Biomedical subjects

A Hjalmarson

Publications and source records attributed to A Hjalmarson.

At least 55 records · Page 3Linked to original sources

PubMed1998

Risk indicators for cerebrovascular complications after coronary artery bypass grafting.

All patients from western Sweden were retrospectively studied in whom CABG was performed between June 1, 1988 and June 1, 1991 without simultaneous valve surgery. The aim was to detect clinical factors prior to and at the time of coronary artery bypass grafting (CABG) which were associated with the risk of neurological complications during the postoperative hospital stay. A neurological complication during the hospital stay was registered if a neurological consultation was made and if this consultation diagnosed a neurological deficit. In all, there were 2121 patients in the study, of whom 81 (3.8%) had a neurological complication. 23 of the latter (28%) died before discharge. Among preoperative factors the following appeared as significant independent predictors of a neurological complication: a history of cerebrovascular disease (p < 0.001), diabetes mellitus (p < 0.01), hypertension (p < 0.05), degree of urgency of the operation (p < 0.01), and age (p < 0.01). Among pre- and post-operative events the following predicted a neurological complication: intensive care unit treatment for more than two days (p < 0.001) and respirator required for more than 24 hours (p < 0.001).

Aged↗

PubMed1998

Effects on heart rate variability of isosorbide-5-mononitrate and metoprolol in patients with recent onset of angina pectoris.

BACKGROUND: Beta-blockers reduce sympathetic tone, increase vagal tone and improve prognosis in ischaemic heart disease. Nitroglycerin, being a vasodilator, may theoretically have an opposite effect and worsen the prognosis. The purpose of the present study was to analyse heart rate variability (HRV), which reflects autonomic tone, in angina patients on isosorbide-5-mononitrate (IS-5-MN) and/or metoprolol. METHODS AND RESULTS: Thirty-two patients (32-81 years old), with recently developed angina (median duration: 3 months), showing no other disease and on no drugs, were Holter-monitored 24-48 h at baseline and after 4-5 days on IS-5-MN (mean daily dose: 33 mg), on metoprolol (mean daily dose: 184 mg) and on the combined treatment. Recordings were analysed on the Marquette Series 8000 Holter scanner. Both IS-5-MN and metoprolol significantly reduced myocardial ischaemia (ST integral) and ventricular tachycardias. Metoprolol induced significant changes in the following parameters (baseline versus metoprolol): high-frequency peak 9 +/- 4 versus 11 +/- 4 ms (p < 0.001), low-to-high frequency ratio 2.5 +/- 0.6 versus 1.9 +/- 0.6 (p < 0.0001), root mean square of RR interval difference 23 +/- 7 versus 31 +/- 9 ms (p < 0.0001), RR intervals differing more than 50 ms from the preceding one 4.8 +/- 3.9 versus 10.0 +/- 7.0% (p < 0.0001), mean of all 5-min standard deviations 50 +/- 12 versus 56 +/- 11 ms (p < 0.001) and mean RR interval 819 +/- 90 versus 1,019 +/- 120 ms (p < 0.00001). The combined treatment caused approximately the same HRV changes as metoprolol alone. IS-5-MN had no significant effect on any HRV parameter, neither alone nor in combination with metoprolol. CONCLUSION: A clinically effective dose of metoprolol had potentially positive effects on HRV with increase in vagal and decrease in sympathetic tone while IS-5-MN had no effect on HRV, neither positive nor negative, neither alone nor in combination with metoprolol.

Adrenergic beta-Antagonists↗

PubMed1998

Significance of reduction in heart rate in cardiovascular disease.

