is associated with coronary artery luminal dimensions among hypercholesterolemic patients.
An enhanced expression of matrix metalloproteinase (MMP)-7 has previously been demonstrated in atherosclerotic and aneurysmal tissue. Because perturbed regulation of MMP-7 may influence the development of these diseases, we searched the MMP-7 promoter for functional polymorphisms. An A to G substitution at position -181 (-181 A/G) and a C to T substitution at position -153 (-153 C/T) with frequencies of 0.50 and 0.10, respectively, were identified. Allele-specific associations were studied in 350 patients undergoing percutaneous transluminal coronary angioplasty. Hypercholesterolemic patients carrying the -181G allele or the -153T allele had smaller reference luminal diameters before percutaneous transluminal coronary angioplasty. Reverse transcription-polymerase chain reaction demonstrated that expression of MMP-7 was confined to differentiated U937 cells. Northern blot analysis could not detect an effect of native or oxidatively modified low density lipoprotein on MMP-7 expression. Thus, the limitation of allele-specific effects on vessel wall remodeling to hypercholesterolemic patients may be secondary to lipid-mediated accumulation of MMP-7-expressing monocyte-derived macrophages within the vessel wall. Both polymorphisms influenced the binding of nuclear proteins. Furthermore, in transient transfection studies, the combination of the 2 rare alleles conferred an increased promoter activity. In conclusion, the present study identified and characterized 2 common polymorphisms in the promoter region of the MMP-7 gene that are functional in vitro and seem to influence coronary arterial dimensions in hypercholesterolemic patients with manifest coronary artery disease.
Adult↗
Brominated flame retardants: a novel class of developmental neurotoxicants in our environment?
Brominated flame retardants are a novel group of global environmental contaminants. Within this group the polybrominated diphenyl ethers (PBDE) constitute one class of many that are found in electrical appliances, building materials, and textiles. PBDEs are persistent compounds that appear to have an environmental dispersion similar to that of polychlorinated biphenyls (PCBs) and dichlorodiphenyltrichloroethane (DDT). Levels of PBDEs are increasing in mother's milk while other organohalogens have decreased in concentration. We studied for developmental neurotoxic effects two polybrominated diphenyl ethers, 2,2',4,4'-tetrabromodiphenyl ether (PBDE 47) and 2,2',4,4',5-pentabromodiphenyl ether (PBDE 99)--congeners that dominate in environmental and human samples--together with another frequently used brominated flame retardant, tetrabromo-bis-phenol-A (TBBPA). The compounds were given to 10-day-old NMRI male mice, as follows: PBDE 47, 0.7 mg (1.4 micromol), 10.5 mg (21.1 micromol)/kg body weight (bw); PBDE 99, 0.8 mg (1.4 micromol), 12.0 mg (21.1 micromol)/kg bw; TBBPA, 0.75 mg (1.4 micromol), 11.5 mg (21.1 micromol)/kg bw. Mice serving as controls received 10 mL/kg bw of the 20% fat emulsion vehicle in the same manner. The present study has shown that neonatal exposure to PBDE 99 and PBDE 47 can cause permanent aberrations in spontaneous behavior, evident in 2- and 4-month-old animals. This effect together with the habituation capability was more pronounced with increasing age, and the changes were dose-response related. Furthermore, neonatal exposure to PBDE 99 also affected learning and memory functions in adult animals. These are developmental defects that have been detected previously in connection with PCBs.
Age Factors↗
Transcriptional regulation of plasminogen activator inhibitor type 1 gene by insulin: insights into the signaling pathway.
Impairment of the fibrinolytic system, caused primarily by increases in the plasma levels of plasminogen activator inhibitor (PAI) type 1, are frequently found in diabetes and the insulin-resistance syndrome. Among the factors responsible for the increases of PAI-1, insulin has recently attracted attention. In this study, we analyzed the effects of insulin on PAI-1 biosynthesis in HepG2 cells, paying particular attention to the signaling network evoked by this hormone. Experiments performed in CHO cells overexpressing the insulin receptor indicate that insulin increases PAI-1 gene transcription through interaction with its receptor. By using inhibitors of the different signaling pathways evoked by insulin-receptor binding, it has been shown that the biosynthesis of PAI-1 is due to phosphatidylinositol (PI) 3-kinase activation, followed by protein kinase C and ultimately by mitogen-activated protein (MAP) kinase activation and extracellular signal-regulated kinase 2 phosphorylation. We also showed that this pathway is Ras-independent. Transfection of HepG2 cells with several truncations of the PAI-1 promoter coupled to a CAT gene allowed us to recognize two major response elements located in the regions between -804 and -708 and between -211 and -54. Electrophoretic mobility shift assay identified three binding sites for insulin-induced factors, all colocalized with putative Sp1 binding sites. Using supershifting antibodies, the binding of Sp1 could only be confirmed at the binding site located just upstream from the transcription start site of the PAI-1 promoter. A construct comprising four tandem repeat copies of the -93/-62 region of the PAI-1 promoter linked to CAT was transcriptionally activated in HepG2 cells by insulin. These results outline the central role of MAP kinase activation in the regulation of PAI-1 induced by insulin.
