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Biomedical subjects

A Hjalmarson

Publications and source records attributed to A Hjalmarson.

At least 145 records · Page 8Linked to original sources
PubMed1991

One-year mortality rate after discharge from hospital in relation to whether or not a confirmed myocardial infarction was developed.

Consecutive patients admitted to our hospital with suspected acute myocardial infarction during 21 months were prospectively evaluated. One-year mortality after discharge from hospital was related to whether or not an infarction developed (infarct versus non-infarct patients). Of patients discharged alive after developing an infarct, there was a mortality of 17% (n = 777) versus 12% (n = 1830) (P less than 0.001) for all patients not developing infarction. In a high risk group (any of the following: age greater than or equal to 75 years, previous history of myocardial infarction, diabetes mellitus or congestive heart failure) patients developing infarction had a mortality of 24% (n = 457) versus 17% (n = 1221) for those who did not (P less than 0.001). In a low risk group (none of the high risk criteria), the corresponding mortality was 8% (n = 316) for patients suffering infarction and 3% (n = 603) for those not having infarction (P less than 0.001). The difference in mortality between patients with and without infarction was most marked in women (21% vs 11%; P less than 0.01) and in hypertensives (25% vs 12%; P less than 0.001), but less marked in men (16% vs 13%; NS) and in patients without hypertension (13% vs 12%; NS). Among patients not suffering infarction, mortality was particularly high in those with previous congestive heart failure (23%) and diabetes mellitus (21%).

Age Factors↗
PubMed1991

Functional analysis of rabbit anti-peptide antibodies which mimic autoantibodies against the beta 1-adrenergic receptor in patients with idiopathic dilated cardiomyopathy.

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.

Amino Acid Sequence↗
PubMed1991

Activity of receptors coupled to guanine nucleotide binding regulatory protein in doxorubicin induced cardiomyopathy.

STUDY OBJECTIVE: The aim was to study the activity of receptors coupled to guanine nucleotide binding regulatory proteins (G proteins) in doxorubicin induced cardiomyopathy, with special attention to G proteins, beta adrenoceptors, muscarinic receptors, and adenylyl cyclase. DESIGN: Messenger RNA of G proteins, densities and high affinity agonist binding of beta adrenoceptors and muscarinic receptors, activity of adenylyl cyclase, calcium influx, and in vivo lipid peroxidation were determined before, in the early stage, and in the later stage of doxorubicin cardiomyopathic heart failure. SUBJECTS: Sprague-Dawley rats between 150-200 g were used. Doxorubicin was given intravenously at two doses of 4 mg.kg-1 and 6 mg.kg-1 every third week (1st, 4th, 7th week) for nine weeks. Doxorubicin treated rats plus corresponding controls were killed at 3 weeks (n = 7), 6 weeks (n = 7), and 9 weeks (n = 6), respectively. MEASUREMENTS AND MAIN RESULTS: Northern blot and dot blot hybridisations of the total RNA revealed that messenger RNA of both stimulatory and inhibitory G proteins were identical between doxorubicin treated rats and controls. No alterations in the densities of beta adrenoceptors and muscarinic receptors were observed, neither did the high affinity agonist binding of beta adrenoceptors and muscarinic receptors change. Furthermore, modulation of adenylyl cyclase was unimpaired. In contrast, Ca(2+)-ATPase and serum water soluble fluorescent substance, a product of in vivo lipid peroxidation, were shown to increase dramatically in doxorubicin treated rats (4 mg.kg-1 for 6 and 9 weeks, 6 mg.kg-1 for 3, 6 and 9 weeks) as compared with corresponding controls. CONCLUSIONS: The findings suggest that, despite increased calcium influx and lipid peroxidation in doxorubicin induced cardiomyopathy, the activity of receptors coupled to G proteins remained normal.

Adenylyl Cyclases↗
PubMed1991

Serum lipids and lipoproteins in relation to restenosis after coronary angioplasty.