Epidemiologic studies suggest that lower heart rate is associated with decreased cardiovascular and all-cause mortality. Heart rate has also been reported to be an independent predictor of outcome after myocardial infarction (MI). Because it is a major determinant of oxygen consumption and metabolic demand, a decrease in heart rate would be expected to decrease cardiac workload. Among patients with restricted coronary blood flow, increased heart rate is associated with more severe myocardial ischemia, angina, and an increase in size of MI. Pharmacologic interventions that reduce heart rate, such as beta blockers, generally reduce mortality and improve outcome. A number of clinical trials using beta blockers after MI has shown a relationship between reduction in heart rate and reduction in mortality. Most beta blockers demonstrate a nearly linear relationship between reductions in mortality and in heart rate. The evidence from trials with calcium antagonists is more equivocal, possibly because until very recently none were available that decreased heart rate without decreasing myocardial contractility. Drugs that do not reduce the heart rate after an MI and in congestive heart failure have not been found to improve survival. In light of the findings thus far reported, reduction in heart rate should be a therapeutic goal in the treatment of cardiovascular disease.

Adrenergic beta-Antagonists↗

PubMed1998

Immunohistochemical localization of angiotensin II receptors (AT1) in the heart with anti-peptide antibodies showing a positive chronotropic effect.

Antibodies were produced against a synthetic peptide corresponding to amino acids (165-191) of the second extracellular loop of the human angiotensin II receptor subtype 1 (AT1) in rabbits. The purified antibodies had an apparent affinity of about 1 nM and were monospecific for the AT1-receptor peptide. Chemical modification of the carboxyl groups (glu at positions 173 and 185) and the sulfhydryl group (cys at position 180) of the AT1-receptor peptide did not alter the relative affinity of the coated AT1-receptor peptide to antibodies. The antibodies specifically stained CHO cells expressing the rat AT1a receptor. Immunoblots on rat kidney revealed that the antibody recognized a protein band of 59 +/- 3 kDa in a dose-dependent manner and this band was no longer detected after preincubating the antibodies with AT1-receptor peptide. Using electron microscopic and immunofluorescence immunocytochemistry techniques, angiotensin II receptors were detected in (1) the sarcolemma, T-tubules and nuclei of rat cardiomyocytes, (2) the transluminal side of endothelial cells and (3) fibroblast cells. These localizations are specific, as the immunostaining did not appear when preimmune rabbit serum was used and was blocked after preincubating antibodies with antigenic peptide. Functionally, these antibodies did not affect the ligand binding properties of the receptors but displayed agonist-like activity as shown by dose-dependent increases in beating frequency in cultured neonatal cardiomyocytes. These results suggest that the antibodies against the second extracellular loop of human AT1 receptors were able to specifically recognize AT1 receptors. In addition, they extend the observation that the second extracellular loop of the G-protein coupled membrane receptors is a specific target for antibodies with agonist-like activity.

Amino Acid Sequence↗

PubMed1997

Effects of beta blockade on sudden cardiac death during acute myocardial infarction and the postinfarction period.

About half of all deaths after myocardial infarction (MI) are sudden cardiac deaths. Most of these are thought to be due to ventricular fibrillation (VF). A number of interventions and many different antiarrhythmic agents have been investigated, but so far only beta-blocker therapy has been found to produce significant reductions in the risk of sudden cardiac death after MI. Reductions in total mortality and sudden cardiac death were first reported in 1981 in 3 placebo-controlled studies, the Norwegian Timolol Study, the American Beta-Blocker Heart Attack Trial (BHAT), and the Göteborg Metoprolol Trial. A few years later, two very large trials, the Metoprolol in Acute Myocardial Infarction (MIAMI) study and the First International Study of Infarct Survival (ISIS-1), which included 6,000 and 16,000 patients, respectively, showed that beta-blocker therapy could reduce mortality within the first 2 weeks after onset of MI. Data from 24 postinfarction studies with long-term follow-up show an average 20% mortality reduction over 2 years. Pooled results of 28 short-term, randomized, placebo-controlled trials in which beta blockers were given intravenously shortly after onset of MI indicate an average 13% mortality reduction within 2 weeks. In the 16 studies in which the sudden cardiac death rate was reported, the beneficial effect of beta blockade was even more marked: a 34% average reduction of risk. Not all studies with beta blockers, however, have demonstrated a significant reduction in the incidence of sudden cardiac death. Such an effect has been clearly demonstrated only for the more lipophilic beta blockers (timolol, metoprolol, and propranolol). Two of these lipophilic beta blockers, metoprolol and propranolol, have also been shown to prevent VF after MI in clinical studies. Based on observations from animal experiments, it has been proposed that beta blockers with a high degree of lipophilicity penetrate the brain and thereby maintain high vagal tone during stress. A combination of direct anti-ischemic effects due to beta1 blockade and preservation of vagal tone appears to prevent VF in these animal models. Further clinical studies are needed to explore this hypothesis.