Base Sequence↗
Gene expression in atherosclerotic lesion of ApoE deficient mice.
BACKGROUND: Atherosclerosis, the major cause of mortality and invalidity in industrialized countries, is a multifactorial disease associated with high plasma cholesterol levels and inflammation in the vessel wall. Many different genes have previously been demonstrated in atherosclerosis, although limited numbers of genes are dealt with in each study. In general, data on dynamic gene expression during disease progress is limited and large-scale evaluation of gene expression patterns during atherogenesis could lead to a better understanding of the key events in the pathogenesis of atherosclerosis. We have therefore applied a mouse gene filter array to analyze gene expression in atherosclerotic ApoE-deficient mice. MATERIALS AND METHODS: ApoE-deficient mice were fed atherogenic western diet for 10 or 20 weeks and aortas isolated. C57BL/6 mice on normal chow were used as controls. The mRNAs of 15 animals were pooled and hybridized onto commercially available Clontech mouse gene array filters. RESULTS: The overall gene expression in the ApoE-deficient and control mice correlated well at both time points. Gene expression profiling showed varying patterns including genes up-regulated at 10 or 20 weeks only. At 20 weeks of diet, an increasing number of up-regulated genes were found in ApoE-deficient mice. CONCLUSIONS: The gene expression in atherogenesis is not a linear process with a maximal expression at advanced lesion stage. Instead, several genes demonstrate a dynamic expression pattern with peaks at the intermediate lesions stage. Thus, detailed evaluation of gene expression at several time points should help understanding the development of atherosclerosis and establishment of preventive intervention.
Animals↗
Rap1p-binding sites in the saccharomyces cerevisiae GPD1 promoter are involved in its response to NaCl.
Mechanisms involved in transcriptional regulation of the osmotically controlled GPD1 gene in Saccharomyces cerevisiae were investigated by promoter analysis. The GPD1 gene encodes NAD(+)-dependent glycerol-3-phosphate dehydrogenase, a key enzyme in the production of the compatible solute glycerol. By analysis of promoter deletions, we identified a region at nucleotides -478 to -324, in relation to start of translation, to be of great importance for both basal activity and osmotic induction of GPD1. Electrophoretic mobility shift and DNase I footprint analyses demonstrated protein binding to parts of this region that contain three consensus sequences for Rap1p (repressor activator protein 1)-binding sites. Actual binding of Rap1p to this region was confirmed by demonstrating enhanced electrophoretic mobility of the protein-DNA complex with extracts containing an N-terminally truncated version of Rap1p. The detected Rap1p-DNA interactions were not affected by changes in the osmolarity of the growth medium. Specific inactivation of the Rap1p-binding sites by a C-to-A point mutation in the core of the consensus showed that this factor is a major determinant of GPD1 expression since mutations in all three putative binding sites for Rap1p strongly hampered osmotic induction and drastically lowered basal activity. We also show that the Rap1p-binding sites appear functionally distinct; the most distal site (core of the consensus at position -386) exhibited the highest affinity for Rap1p and was strictly required for low salt induction (< or =0.6 m NaCl), but not for the response at higher salinities (> or =0.8 m NaCl). This indicates tha different molecular mechanisms might be operational for low and high salt responses of the GPD1 promoter.
Binding Sites↗
Allele-specific regulation of matrix metalloproteinase-12 gene activity is associated with coronary artery luminal dimensions in diabetic patients with manifest coronary artery disease.
Both the processes of atherosclerosis and plaque rupture are indicated to be influenced by matrix metalloproteinase (MMP) activity. We therefore searched for common functional variation in the matrix metalloelastase (MMP-12) gene locus that may be implicated in coronary artery disease. Single-strand conformation polymorphism analysis of DNA from healthy individuals detected a common polymorphism within the MMP-12 gene promoter (an A-to-G substitution at position -82). The frequency of the G allele was 0. 19. The polymorphism influences the binding of the transcription factor activator protein-1 (AP-1) in electromobility shift assay. A higher binding affinity of AP-1 to the A allele was associated with higher MMP-12 promoter activity in vitro in transient transfection studies in U937 and murine lung macrophage (MALU) cells. Phorbol 12-myristate 13-acetate (PMA) and insulin, 2 known activators of AP-1, increased the binding of AP-1 to the MMP-12 promoter, with higher affinity for the A allele. In transfection experiments, both the A and the G alleles responded to insulin and PMA, the A allele showing higher promoter activity than the G allele. Furthermore, Western blot analysis demonstrated that insulin increased MMP-12 protein production. To analyze whether the -82 A/G polymorphism is associated with coronary artery disease, 367 consecutive patients who underwent percutaneous transluminal coronary angiography with stent implantation were genotyped. In patients (n=71) with diabetes, the A allele was associated with a smaller luminal diameter. In conclusion, a common functional polymorphism within the MMP-12 promoter influences coronary artery luminal dimensions in diabetic patients with manifest coronary artery disease.
