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Biomedical subjects

A Hjalmarson

Publications and source records attributed to A Hjalmarson.

At least 235 records · Page 13Linked to original sources
PubMed1985

Adenylate cyclase modulation by ammonium ion: GTP-like effect on muscarinic and alpha 2-adrenergic receptors.

The stimulatory influence of ammonium sulphate on adenylate cyclase activity has been investigated. By competition binding experiments on the beta-adrenergic stimulatory receptor in rat myocardial membranes, no influence could be detected of ammonium sulphate neither in receptor coupling to the stimulatory guanine nucleotide binding protein nor in the GTP-induced uncoupling. In order to detect an impaired inhibition instead of an increased stimulation of adenylate cyclase activity by ammonium sulphate the investigation was extended to inhibitory receptors. The same type of effect by ammonium sulphate was detected on both the muscarinic cholinergic receptor in rat myocardial membranes as well as on the alpha 2-adrenergic receptor in human platelets. The influence of ammonium sulphate noted in competition binding studies and off-kinetics experiments was GTP-like, i.e. causing a decrease in agonist-receptor affinity leaving all the inhibitory receptors in the low affinity state. In conclusion, this paper indicates that the observed stimulatory effect of ammonium sulphate is exerted by the ammonium ion on the inhibitory guanine nucleotide binding protein, impairing the negative control of adenylate cyclase activity.

Adenylyl Cyclases↗
PubMed1985

Prediction of the severity of acute myocardial infarction.

In 698 patients with suspected and definite acute myocardial infarction we tried to predict the severity of the infarction from clinical history and simple bedside evaluation soon after arrival in hospital. The severity of the infarction was judged from serum enzyme activity, 2-year survival, incidence and severity of congestive heart failure and incidence of severe ventricular arrhythmias during initial hospitalization. Entry characteristics which were positively associated with the severity of the infarction were intensity of pain, sign of congestive heart failure, high heart rate, ECG signs of acute myocardial infarction and presence of Q waves. Elderly patients and those with a history of hypertension also had a more severe clinical course.

Adult↗
PubMed1985

The diagnostic value of different enzymes and standard ECG in acute myocardial infarction.

Serum (S) enzyme activity of aspartate aminotransferase (ASAT, E.C. 2.6.1.1.), heat stable lactate dehydrogenase (LD, E.C. 1.1.1.27.), creatine kinase (CK, E.C. 2.7.3.2.) and CK-B subunit and the respective standard electrocardiograms (ECG) were compared in 463 patients with suspected acute myocardial infarction (MI) in order to evaluate sensitivity and specificity. Serum ASAT was analysed daily for 3 days, S-heat stable LD every 12 h for 48-108 h, S-CK and S-CK-B every 6 h for 48 h and ECG once daily for 3 days. All four enzymes had a high sensitivity, varying from 99% for LD to 97% for CK-B. The highest specificity was observed for CK-B and CK (98%) as compared with heat stable LD (91%) and ASAT (74%). Standard ECG showed a high specificity (96%) and a low sensitivity (80%).

Adult↗
PubMed1985

Estimated appearance of raised serum enzyme activity in relation to onset of symptoms in acute myocardial infarction.

In 709 patients with definite acute myocardial infarction (MI) the appearance of raised serum enzyme activity was related to onset of symptoms. Heat stable lactate dehydrogenase (LD), creatine kinase (CK) and CK B were analysed. A gradual increase in the incidence of raised enzyme activity in the first blood sample was seen for up to 18 hours after the onset of MI for all 3 enzymes. The incidence of raised enzyme activity in the first blood sample was higher for CK and CK B than for heat stable LD up to 24 hours after onset of MI, but thereafter a similar incidence was found. The median time between onset of symptoms and estimated appearance of raised serum enzyme activity was 6.2 hours for heat stable LD versus 4.3 hours for CK and 4.1 hours for CK B. A wide variation was however found. Infarct localization and chronic treatment with betablockade might affect these results. The clinical course including short- and long-term survival was similar in patients with early and later appearance of enzymes.

Adrenergic beta-Antagonists↗
PubMed1985

Relationship between different enzymatic estimations of the infarct size.

In 592 patients with an acute myocardial infarction different enzymatic estimations of the infarct size were compared. Heat stable lactate dehydrogenase (LD) was analysed every 12 hours for 48-108 hours. Aspartate amino transferase (ASAT) was analysed once daily for 3 days. In a subgroup creatine kinase (CK) and creatine kinase subunit B (CK B) were analysed every 6 hours for 48 hours. A strong positive correlation was observed between the peak activity of the different enzymes (r-values varying between 0.81 and 0.85). The peak activity of heat stable LD, CK and CK B were strongly related to the area under the enzyme curve (r-values varying between 0.94 and 0.98). A substantial decrease in estimated infarct size was observed in a large number of patients when intervals between sampling increased, most often found for CK B. It is concluded that the calculated peak activity of heat stable LD, ASAT, CK and CK B seems to give a similar information about the infarct size in the majority of patients with acute myocardial infarction. Analyses of the area under the enzyme curve do not deviate from calculated peak enzyme activity.