Adrenergic beta-Antagonists↗

PubMed1997

Effect of metoprolol on the prognosis for patients with suspected acute myocardial infarction and indirect signs of congestive heart failure (a subgroup analysis of the Göteborg Metoprolol Trial).

The aim of this study is to describe the impact of early treatment with metoprolol on prognosis during 1 year of follow-up in patients with suspected acute myocardial infarction (AMI) and indirect signs of congestive heart failure (CHF). Patients aged 40-74 years who presented within 48 hours of onset of symptoms raising suspicion of AMI were assessed for inclusion. All patients participated in the Göteborg Metoprolol Trial and had indirect indices of CHF according to various clinical criteria. As soon as possible after hospital admission, patients received either placebo or metoprolol (15 mg) divided into 3 intravenous injections, then oral treatment, 200 mg daily for 3 months. Thereafter, most patients in both treatment groups received metoprolol in an open manner. Among the 1,395 randomized patients, 262 (19%) had signs of mild-to-moderate CHF before randomization. Of these, 131 were randomized to metoprolol and 131 to placebo. During the first 3 months, mortality was 10% among patients randomized to metoprolol versus 19% among patients randomized to placebo (p = 0.036). The corresponding figures for the first year were 14% and 27%, respectively (p = 0.0099). Patients randomized to placebo who showed signs of CHF had a 1-year mortality rate of 28% compared with 10% among patients without such signs (p <0.001). The results suggest that early treatment with metoprolol markedly reduces mortality in patients having suspected AMI and signs of CHF.

Adrenergic beta-Antagonists↗

PubMed1997

Detection of interstellar ethylene oxide (c-C2H4O).

We report the identification of 10 transitions that support the detection of the small cyclic molecule ethylene oxide (c-C2H4O) in Sgr B2N. Although one of these transitions is severely blended, so that an accurate intensity and line width could not be determined, and two other lines are only marginally detected, we have done Gaussian fits to the remaining seven lines and have performed a rotation diagram analysis. Our results indicate a rotation temperature T(rot) = 18 K and a molecular column density N(c-C2H4O) = 3.3 x 10(14) cm-2, corresponding to a fractional abundance relative to molecular hydrogen of order 6 x 10(-11). This is a factor of more than 200 higher than the abundance for this molecule suggested by the "new standard" chemistry model of Lee, Bettens, & Herbst. This result suggests that grain chemistry might play an effective role in the production of c-C2H4O. No transitions of this molecule were detected in either Sgr B2M or Sgr B2NW.

Astronomical Phenomena↗

PubMed1997

Anti-M2 muscarinic receptor antibodies inhibit beta-adrenoceptor-mediated inotropic response in rat myocardium.