Restenosis after coronary angioplasty (PTCA) is a major problem, limiting the long-term efficacy of the procedure. Lipoprotein levels are associated with the development of atherosclerosis and may also be associated with restenosis. In this study the serum levels of cholesterol (CH), triglycerides (TG), high density lipoprotein (HDL) and low density lipoprotein (LDL) were analysed in 157 patients undergoing 161 PTCA procedures. Follow-up coronary angiograms were performed after 6.0 +/- 4.3 months. The restenosis rate was 33%. Treatment with aspirin and a residual stenosis of 25-49% immediately after successful PTCA were the only variables associated with restenosis (P less than 0.05), otherwise the clinical and angiographic characteristics were similar with and without restenosis. There was no relationship between restenosis and the levels of CH, TG, HDL or LDL (P greater than 0.05). In univariate and multivariate analysis of males (n = 121) and females (n = 40) separately, restenosis was associated with low HDL in men and high HDL in women (P less than 0.05), but not with CH, TG or LDL (P greater than 0.05). We conclude that the serum levels of CH, TG and LDL do not seem to be related to restenosis after PTCA. It is suggested that low HDL in males and high HDL in females is related to restenosis.

Adult↗
PubMed1991

New therapeutic strategies in chronic heart failure: challenge of long-term beta-blockade.

It is claimed that long-term treatment with beta-blockers improves cardiac function and exercise capacity in patients with various forms of congestive heart failure. This was first reported by Waagstein and coworkers in patients with idiopathic dilated cardiomyopathy in 1975 and was later confirmed in 8 further studies in this type of patient. A total of 211 patients with idiopathic dilated cardiomyopathy were treated for 12-19 months. About two thirds of the patients have improved to some extent. Seven other studies reported favourable long-term effects of beta-blockers in 120 patients with other forms of dilated cardiomyopathy, e.g. caused by coronary artery disease, adriamycin, diabetes, or valvular heart disease. Pooled data from 10 studies on 153 patients with various forms of cardiomyopathy, showed that ejection fraction was improved by 40% from 27 to 38%. Only two studies were inconclusive, both with only one month's treatment. In all studies with favourable effects of long-term beta-blockade, treatment was given for more than 2 months and in most cases for about 6 months. A number of beta-blockers have been used in the studies, including acebutulol, alprenolol, bucindolol, labetalol, metoprolol, practolol and propranolol. In most cases, a rather low dose was given initially and there was a stepwise increase in the dosages. After 6-8 weeks most patients were given beta-blockers in daily doses comparable to those given in patients with angina pectoris and hypertension. There is at present no indication that one beta-blocker is superior to others. It therefore seems reasonable to believe that the effects are due to beta 1-blockade.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1991

Effect of acupuncture in patients with angina pectoris.

Twenty-one patients with stable effort angina pectoris were randomized in a crossover study to 4 weeks traditional Chinese acupuncture or placebo tablet treatment. The patients had at least five anginal attacks per week in spite of intensive treatment. Acupuncture was given three times per week at main points Neiguan (Pericardium 6), Tongli (Heart 5), Xinshu (Urinary Bladder 15), Pishu (Urinary Bladder 20) and Zusanli (Stomach 36). Previous antianginal treatment remained unchanged during the whole study. During the acupuncture period, the number of anginal attacks per week was reduced from 10.6 to 6.1 compared with placebo (P less than 0.01). Accordingly, the performance before onset of pain during exercise test increased from 82 W to 94 W (P less than 0.05). However, maximal performance did not increase after acupuncture. Intensity of pain at maximal workload decreased from 1.4 to 0.8 (scale 0-4, P less than 0.01). Further, ST-segment depressions at maximal comparable load decreased from 1.03 to 0.71 mm after acupuncture (P less than 0.01). A life quality questionnaire confirmed improved feeling of well-being. Thus, acupuncture showed an additional beneficial effect in patients with severe, intensively treated angina pectoris.

Acupuncture Analgesia↗
PubMed1991

Patients admitted to the emergency room with symptoms indicative of acute myocardial infarction.