Adult↗
PubMed1984

Early intervention with a beta-blocking drug after acute myocardial infarction.

Several controlled studies with long-term administration of beta blockers in postinfarction patients have demonstrated a reduction in cardiac events and mortality. During acute myocardial infarction (AMI), conventional treatment is directed mainly at such complications as pump failure and arrhythmias. Another approach attempts to influence the natural evolution of impending myocardial necrosis by interrupting the process in its reversible phase. In a double-blind trial with metoprolol in suspected or definite AMI, 1,395 patients were studied, 698 of whom received metoprolol and 697 placebo. The 3-month mortality was 36% lower in the metoprolol group (p = 0.024). A reduction in severe ventricular arrhythmias (ventricular fibrillation and tachycardia) was also seen. Chest pain was reduced and there was less need of analgesic drugs in the metoprolol group. Intervention within 12 hours resulted in a limitation of infarct size, a decreased need for furosemide and a shortened hospital stay. A significant reduction in mortality was maintained after 2 years of follow-up despite the same treatment in both groups between 3 and 24 months. Early institution of metoprolol in AMI has resulted in reduced mortality and morbidity.

Adrenergic beta-Antagonists↗
PubMed1984

Göteborg Metoprolol Trial: enzyme-estimated infarct size.

In 1,375 patients serum activity of heat-stable lactate dehydrogenase (LD; E.C.1.1.1.27.) was analyzed every twelfth hour for 48 to 108 hours. The mean maximum LD activity was 11.1 +/- 0.4 mu kat X 1(-1) in the metoprolol group vs 12.4 +/- 0.5 mu kat X 1(-1) in the placebo group (p = 0.054). In patients in whom treatment was started 12 hours or less after the onset of pain, a 17% reduction in LD activity was observed (p = 0.009) and similar results were found in patients randomized 8 hours or less. Groups in which the effect after metoprolol treatment was more pronounced were those with an initially higher heart rate and also those with anterior myocardial infarction.

Aged↗
PubMed1984

Göteborg Metoprolol Trial: electrocardiographically estimated infarct size.

In 236 patients with anterior myocardial infarction (MI), infarct size was estimated by analyzing the R- and Q-wave amplitude in 24 precordial leads 4 days after randomization. In 254 patients with inferior MI, the final R- and Q-wave amplitude was evaluated in leads II, III and aVF. Electrocardiographic signs of a smaller MI were observed in anterior MI in the metoprolol group compared with the placebo group when treatment was started 12 hours or less after the onset of pain, but no difference was found when treatment was started later. There was no sign of an effect of metoprolol in inferior MI. An immediate reduction in ST-segment elevation was observed after metoprolol treatment regardless of infarct localization or delay between the onset of pain and treatment.

Clinical Trials as Topic↗
PubMed1984

Göteborg Metoprolol Trial: effects on arrhythmias.

During the initial hospitalization, ventricular fibrillation (VF) developed in 6 metoprolol-treated patients (0.9%) vs 17 placebo-treated patients (2.4%) after inclusion in the study (p = 0.035). There were 6 episodes of VF in the metoprolol group compared with 41 episodes in the placebo group (p less than 0.001). During the same period, 14 metoprolol-treated patients had treated ventricular tachycardia vs 26 placebo-treated patients (p = 0.076). Similar favorable results were found when the incidence of severe ventricular arrhythmias during the first rehospitalization within the 3-month double-blind treatment period was analyzed.

Adult↗
PubMed1984

Göteborg Metoprolol Trial: effects on chest pain.

The effect of metoprolol on chest pain was compared with that of placebo in all randomized patients. The pain score before and 15 minutes after the injection of trial medication was registered and a reduction in chest pain was observed in the metoprolol group. Increasing chest pain after blind injection was observed in only 16 and 9 patients from the placebo and metoprolol groups, respectively. Comparison with the placebo as well as detailed analysis of clinical data revealed that in these patients the increasing pain could not be explained by coronary spasm evoked by beta-blockade. Similarly, metoprolol did not exhibit any unfavorable effect on the 14 patients who were withdrawn (together with the 28 patients given placebo) from blind treatment due to angina pectoris. Either metoprolol does not induce coronary vasospasm or spasm does not play a role in these patients with definite and suspected acute myocardial infarction as well as unstable angina pectoris. Metoprolol reduced the need for analgesics during the first 4 days and shortened the duration of pain. The effects were similar in patients with early and late treatment, but may depend on initial heart rate, blood pressure and site of infarction.

Administration, Oral↗
PubMed1984

Göteborg Metoprolol Trial: clinical observations.