The modulation of the inotropic effect by affinity-purified antibodies against a synthetic peptide corresponding to the second extracellular loop of the human muscarinic M2 receptors was studied in adult rat ventricular myocardium. These anti-muscarinic M2 receptor antibodies shifted the dose-response relationship of the beta-adrenoceptor agonist isoproterenol to higher concentrations whereas preimmune rabbit immunoglobulin G (IgG) or antibodies against the N-terminus of the beta 1-adrenoceptor had no effect. This effect of anti-muscarinic M2 receptor antibodies was fully blocked after preincubation with the antigenic peptide. No significant change of maximal inotropic response to isoproterenol was observed in the presence of anti-muscarinic M2 receptor antibodies. The anti-muscarinic M2 receptor antibodies did apparently not hamper the access of the muscarinic receptor agonist carbachol. The muscarinic receptor antagonist atropine attenuated the effect of the anti-muscarinic M2 receptor antibodies. The present study demonstrates for the first time in intact adult ventricular myocardium a specific stimulatory muscarinic activity of antibodies raised against a part of the muscarinic M2 receptor protein.

Adrenergic beta-Agonists↗

PubMed1997

Heart rate variability after acute myocardial infarction in patients treated with atenolol and metoprolol.

UNLABELLED: Heart rate variability (HRV) reflects autonomous activity that influences the heart. It has been shown that HRV is depressed during acute myocardial infarction (AMI) and that it recovers with time. Beta-blockers reduce mortality after AMI and changes in sympathico-vagal activity have been suggested to be of importance. Under certain animal experimental conditions, metoprolol has been reported to increase vagal tone more than atenolol, which could have clinical implications. The purpose of the present study was to compare the effects of atenolol and metoprolol treatments on HRV during 6 weeks after AMI and to follow the post MI changes in HRV in patients on betablockers. METHODS: In an open, randomised cross-over study, 28 patients were randomised to 3+3 weeks' treatment with atenolol or metoprolol starting 2-5 days after AMI. Twenty-four hour Holter recordings were made before randomisation and after 3 and 6 weeks. HRV was analysed as HR, SDRR, SDANN, SD, rMSSD and pNN50 in the time domain and as coefficient of component variance (CCV) of HF and LF, and as LF/HF ratio in the frequency domain. RESULTS: The average daily dose in our study population was 106 mg of metoprolol and 54 mg of atenolol. There were trends toward lower heart rates daytime, lower LF/HF ratio daytime and higher rMSSD on atenolol compared to metoprolol. In the total group of 28 patients we found during the first 3 weeks, a significant increase of SDNN, SDANN (p<0.0001) and LF/HF ratio daytime and CCV-HF night-time (p<0.01). All differences and trends were unchanged between 3 and 6 weeks. CONCLUSIONS: There was no evidence of more increased vagal tone with metoprolol compared to atenolol as has been suggested from animal models. In patients also on chronic treatment with beta blockers, an increase of HRV was seen during the first weeks post MI.

Adrenergic beta-Antagonists↗

PubMed1997

Peptides derived from cardiovascular G-protein-coupled receptors induce morphological cardiomyopathic changes in immunized rabbits.

An experimental model of early-stage cardiomyopathy was created by immunizing rabbits for 1 year with synthetic peptides corresponding to the sequence of the second extracellular loop of either beta-adrenoceptors or M2-muscarinic receptors. Thirty male rabbits were used and divided into three groups: a control group (n = 10), a group immunized with the peptide corresponding to the beta-adrenoceptor (beta 1 group) (n = 10) and a group immunized with the peptide corresponding to the M2-muscarinic receptor (M2 group) (n = 10). If the sera from both groups of immunized rabbits high-titres of anti-peptide antibodies were found throughout the study period but not in the sera from control rabbits or in the preimmune sera of immunized rabbits. No significant cross-reaction with peptides other than those used for immunization was found. The myocardial receptor density of both immunized groups displayed a strong trend toward receptor up-regulation. This was significant in the beta 1 group but not in the M2 group. Both groups of immunized rabbits displayed significantly enlarged ventricles and thinner walls, as compared with the control group. However, in contrast to the beta 1 group, which showed enlarged cavities in both left and right ventricles, the M2 group was mainly affected in the right ventricles. Moreover, morphological examinations of the hearts of rabbits from both immunized groups demonstrated focal myofibrillar lysis, loss of myofilament, mitochondrial swelling and condensation, sarcoplasmic vacuolation, deposition of dense granules in the sarcoplasm and the myofibrils. One of the sex control rabbit hearts which were examined showed mild degenerative changes in the myocardium and scant mononuclear cell infiltration. However, when all the control rabbit hearts were examined by electron microscopy, no significant alterations were found. These results suggest that immunization by peptides, corresponding to the target sequences for anti-receptor autoantibodies in idiopathic dilated cardiomyopathy, induces morphological changes in the heart similar to those found in the human disease.