All 7157 patients (55% men) admitted to the emergency room with chest pain or other symptoms indicative of acute myocardial infarction during a period of 21 months were registered consecutively. Chest pain was reported by 93% of the patients. On the basis of history, clinical examination, and electrocardiogram in the emergency room, all patients were prospectively classified in one of four categories: (i) obvious infarction (4% of all patients); (ii) strongly suspected infarction (20%); (iii) vague suspicion of infarction (35%); and (iv) no suspected infarction (41%). In patients with no suspected infarction (n = 2910), musculoskeletal (26%), obscure (21%) and psychogenic origins (16%) of the symptoms occurred most frequently. We conclude that few of the patients had an obvious infarction on admission, and that a musculoskeletal origin of the symptoms occurred most frequently in patients with no suspected infarction.

Adolescent↗
PubMed1991

Prognosis in suspected acute myocardial infarction in relation to delay time between onset of symptoms and arrival in hospital.

During a 21-month period, the prognosis in all patients admitted to a hospital ward from the emergency room with suspected acute myocardial infarction (AMI) was prospectively recorded and related to the time between onset of symptoms and arrival in hospital. They were classified as early arrivers (less than or equal to 2 h), intermediate arrivers (2-8 h) and late arrivers (greater than 8 h). Among patients developing a confirmed AMI (n = 909) the 1-year mortality rate was 26.0% in early arrivers, 28.1% in intermediate arrivers and 32.6% in late arrivers. The corresponding figures for patients in whom AMI was ruled out (n = 2,035) were 15.2, 15.1 and 17.6%, respectively. In AMI patients, various morbidity aspects during hospitalization and 1 year of follow-up appeared mainly independent of delay time, whereas among those in whom AMI was ruled out congestive heart failure during hospitalization was most common in early arrivers. We conclude that patients with suspected AMI who do not arrive early in hospital have a high 1-year mortality rate regardless of whether they develop AMI or not. Whether their prognosis can be improved by shortening of delay time remains to be clarified.

Aged↗
PubMed1991

Prognosis in patients with ST-T changes but no rise in serum enzyme activity as compared with non-Q-wave infarction.

We evaluated the prognosis for 419 patients admitted to hospital due to suspected acute myocardial infarction (AMI) who developed ST-T changes, but no rise in serum enzyme activity, and compared it to that of 508 patients developing non-Q-wave AMIs. We conclude that these patients have a high 1-year mortality (13%), although significantly lower than in patients with non-Q-wave AMIs (31%). The mortality is higher in patients with only ST depression (n = 86; 22%) than in patients with only T-wave inversion (n = 264; 8%).

Aged↗
PubMed1991

Long-term follow-up of health-related quality of life in patients with suspected acute myocardial infarction when the diagnosis was not confirmed.

This study describes the outcome in terms of health-related quality of life (QL) five years after onset of symptoms in 397 patients with an initial suspicion of acute myocardial infarction (MI) but in whom the diagnosis was not confirmed. The patients were approached by means of a postal inquiry that comprised two questionnaires. The most pronounced impairment in health-related QL was expressed as decreased energy, whereas social life was the least affected area. The overall QL was very similar to that in patients who had a confirmed MI. Subsets of patients with impaired QL were those given the diagnosis of angina pectoris or possible infarction.

Acute Disease↗
PubMed1991

Myocardial infarction. Effects of beta-blockade.

By the mid 1960s a beneficial effect of post-myocardial infarction treatment with beta-blockade had been proposed. However, it was not until 1981 that large clinical trials clearly demonstrated a beneficial effect both in terms of reduction in mortality and morbidity. Today treatment with beta-blockers both in the acute phase of acute myocardial infarction as well as in the stable post-myocardial infarction patient is well established. In this review article, different aspects of early and late treatment with beta-adrenoceptor blockers are discussed. The cardioprotective effects of beta-blockers on mortality and morbidity should not be considered class effects valid for all beta-blockers. Pooled data have clearly demonstrated that beta-blockers with intrinsic sympathomimetic activity have less marked effects. Impressive effects on mortality and morbidity have been obtained with propranolol, timolol, and metoprolol, which are noncardioselective as well as more beta 1-selective (metoprolol), but they are all lacking intrinsic sympathomimetic activity and, furthermore, have a relatively high degree of lipophilicity. It is clear that acute beta-adrenoceptor blockade in suspected acute myocardial infarction reduces mortality and morbidity as well as complications such as chest pain and ventricular arrhythmias during the acute phase. In post-myocardial infarction treatment, it is clear that both mortality and morbidity are reduced. Reports from extended follow-ups after termination of initial double-blind beta-blocker studies in postinfarction patients indicate that withdrawal of the active treatment may increase mortality after cessation of treatment. This is observed despite measures having been taken to avoid so-called acute withdrawal phenomena.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1990

