| 1. |
- Chiale, P A, et al.
(författare)
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High prevalence of antibodies against beta 1- and beta 2-adrenoceptors in patients with primary electrical cardiac abnormalities.
- 1995
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Ingår i: Journal of the American College of Cardiology. - : Elsevier BV. - 0735-1097. ; 26:4, s. 864-9
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: This study sought to determine the prevalence of autoantibodies directed against the beta-adrenoceptors in patients with primary electrical cardiac abnormalities, including atrial arrhythmias, ventricular arrhythmias and conduction disturbances, in the absence of any other cardiac abnormality. BACKGROUND: Using synthetic peptides corresponding to the predicted sequences for the second extracellular loop of the human beta 1- and beta 2-adrenoceptors as antigenic targets, autoantibodies directed against the beta-adrenoceptors were recently shown to occur in patients with idiopathic dilated cardiomyopathy and Chagas' heart disease. METHODS: Eighty-six patients (57 with primary electrical abnormalities, 29 with idiopathic dilated cardiomyopathy) and 101 healthy and cardiopathic control subjects were studied. Antibodies against the beta 1- and beta 2-peptides were detected with an enzyme immunoassay performed in blinded manner. In nine selected (seropositive) cases, the immunoglobulin G (IgG) fraction was tested for functional effects on the rate of beating of cultured neonatal rat cardiomyocytes. RESULTS: Antibodies recognizing the beta 1- and beta 2-peptides were found in 11 (52.3%) of 21 patients with ventricular arrhythmias (p < 0.01), 5 (35.7%) of 14 patients with conduction disturbances (p < 0.05), 3 (13.6%) of 22 patients with atrial arrhythmias (p > 0.05) and 11 (37.9%) of 29 patients with dilated cardiomyopathy (p < 0.05) compared with 15 (14.8%) of 101 control subjects. A rapid increase in the rate of beating of the cultured cardiomyocytes was induced by IgG from a selected group of patients, suggesting an agonist-like interaction with a functional epitope. This response was mediated by stimulation of both the beta 1- and beta 2-adrenoceptors in the patients with primary ventricular arrhythmias but only the beta 1-adrenoceptors in the patients with idiopathic dilated cardiomyopathy. CONCLUSIONS: Primary ventricular arrhythmias and conduction disturbances, like idiopathic cardiomyopathy, show a high prevalence of antibodies interacting with functional epitopes of the beta-adrenoceptors, suggesting a common or similar abnormal immunoregulatory process.
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| 2. |
- Eliasson, Björn, 1959, et al.
(författare)
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Effect of smoking reduction and cessation on cardiovascular risk factors.
- 2001
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Ingår i: Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco. - : Informa UK Limited. - 1462-2203. ; 3:3, s. 249-55
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Tidskriftsartikel (refereegranskat)abstract
- This open study examined the effect of smoking reduction and smoking cessation on established cardiovascular risk factors. Fifty-eight healthy adult smokers (smoking >or=15 cigarettes/day for at least 3 years) were provided with nicotine nasal spray (to be used ad libitum) and asked to stop smoking. The primary goal during the first 8 weeks, however, was to reduce their daily smoking by at least 50%. Subjects were then followed for another 8 weeks; at this point, 33 participants had successfully stopped smoking. Cardiovascular risk factors including fibrinogen, hemoglobin, hematocrit, triglycerides, and cholesterol were measured at baseline and at 9 and 17 weeks. After 8 weeks of smoking reduction, the mean number of cigarettes smoked per day had decreased from 21.5 +/- 0.6 (baseline) to 10.8 +/- 0.6 (p < 0.001). This was accompanied by significant improvements in fibrinogen (from 2.9 +/- 0.1 g/l at baseline to 2.6 +/- 0.1 g/l, p = 0.011), white blood cells (from 7.0 +/- 0.4 to 6.2 +/- 0.3 x 10(9)/l, p = 0.005) and the high-density/low-density lipoprotein (HDL/LDL) ratio (0.33 +/- 0.03 to 0.37 +/- 0.03, p < 0.005). Following 8 weeks of abstinence from smoking, the mean white blood cell count was further reduced (to 6.1 +/- 0.3 x 10(9)/l, p = 0.026 vs. baseline) and there were also significant improvements in HDL (from 1.16 +/- 0.06 mmol/l at baseline to 1.32 +/- 0.06, p < 0.001) and LDL (from 3.78 +/- 0.16 mmol/l at baseline to 3.52 +/- 0.17, p = 0.015). In conclusion, 8 weeks of smoking reduction resulted in clinically significant improvements in established cardiovascular risk factors. These improvements were even greater after an additional period of abstinence from smoking.