Amino Acid Sequence↗

PubMed1997

Improvement of ED prediction of cardiac mortality among patients with symptoms suggestive of acute myocardial infarction.

A study was undertaken to evaluate the 1-year risk of cardiac death for patients with chest pain/suspected acute myocardial infarction in the emergency department (ED) and express the prognosis in a statistical model. Clinical variables and electrocardiogram were correlated to cardiac death during 1 year. Cox regression model was used to estimate the risk of death as a continuous function of a risk score and the time interval. From these, the prognosis for each patient can be calculated. There were 6,794 visits by 5,303 patients followed for 1 year, during which 604 patients died. The absolute risk of cardiac death can be calculated from the independent predictors for cardiac death: age; sex; histories of diabetes mellitus, hypertension, and congestive heart failure; and symptoms, electrocardiographic pattern, and degree of suspicion of acute myocardial infarction on admission. This model allows estimation of the prognosis for every patient with chest pain/suspected acute myocardial infarction from data easily available in the ED.

Adolescent↗

PubMed1997

Growth hormone improves cardiac function in rats with experimental myocardial infarction.

Accumulating evidence suggests from experimental and clinical studies beneficial effects of growth hormone (GH) on contractility, although concomitant cardiac hypertrophy, generally considered to be a cardiovascular risk factor, has also been reported. In the present study, we combine a rat model with impaired cardiac performance after myocardial infarction (MI) with echocardiographic evaluation of GH effects on cardiac structure and function. We have used a rat model with ligation of the left coronary artery in normal, growing male rats resulting in subsequent impaired cardiac performance. After 6 weeks' recovery, blind transthoracic echocardiography was performed to determine infarction size, cardiac geometry and performance. Rats with no signs of myocardial infarction were excluded from the study. After randomization, the rats were treated with daily s.c. injections of saline (n = 8) or recombinant human growth hormone (rhGH) (n = 6) at a dose of approximately 1 mg kg-1 body weight for 1 week. A new blind echocardiography examination was performed after treatment demonstrating a 13% increase in ejection fraction (EF) and a 50% increase in cardiac index in GH-treated rats compared with control rats (P < 0.01). Moreover, GH caused a significant decrease in end-systolic volume. There were no significant changes in left ventricular (LV) or interventricular wall thickness, LV dimensions, heart rate or diastolic function. No effects were seen on LV weight, cardiac insulin-like growth factor (IGF) I, IGF-I receptor and GH receptor mRNA content. GH in a physiological dose improves systolic function in an experimental model of heart failure without signs of hypertrophy, suggesting a potential role as a therapeutic agent in the treatment of heart failure and merits further investigation.

Animals↗

PubMed1997

Predictors of hospital readmission two years after coronary artery bypass grafting.