Subgroups of patients with atypical circadian patterns of symptom onset in acute myocardial infarction.

Circadian variation of onset of acute myocardial infarction has been noted in many studies and may carry important implications. However, only a few previous studies have attempted subgroup analysis. In 4,796 patients with documented acute myocardial infarction, the time of symptom onset was recorded. As in other studies, a peak occurred in the morning hours from 6 A.M. to noon with 28% of the population (1.16 times the average percent for the other time periods) experiencing symptom onset in that period (p less than 0.001). There was a second lower peak (25%) in the evening hours between 6:01 P.M. and midnight, also observed in some previous studies. Whether the presence of subgroups with specific clinical characteristics would exhibit different patterns and thereby contribute to these peaks in the overall population was then determined. In patients with a history of congestive heart failure (n = 606) or with non-Q-wave infarction (n = 832), a pronounced peak (29%) occurred only in the evening hours. In patients greater than 70 years of age (n = 1,422), smokers (n = 2,057), diabetics (n = 767), women (n = 1,213) and patients taking beta blocking drugs (n = 847), 2 nearly equal peaks were observed. Finally, in patients with previous myocardial infarction (n = 1,104), no peaks were observed. In a subgroup of patients (n = 1,084) free from the most important modifying factors, there was a single very pronounced late morning peak (32%), 1.39 times the average percent for the other time periods (p less than 0.001), without evidence of a second evening peak.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1990

Role of beta-adrenergic blockers after percutaneous transluminal coronary angioplasty.

Restenosis after percutaneous transluminal coronary angioplasty (PTCA) cannot currently be prevented. Different medical regimens have been largely unsuccessful. Experimental studies suggest roles for beta-adrenergic blockers and calcium antagonists. Controlled clinical studies have failed to show any decrease in restenosis rate for calcium antagonists. Corresponding studies for beta blockers are lacking. This study evaluates 541 consecutive PTCA procedures, 455 (86%) in patients treated with beta blockers after PTCA (76% metoprolol, 14% atenolol, 4% sotalol, 6% others) and 86 (14%) in patients without beta blockers. Angiographic success was achieved in 483 of 620 lesions (78%), and was not significantly different with or without beta blockers (79 vs 73%, p greater than 0.05). The procedure success rate and the complication rates (myocardial infarction, emergency coronary artery bypass grafting, death) did not differ with or without beta blockers (p greater than 0.05). Follow-up angiograms for 426 of the 483 successfully dilated lesions (88%) revealed that a total of 155 stenoses had recurred (36%). The restenosis rate was not significantly different with (368) or without (58) beta blockers (36 vs 38%, p greater than 0.05). For beta blockers with calcium antagonists (84% nifedipine, 13% diltiazem, 2% verapamil, 1% others), the restenosis rate was 97 of 250 (39%) vs 36 of 118 (31%) (p greater than 0.05). This retrospective study indicates that treatment with beta-adrenergic blockers after PTCA, alone or in combination with calcium antagonists, does not influence either the success rate or the restenosis rate and can be continued if indicated from an antiischemic viewpoint.

Adrenergic beta-Antagonists↗
PubMed1990

Influence of heart rate on mortality after acute myocardial infarction.