Adult↗
Exposure to nicotine during a defined period in neonatal life induces permanent changes in brain nicotinic receptors and in behaviour of adult mice.
Neonatal exposure to low doses of nicotine has been shown to prevent the development of low-affinity nicotine-binding sites, and to elicit a different behaviour response to nicotine in the mice as adults. This study has identified a defined period during the development of neonatal mouse brain for the induction of these permanent changes. Neonatal mice, aged either 3, 10, or 19 days were exposed to nicotine, 66 micrograms nicotine-base/kg b.wt., s.c. twice daily, on 5 consecutive days. In the cerebral cortex, high- and low-affinity (HA and LA) nicotine-binding sites were assayed (3H-nicotine/nicotine) in neonatal male mice aged 8, 15, and 24 days and in adult mice aged 4 months. Spontaneous behaviour and nicotine-induced behaviour were observed in 4-month-old male mice. The spontaneous behaviour test did not indicate any difference between saline- and nicotine-treated mice, whereas the nicotine-induced behaviour test revealed a hypoactive response to nicotine, though only in mice given nicotine on days 10-14. The response of controls and the other age categories to nicotine was an increased activity. At no time during the neonatal period could LA nicotine-binding sites be found following nicotine treatment, but the persistence of this effect was evident only in adult mice exposed on days 10-14.
Animals↗
Maze learning and motor activity deficits in adult mice induced by iron exposure during a critical postnatal period.
Newborn mice were administered Fe(2+) (iron succinate: 7.5 mg/kg, b. wt) on either Days 3-5, 10-12 or 19-21, or vehicle (saline) at the same times, postnatally. Spontaneous motor behaviour and radial arm maze learning were tested at the age of 3 months. It was found that mice treated with Fe(2+) during postnatal Days 10-12 were markedly hypokinetic during the 1st 20-min test period and hyperkinetic during the 3rd and final 20-min test period. These mice showed an almost complete lack of habituation of spontaneous motor activity parameters to the test chambers. In the radial arm maze, the Days 10-12 treatment group evidenced significantly both more errors in arm choices and longer latencies to acquire all eight pellets; these mice showed also a severe trial-to-trial retention deficit as indexed by retention quotients. These behavioural deficits were observed also in animals treated with Fe(2+) during postnatal Days 3-5, but the effects were less pronounced, indicating the higher susceptibility of the brain for Fe(2+)-induced damage during Days 10-12 postpartum. Treatment with Fe(2+) on Days 19-21 did not induce behavioural alterations in comparison with its respective control (vehicle) group. Analysis of total brain iron content indicated significantly more iron (microg/g) accumulation in the basal ganglia, but not frontal cortex, of mice from the Days 3-5 and 10-12 Fe(2+) (7.5 mg/kg) treatment groups. The contribution of iron overload during the immediate postnatal to later functional deficits seems to implicate symptoms of Parkinsonism but the kinetics of iron uptake to the brain and its regional distribution at this critical period of development awaits elucidation.
Animals↗
Excessive fat accumulation is associated with the TNF alpha-308 G/A promoter polymorphism in women but not in men.
AIMS/HYPOTHESIS: Tumour necrosis factor alpha (TNF alpha) is a candidate gene for the development of obesity, which in turn is a major risk factor for diabetes mellitus. The aim of our study was to investigate whether a previously known NcoI-sensitive polymorphism (-308 G/A) in the promoter region of the TNF alpha gene was related to body weight. METHODS: Genotyping was done in 239 male and 342 female non-diabetic subjects with a marked variation in body mass index (BMI). RESULTS: We found three genotypes; AA (n = 13), AG (n = 158) and GG (n = 410). When the material was divided according to sex, allele specific phenotypic differences were confined to women. The female subjects carrying the AA genotype were markedly more obese than both the AG and GG carriers (mean BMI = 41.4 vs 32.3 and 31.7 kg/m2, respectively, p = 0.02). The body fat content of female AA carriers was increased by one-third compared with AG/GG carriers (p = 0.02). We found no differences between genotypes with respect to waist-to-hip ratio, blood pressure or metabolic variables. Among obese female subjects (BMI > 27 kg/m2), we also found that the BMI and body fat content of AA carriers (n = 7) were also higher than for AG/GG carriers. CONCLUSION/INTERPRETATION: The AA-variant at position -308 in the promoter region of the TNF alpha gene could be an important genetic factor behind excessive fat accumulation in women.