OBJECTIVE: To determine the clinical factors before, and in association with, coronary artery bypass grafting (CABG) that increase the risk of readmission to hospital in the first two years after surgery. PATIENTS: All patients in western Sweden who had CABG without simultaneous valve surgery between 1 June 1988 and 1 June 1991. METHODS: All patients who were readmitted to hospital were evaluated by postal inquiry and hospital records. RESULTS: A total of 2121 patients were operated on, of whom 2037 were discharged from hospital. Information regarding readmission was missing in four patients, leaving 2033 patients; 44% were readmitted to hospital. The most common reasons for readmission were angina pectoris and congestive heart failure. There were 12 independent significant predictors for readmission: clinical history (a previous history of either congestive heart failure or myocardial infarction, or CABG); acute operation; postoperative complications (time in intensive care unit greater than two days, neurological complications); clinical findings four to seven days after the operation (arrhythmia, systolic murmur equivalent to mitral regurgitation); medication four to seven days after the operation (antidiabetics, diuretics for heart failure, other antiarrhythmics (other than beta blockers, calcium antagonists, and digitalis), and lack of treatment with aspirin). CONCLUSION: 44% of patients were readmitted to hospital two years after CABG. The most common reasons for readmission were angina pectoris and congestive heart failure. Four clinical markers predicted readmission: clinical history; acute operation status; postoperative complications; and clinical findings and medication four to seven days after operation.

Adrenergic beta-Antagonists↗

PubMed1997

The role of beta-blockers in left ventricular dysfunction and heart failure.

It was first reported by our group in 1975 that heart failure due to idiopathic dilated cardiomyopathy (IDC) could be improved by long term treatment with a beta-blocker, starting at a low dose and continuing with a stepwise up-titration. Since then, many studies have been performed in patients with heart failure of various aetiologies and the beneficial effects of long term beta-blockade have been confirmed. About 3000 patients have been included in randomised studies in which beta-blockade, given for more than 2 months, mostly elicited significant improvements in functional class, exercise capacity, cardiac function, quality of life and/or morbidity. When started at a very low dose (one-tenth to one-twentieth of the doses generally used in angina or hypertension), the treatment is well tolerated in most patients. In these studies, various types of beta-blockers were used, including beta1-selective blockers and nonselective blockers with additional properties (vasodilator and antioxidative) such as metoprolol, bisoprolol, bucindolol and carvedilol. Several large studies have also reported benefits on mortality and morbidity. In the Metoprolol in Dilated Cardiomyopathy (MDC) trial, metoprolol treatment in patients with IDC resulted in a 34% reduction of the primary combined endpoint, total number of deaths and need for cardiac transplantation. In the Cardiac Insufficiency Bisoprolol Study (CIBIS), in patients with idiopathic as well as ischaemic cardiomyopathy, there was a nonsignificant 20% reduction in mortality. In the US carvedilol studies (n = 1094), also in patients with ischaemic and idiopathic cardiomyopathy, carvedilol reduced mortality by 65%, which was highly significant. A nonsignificant reduction in mortality was observed in the Australia-New Zealand (ANZ) Heart Failure Study with carvedilol. In all these studies there was a reduction in hospitalisations, with all drugs being generally well tolerated. It can thus be concluded that the beneficial effects of beta-blockers on cardiac function and morbidity have been documented in a large number of studies in selected groups of patients. The treatment has been accepted in some countries by the regulatory authorities. Larger, placebo-controlled studies are needed to convincingly demonstrate a reduction in total mortality as observed in the pooling of the 4 US carvedilol studies. Such studies are in progress for various beta-blockers, which may lead to acceptance of their routine clinical use in patients with congestive heart failure.

Adrenergic beta-Antagonists↗

PubMed1996

Changes in early and late diastolic filling patterns induced by long-term adrenergic beta-blockade in patients with idiopathic dilated cardiomyopathy.