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| 3. |
- From Attebring, Mona, 1947, et al.
(författare)
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Smoking habits and predictors of continued smoking in patients with acute coronary syndromes
- 2004
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Ingår i: J Adv Nurs. - : Wiley. - 0309-2402 .- 1365-2648. ; 46:6, s. 614-23
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Most patients with acute coronary syndrome quit smoking when hospitalized, although several have been found to relapse and resume smoking within 3 months. AIM: This paper reports a study to identify factors that can predict who will resume smoking after hospitalization for an acute coronary syndrome. METHODS: Patients (n = 1320) below the age of 75 years, admitted to a Swedish university hospital coronary care unit with acute coronary syndromes, between September 1995 and September 1999, were consecutively included. Data were collected from hospital medical records and included information on previous clinical history, former illnesses and smoking. During their hospitalization, an experienced nurse interviewed the patients by using a structured questionnaire to obtain additional information. Patients were followed up 3 months after the discharge. Those who continued to smoke (non-quitters) were compared with those who had stopped (quitters) with regard to age, sex, medical history, clinical course, and intention to quit. To identify factors independently related to continued smoking, a logistical regression in a formal forward stepwise mode was used. RESULTS: Of the patients admitted, 33% were current smokers. Three months after discharge, 51% of these patients were still smoking. There were no significant differences in age, gender or marital status between non-quitters and quitters. In a multivariate analysis, independent predictors of continued smoking were: non-participation in the heart rehabilitation programme (P = 0.0008); use of sedatives/antidepressants at time of admission (P = 0.001); history of cerebral vascular disease (P = 0.002), history of previous cardiac event (P = 0.01); history of smoking-related pulmonary disease (P = 0.03) and cigarette consumption at index (P = 0.03). CONCLUSIONS: Smoking patients who do not participate in a heart rehabilitation programme may need extra help with smoking cessation. The findings may provide means of identifying patients in need of special intervention.
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| 4. |
- Hjalmarson, Agneta, 1943
(författare)
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Rökstopp inför operation minskar risk för komplikationer: Rökare bör erbjudas rökavvänjning
- 2014
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Ingår i: Läkartidningen. - : Swedish Medical Association. - 0023-7205. ; :29-31
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Tidskriftsartikel (refereegranskat)abstract
- Smoking cessation before surgery is beneficial for patients. The longer the period of pre-operative abstinence, the better. Both brief and intensive interventions resulted in more patients quitting smoking at time of surgery. However, a significant reduction in risk of surgical complications, and an increase in cessation rates at 12 months, was only reported by the studies offering patients intensive smoking cessation treatment, including nicotine replacement therapy, for 4–8 weeks before surgery and a similar time-period after surgery. The Swedish National Board of Health and Welfare recommends that smokers scheduled for surgery should be offered intensive cessation treatment. This, though, requires more treatment time than brief advice, and also trained staff, something which can be offered at tobacco preventive units and at many primary care facilities. For patients to profit from this, they must be aware that treatment is available and be encouraged to use it.
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| 5. |
- Jacobsson, B, et al.
(författare)
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Abnormality of adenylate cyclase regulation in human platelet membranes in renal insufficiency.
- 1985
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Ingår i: European journal of clinical investigation. - 0014-2972. ; 15:2, s. 75-81
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Tidskriftsartikel (refereegranskat)abstract
- Adenylate cyclase in human platelets is under dual control of prostaglandins (PGI2 and PGE1) and catecholamines. The adenylate cyclase complex in membranes of platelets from ten patients with uraemia was investigated. The activation of the platelet cyclase by PGE1 is increased in the uraemic state, Vmax 4436 +/- 607 pmol cAMP mg-1 15 min-1. In the normal state Vmax is 2098 +/- 309 pmol cAMP mg-1 15 min-1. The alpha 2-adrenergic receptor was assayed with 3H-yohimbine binding. The density of receptors was equal in the uraemic (175 fmol mg-1 membrane protein) and the normal (170 fmol mg-1 membrane protein) states. Norepinephrine/3H-yohimbine competition binding revealed that catecholamines were bound with normal affinity in platelets in uraemia. Yet the inhibition of adenylate cyclase through the alpha 2-adrenergic receptor was diminished since Vmax values of adenylate cyclase with PGE1 and PGE2 + norepinephrine did not significantly differ. In the normal state, norepinephrine significantly (P less than 0.05) inhibited the PGE1 stimulated cyclase. It is concluded that platelet adenylate cyclase in the uraemia has an increased capacity for activation which is the result of both a sensitized stimulatory mechanism (prostaglandin mediated) and a deficient inhibitory mechanism (catecholamine mediated). It is suggested that a defect exists in the inhibitory nucleotide binding protein (NI) which is the coupling unit between the adenylate cyclase catalytic subunit (C).