Elevated heart rate (HR) during hospitalization and after discharge has been predictive of death in patients with acute myocardial infarction (AMI), but whether this association is primarily due to associated cardiac failure is unknown. The major purpose of this study was to characterize in 1,807 patients with AMI admitted into a multicenter study the relation of HR to in-hospital, after discharge and total mortality from day 2 to 1 year in patients with and without heart failure. HR was examined on admission at maximum level in the coronary care unit, and at hospital discharge. Both in-hospital and postdischarge mortality increased with increasing admission HR, and total mortality (day 2 to 1 year) was 15% for patients with an admission HR between 50 and 60 beats/min, 41% for HR greater than 90 beats/min and 48% for HR greater than or equal to 110 beats/min. Mortality from hospital discharge to 1 year was similarly related to maximal HR in the coronary care unit and to HR at discharge. In patients with severe heart failure (grade 3 or 4 pulmonary congestion on chest x-ray, or shock), cumulative mortality was high regardless of the level of admission HR (range 61 to 68%). However, in patients with pulmonary venous congestion of grade 2, cumulative mortality for patients with admission HR greater than or equal to 90 beats/min was over twice as high as that in patients with admission HR less than 90 beats/min (39 vs 18%, respectively); the same trend was evident in patients with absent to mild heart failure (mortality 18 vs 10%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1990

Prognosis during one year for patients with myocardial infarction in relation to the development of Q waves: experiences from the Miami trial.

From a randomized multicenter trial with metoprolol in suspected acute myocardial infarction (n = 5778) we report on the outcome during a one-year follow-up in patients with confirmed infarction (n = 4106) in relation to whether or not they developed Q waves. Patients with Q waves had another pattern of risk factors, including lower age and a lower occurrence of previous infarction, angina pectoris, and congestive heart failure. After one year follow-up, 14.3% of the patients with Q waves had died versus 9.0% of those without Q waves (p less than 0.001). Reinfarction during the first year occurred in 8.2% of patients with Q waves and 12.5% of patients without Q waves (p less than 0.001). After one year, other morbidity aspects appeared relatively independent of the original presence of Q waves. In conclusion, during the first year after development of acute myocardial infarction the appearance of Q waves during the first three days is associated with a higher mortality and a lower reinfarction rate, whereas other morbidity aspects appear to be relatively independent of its presence.

Electrocardiography↗
PubMed1990

An update to silent myocardial ischemia: pathophysiological, diagnostic, and therapeutic approaches.

Silent myocardial ischemia (SMI) is a common ischemia process which can be defined as objective evidence of myocardial ischemia without chest pain or other equivalent indications. SMI can occur in totally asymptomatic patients, as well as in patients who have documented coronary artery disease (CAD) and who, on exercise and/or during Holter monitoring, may show ischemic changes. The precise mechanism for pathogenesis and pathophysiology of SMI remains to be clarified. A great deal has been learned about the role of beta-adrenergic receptors, adenylyl cyclase, and guanine nucleotide binding proteins (G proteins) in the myocardial ischemic process of SMI. Moreover, standard exercise test and long-term ECG recordings have proved to be of great value, especially when performed jointly, however, in this field there is still room for expanded knowledge. Pharmacological interventions to date have demonstrated the beneficial effects of beta-adrenergic receptor antagonists and/or calcium antagonists as contributing substantially to reducing both frequency and duration of SMI episodes. However, therapeutic options to improve the prognosis of SMI appear to be limited.

Adenylyl Cyclases↗
PubMed1990

Heart rate and beta-adrenergic mechanisms in acute myocardial infarction.

Increased heart rate is an independent predictor of mortality in patients with acute myocardial infarction. Elevated heart rate is due to increased sympathetic activity and/or decreased parasympathetic activity. In placebo-controlled trials beta-blockers are known to reduce mortality as well as morbidity and these effects are most evident among patients with elevated heart rate. Studies on circadian variation have demonstrated that there is an increased sympathetic activity in the morning as well as a more frequent onset of ischemic attacked including acute myocardial infarction and sudden death. There seems to be a close relationship between increased sympathetic activity and the onset of ischemic events which can be prevented by prophylactic institution of a beta-blocker.

Adrenergic beta-Antagonists↗