BACKGROUND: beta-Blockers have been used in patients with idiopathic dilated cardiomyopathy to improve cardiac performance and theoretically would be beneficial to diastolic function. However, there are few reports on changes in diastolic function during chronic pharmacological treatment of congestive heart failure. METHODS AND RESULTS: The present study was a substudy in the international Metoprolol in Dilated Cardiomyopathy Trial. Transmitral Doppler echocardiography was used to evaluate diastolic function in 77 patients randomly assigned to placebo (n = 37) or metoprolol (n = 40). The patients were treated for 12 months. Changes in Doppler flow variables in the metoprolol group implied a less restrictive filling pattern, expressed as an increase in E-wave deceleration time (placebo, 185 +/- 126 to 181 +/- 64 ms; metoprolol, 152 +/- 63 to 216 +/- 78 ms; P = .01, placebo versus metoprolol). Maximal increase in deceleration time had occurred by 3 months, whereas systolic recovery was achieved gradually and maximal effect was seen by 12 months of treatment. Although deceleration time was correlated to heart rate at baseline, changes in deceleration time were not significantly correlated to changes in heart rate during treatment. CONCLUSIONS: During the first 3 months of treatment, maximal effects on diastolic variables were reached, whereas the most prominent effect on systolic function was seen late in the study. It is suggested that effects on diastolic filling account for subsequent later myocardial systolic recovery. The E-wave deceleration time, which in recent studies has been shown to be a powerful predictor of survival, was significantly improved in the metoprolol-treated patients.

Adrenergic beta-Antagonists↗

PubMed1996

A synthetic peptide corresponding to the second extracellular loop of the human M2 acetylcholine receptor induces pharmacological and morphological changes in cardiomyocytes by active immunization after 6 months in rabbits.

We have previously shown the presence of functional autoantibodies against the second extracellular loop of the human M2 acetylcholine receptor as an autoimmune epitope in 39% of patients with idiopathic dilated cardiomyopathy (DCM). To see if this autoimmune DCM can be experimentally reproduced, a synthetic peptide corresponding to the above autoimmune epitope was used as an autoantigen to immunize rabbits monthly for 6 months. Affinity-purified antibodies were able to display the negative chronotropic effects on neonatal rat cardiomyocytes in culture. The density of the M2 acetylcholine receptors was increased in the immunized rabbits compared to controls but the receptors showed only low-affinity binding sites for the agonist carbachol. Ultrastructural changes such as moderate sarcolemma alterations, mitochondrial swelling, disruption of cristae, and formation of myelin-like structures in the myocardial cells of rabbits immunized for 6 months suggest an immune-induced cardiotoxicity. With only a limited infiltration of inflammatory cells, these results point toward a pathophysiological role of anti-M2 acetylcholine receptor autoantibodies.

Amino Acid Sequence↗

PubMed1996

Beta 1-adrenoceptor autoimmunity in cardiomyopathy.

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.

Autoantibodies↗

PubMed1996

Complications prior to revascularization among patients waiting for coronary artery bypass grafting and percutaneous transluminal coronary angioplasty.

AIM: To describe the occurrence of death, development of acute myocardial infarction and need for hospitalization among patients on the waiting list for coronary artery bypass grafting and percutaneous transluminal coronary angioplasty. PATIENTS AND METHODS: All the patients on the waiting list for possible coronary revascularization in September 1990 in western Sweden. RESULTS: Of 718 patients waiting for either coronary artery bypass grafting or percutaneous transluminal coronary angioplasty, 15 (2.1%) died between the actual week in September 1990 and prior to revascularization and 12 (1.7%) developed a non-fatal acute myocardial infarction during the same period. All 15 patients who died before undergoing revascularization died a cardiac death. Death and/or the development of an acute myocardial infarction was significantly more frequent among the elderly, among patients with a low ejection fraction and among patients with a history of diabetes mellitus. In all, 29% required hospitalization prior to the procedure. The most common reason was symptoms of angina pectoris requiring hospitalization in 23% of the patients. CONCLUSION: Among patients on the waiting list before either coronary artery bypass grafting or percutaneous transluminal coronary angioplasty, 15 (2.1%) died prior to the procedure and 1.7% developed a non-fatal acute myocardial infarction. The risk of either death or developing an acute myocardial infarction was highest among patients in the older age groups, among patients with a history of diabetes mellitus and among patients with a lower ejection fraction.

Adult↗