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| 6. |
- Libungan, Berglind, et al.
(författare)
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Secondary prevention in coronary artery disease. Achieved goals and possibilities for improvements.
- 2012
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Ingår i: International journal of cardiology. - : Elsevier BV. - 1874-1754 .- 0167-5273. ; 161:1, s. 18-24
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Tidskriftsartikel (refereegranskat)abstract
- AIM: To describe presence of risk indicators of recurrence 6months after hospitalisation due to coronary artery disease at a university clinic. METHODS: The presence of risk indicators, including tobacco use, lipid levels, blood pressure and glucometabolic status, including 24-hour blood pressure monitoring and an oral glucose-tolerance test, was analysed. RESULTS: Of 1465 patients who were screened, 402 took part in the survey (50% previous myocardial infarction and 50% angina pectoris). Mean age was 64years (range 40-85years) and 23% were women. Present medications were: lipid lowering drugs (statins; 94%), beta-blockers (85%), aspirin or warfarin (100%) and ACE-inhibitors or angiotensin II blockers (66%). Values above target levels recommended in guidelines were: a) low density lipoprotein (LDL) in 40%; b) mean blood pressure (day or night) in 38% and c) smoking in 13%. Of all patients, 66% had at least one risk factor (LDL or blood pressure above target levels or current smoking). An abnormal glucose-tolerance test was found in 59% of patients without known diabetes. If no history of diabetes, 85% had either LDL or blood pressure above target levels, current smoking or an abnormal glucose-tolerance test. However, with treatment intensification to patients with elevated risk factors 56% reached target levels for blood pressure and 79% reached target levels for LDL. CONCLUSION: Six months after hospitalisation due to coronary artery disease, despite the high use of medication aimed at prophylaxis against recurrence, the majority were either above target levels for LDL or blood pressure or continued to smoke.
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| 7. |
- Magnusson, Yvonne, 1957, et al.
(författare)
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Antigenic analysis of the second extra-cellular loop of the human beta-adrenergic receptors.
- 1989
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Ingår i: Clinical and experimental immunology. - 0009-9104. ; 78:1, s. 42-8
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Tidskriftsartikel (refereegranskat)abstract
- Polyclonal antibodies were raised in rabbits by immunization with free peptides corresponding to positions 197-222 of the human beta 1-adrenergic receptor (beta 1 peptide) and the corresponding sequence (172-197) of the human beta 2-adrenergic receptor (beta 2 peptide). While the beta 2 peptide yielded antibodies that cross-reacted with the beta 1 peptide, the antibodies against the beta 1 peptide did not cross-react with the beta 2 sequence. Cross-reactivity of the anti-beta 2 peptide antibodies and the selectivity of the anti-beta 1 peptide antibodies were also revealed in the recognition by immunoblots of the beta 1- and beta 2-adrenergic receptors of different species or of the receptor gene products expressed in a bacterial vector. These antibodies could be used immunohistochemically to visualize the beta-adrenergic receptors on rabbit heart. The anti-beta 2 peptide antibodies did not show any functional effect on the beta-adrenergic receptors; the anti-beta 1 peptide antibodies were able to displace agonist affinity to higher values. Recognition of truncated peptides by the anti-beta 1 and anti-beta 2 peptide antibodies suggested that the cross-reaction of the anti-beta 2 peptide antibodies was due to the recognition of a common epitope on the C-terminal part of the peptides. The anti-beta 1 peptide antibodies recognized the N-terminal part of the peptide better than the C-terminal part. These results suggest that the second extracellular loop postulated in the structure of the human beta-adrenergic receptor contains the T and B cell epitopes necessary for induction of an immune response. The selectivity and the functional properties of the antibodies raised against that loop in the beta 1 adrenergic receptor could have relevance in induction of auto antibodies in certain cardiomyopathic conditions.
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| 8. |
- Magnusson, Yvonne, 1957, et al.
(författare)
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Autoimmunity in idiopathic dilated cardiomyopathy. Characterization of antibodies against the beta 1-adrenoceptor with positive chronotropic effect.