Adipose Tissue↗
Neonatal nicotine administration influences ethanol-induced behaviors.
Neonatal mice were administered nicotine (66 microg (-)-nicotine base/kg body weight (bw) s.c. twice daily at 0800 and 1700 h on postnatal days 10 and 14) and control mice received saline (10 ml 0. 9% NaCl/kg bw s.c.) on the same occasions. Behavioral testing was initiated 3 months after birth. In Experiment 1, neonatal nicotine administration did not affect spontaneous motor activity but altered the peak dose stimulatory effect of ethanol upon locomotion and rearing activity from 3.0 mg/kg, in the control mice, to 1.5 mg/kg. Administration of the nicotine antagonist, mecamylamine (MEC, 2.0 mg/kg), had no effect upon the peak dose stimulatory effect (i.e., 1. 5 mg/kg) evidenced in the nicotine-treated mice, but attenuated the stimulatory effect of the 3.0 mg/kg dose of ethanol in the control mice. In Experiment 2, the effects of neonatal nicotine administration upon ethanol intake and preference were assessed. In the single fluid access (one-bottle) test, nicotine-treated mice consumed both more ethanol (2%, 4%, or 6% concentrations) and more tap water than control mice. In the two-bottle ethanol preference test, nicotine-treated mice consumed more ethanol and tap water. Further analysis of the high-preferring (HP) ethanol mice indicated higher ethanol intake and preference in the nicotine-treated mice but no differences in tap water or total fluid intake. The present findings are considered together with prevailing notions of nicotine receptor alterations and possible cross-sensitization effects modulating substance abuse.
Animals↗
The Q/E27 polymorphism in the beta2-adrenoceptor gene is associated with increased body weight and dyslipoproteinaemia involving triglyceride-rich lipoproteins.
OBJECTIVES: To investigate whether a substitution of glutamine by glutamic acid at amino acid position 27 (Q/E27) and an arginine to glycine transition at amino acid 16 (R/G16) in the beta2-adrenoceptor gene are associated with lipid and lipoprotein disturbances and/or increased body weight in men. DESIGN: Population-based study. SETTING: Department of medicine at a university hospital. SUBJECTS: A total of 180 healthy men, aged 30-45 years, were recruited at random from a register containing all permanent residents in Stockholm County (response rate of 70%). MAIN OUTCOME MEASURES: Frequency of beta2-adrenoceptor genotypes and alleles in relation to plasma lipid and lipoprotein levels and body mass index. RESULTS: Individuals carrying the E27 allele and/or the G16 allele had significantly higher body mass index (BMI). Furthermore, carriers of the E27 allele had significantly higher plasma concentrations of cholesterol, triglycerides, VLDL cholesterol and VLDL triglycerides than did subjects homozygous for the Q allele. CONCLUSION: The E27 allele of the beta2-adrenoceptor gene is associated with slightly to moderately elevated BMI and dyslipoproteinaemia involving triglyceride-rich lipoproteins in healthy younger and middle-aged men.
Adult↗
Clinical outcome after successful coronary angioplasty: impact of intracoronary stent implantation.
The clinical outcome after successful conventional coronary balloon angioplasty is compared with that of stent implantation after 30 days and 12 months. The study took place at the Divisions of Cardiology and Thoracic Radiology, Norrland University Hospital, Umeå, a referral centre for northern Sweden. The first 100 consecutive patients with stable or unstable angina undergoing successful percutaneous transluminal coronary angioplasty (PTCA) in 1994 and the first 100 consecutive patients undergoing successful coronary stent implantation in 1995 were included. The cardiac endpoints studied were death, myocardial infarction, need for repeat PTCA or coronary artery bypass grafting (CABG). Significantly more adverse cardiac events were observed in the PTCA group compared with the stent group. Event-free 12 months' follow-up (no deaths, myocardial infarction or re-intervention) was 64% in the PTCA group and 86% in the stent group (p < 0.005). The main explanation for the observed difference was a reduction in the need for a repeat PTCA (7 vs 18, p < 0.05) or CABG (4 vs 12, p < 0.05) in the stent group. Patients with stable or unstable angina who can be treated with a stent have a better clinical outcome than those treated with coronary balloon angioplasty only.
Angina Pectoris↗