- 1994
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Ingår i: Circulation. - 0009-7322. ; 89:6, s. 2760-7
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Autoantibodies against the beta 1-adrenoceptor have been detected in the sera of patients with idiopathic dilated cardiomyopathy (DCM). The mechanisms by which these autoantibodies can alter normal receptor function are investigated, and the results are interpreted in the light of the beneficial effects of beta 1-blockade in some of these patients. METHODS AND RESULTS: Autoantibodies against the beta 1-adrenoceptor, affinity purified from sera of patients with idiopathic DCM, were analyzed in a functional test system of spontaneously beating neonatal rat heart myocytes. Antibodies from rabbits immunized with peptides derived from the amino acid sequence of this receptor were also analyzed. Autoantibodies, against the second extracellular loop increased the beating frequency of isolated myocytes in a concentration-dependent manner, to approximately 80% of maximal isoproterenol stimulation. Rabbit anti-peptide antibodies against the second extracellular loop increased the beating frequency correspondingly. Autoantibodies and rabbit anti-peptide antibodies against the second extracellular loop were able to immunoprecipitate the unliganded receptor but not the antagonist-occupied receptor. In contrast, rabbit antibodies against the extracellular N-terminal sequence 34-57 of the beta 1-adrenoceptor were able to immunoprecipitate both the unliganded and the antagonist-occupied receptor although with no effect on the beating frequency of myocytes. The positive chronotropic effect of the antibodies was completely neutralized both by the addition of increasing concentrations of the beta 1-selective antagonist bisoprolol and by preincubation with the peptide corresponding to the second extracellular loop. The antibody-induced increase in beating frequency remained unchanged for more than 6 hours. This should be compared with the isoproterenol-stimulated beating frequency, which undergoes desensitization within 60 minutes. Addition of isoproterenol to autoantibody-stimulated myocytes resulted in only a small increase in beating frequency and did not cause desensitization. Antibodies had only a marginal effect on cyclic AMP production of stimulated cardiomyocytes compared with the 10-fold increase obtained after stimulation with isoproterenol. CONCLUSIONS: The second extracellular loop of the beta 1-adrenoceptor is a specific target for antibodies with stimulatory activity detected in patients with idiopathic DCM. The antibodies have a positive chronotropic effect on isolated rat heart myocytes. Autoantibody stimulation does not cause the normal agonist-induced desensitization phenomena of the effector system. These findings could contribute to our understanding of the pathophysiological mechanisms of the autoantibodies and of the beneficial effect of beta 1-blocking agents in the treatment of patients with idiopathic DCM.
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| 9. |
- Magnusson, Yvonne, 1957, et al.
(författare)
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Beta 1-adrenoceptor autoimmunity in cardiomyopathy.
- 1996
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Ingår i: International journal of cardiology. - 0167-5273. ; 54:2, s. 137-41
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Forskningsöversikt (refereegranskat)abstract
- A growing body of studies have confirmed that autoantibodies against beta 1-adrenoceptors are present in different types of cardiomyopathy. This suggests that they play a role in the pathophysiology of the disease. This article will review the data indicating the presence of anti-beta 1-adrenoceptor autoantibodies in cardiomyopathy. It will focus upon their structural and functional properties which could explain their possible role in the induction and development of cardiomyopathic diseases.
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| 10. |
- Magnusson, Yvonne, 1957, et al.
(författare)
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Functional analysis of rabbit anti-peptide antibodies which mimic autoantibodies against the beta 1-adrenergic receptor in patients with idiopathic dilated cardiomyopathy.
- 1991
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Ingår i: Journal of autoimmunity. - 0896-8411. ; 4:6, s. 893-905
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Tidskriftsartikel (refereegranskat)abstract
- A synthetic peptide corresponding to the second extracellular loop of the beta 1-adrenergic receptor was used as an antigen for antibody production in three rabbits. Antibodies of high titers were obtained in all rabbits. Only one rabbit yielded antibodies which decreased radioligand binding on the receptor in a similar way to that described for autoantibodies in patients with dilated cardiomyopathy. These antibodies recognized the receptor protein in immunoblots. Epitope mapping indicated that the N-terminal sequence of the loop used as antigen was the target of the major antigen fraction. Incubation of antibodies with C6 glioma cell membranes or inner membranes of E. coli, which express the human beta 1-adrenergic receptor, resulted in a decrease in number of radioligand binding sites. This decrease was dependent on the concentration of antibody and of Mg++ ions. It was not affected by the GTP analog GppNHp or the beta 1 subtype-specific antagonist metoprolol. The agonist, isoproterenol, also induced a decrease but the effects of antibody and agonist were not additive. These results suggest that the antibodies induce a Mg(++)-dependent, 'active', labile conformation of the receptor, independent from coupling to the GTP regulatory protein, but similar to that induced by the agonist isoproterenol. This interpretation was corroborated by the beta 1-adrenergic receptor agonist-like effect of the antibodies on cardiomyocytes in culture.
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