Heart rate, systolic blood pressure and rate-pressure product were analyzed during the first 18 hours and 4 days after intravenous metoprolol or placebo. On injection of metoprolol there was an immediate decrease in mean heart rate from 72.9 +/- 0.6 to 62.7 +/- 0.4 beats/min, but no change was found in the placebo group. The difference in heart rate remained during the first 4 days. Systolic blood pressure was reduced from 144.1 +/- 0.9 to 134.6 +/- 0.9 mm Hg after intravenous metoprolol and was lower than that in the placebo group during 4 days of follow-up. Indirect signs of congestive heart failure tended to be less severe in patients given metoprolol within 12 hours of the onset of symptoms than in those given placebo. The duration of hospitalization also tended to be shorter in patients given early metoprolol treatment than in those given placebo early.

Blood Pressure↗
PubMed1984

Göteborg Metoprolol Trial: tolerance.

During a 3-month follow-up, 131 patients (19.1%) withdrew from blind treatment in both metoprolol- and placebo-treated groups. More metoprolol-treated than placebo-treated patients withdrew because of cardiovascular adverse experience mainly during the very early phase. In all, 45 (6.5%) metoprolol-treated vs 14 (2.0%) placebo-treated patients were not given either a full intravenous dose or a full oral dose 15 minutes later. Bradycardia and hypotension were more common in the metoprolol group, whereas severe atrioventricular block did occur in a similar number of patients in both groups and severe congestive heart failure was more common in the placebo group. Results indicate that tolerance is generally good after intravenous and oral treatment with metoprolol in patients with suspected acute myocardial infarction.

Administration, Oral↗
PubMed1984

The detection of interstellar methylcyanoacetylene.

A new interstellar molecule, methylcyanoacetylene (CH3C3N), has been detected in the molecular cloud TMC-1. The J = 8 --> 7, J = 7 --> 6, J = 6 --> 5, and J = 5 --> 4 transitions have been observed. For the first three of these, both the K = 0 and K = 1 components are present, while for J = 5 --> 4, only the K = 0 line has been detected. The observed frequencies were calculated by assuming a value of radial velocity VLSR = 5.8 km s-1 for TMC-1, typical of other molecules in the cloud. All observed frequencies are within 10 kHz of the calculated frequencies, which are based on the 1982 laboratory constants of Moises et al., so the identification is secure. The lines are broadened by hyperfine splitting, and the J = 5 --> 4, K = 0 transition shows incipient resolution into three hyperfine components. The rotational temperature determined for these observations is quite low, with 2.7 K < or = Trot < or = 4 K. the total column density is approximately 5 x 10(12) cm-2.

Acetylene↗
PubMed1984

Relationship between electrocardiographically estimated infarct size and clinical findings in anterior myocardial infarction.

In 292 patients with anterior myocardial infarction (MI) and no previous MI the electrocardiographically estimated infarct size was correlated with clinical findings during hospitalization and 3-month follow-up. Patients with ECG-defined transmural MI had a higher incidence of different types of complications, such as congestive heart failure (CHF), hypotension, pericarditis, and a longer duration of hospitalization than patients with nontransmural MI. In a subgroup including 182 patients of the total series, a precordial map containing 24 electrodes was used. The sum of R waves (sigma R), the sum of Q waves (sigma Q), the number of Q waves, and sigma R - sigma Q were calculated 4 days after arrival in hospital to estimate the size of infarction. There was generally a correlation between these ECG variables and different clinical findings, such as incidence of CHF, hypotension, pericarditis, and the duration of hospitalization. It is concluded that the ECG determined infarct size in anterior MI in a majority of patients correlates with the incidence of different types of complications in acute myocardial infarction. In the individual patient, however, the risk of developing complications cannot be predicted by ECG changes.

Adult↗
PubMed1984

Relationship between electrocardiographically estimated infarct size and clinical findings in inferior myocardial infarction.

In 270 patients with acute inferior wall myocardial infarction (MI) and no previous MI, Q- and R-wave changes in leads II, III, and aVF in a 12-lead standard ECG were related to the clinical course during hospitalization and 3-month follow-up. Patients with ECG-defined transmural MI showed a higher incidence of tachycardia, high degree of AV block, congestive heart failure (CHF), and pericarditis than patients with nontransmural MI. In a subgroup including 226 patients, the series was divided into quartiles according to the sum of Q- and R-wave changes in leads II, III, and aVF 4 days after arrival in hospital. A weak correlation between ECG-determined infarct size and the incidence of complications such as congestive heart failure (CHF), need for furosemide, and pericarditis, as well as the duration of hospitalization was observed. It is concluded that ECG-determined infarct size from leads II, III, and aVF in inferior MI is associated with the clinical course, although it cannot predict the outcome in the individual patient.

Adult↗
PubMed1984

Hemodynamic and clinical findings after combined therapy with metoprolol and nifedipine in acute myocardial infarction.

In a double-blind trial, 30 patients with suspected acute myocardial infarction with onset of symptoms within the previous 24 h were randomized to treatment with 10 mg nifedipine/placebo orally 4 times a day during hospitalization. All patients were given 15 mg metoprolol intravenously 20 min after the initial administration of nifedipine/placebo, and thereafter, 50 mg 4 times a day. The combined therapy resulted only in moderate changes in systolic blood pressure and heart rate compared with metoprolol alone. Three of the 15 patients in the nifedipine group versus 2 of the 15 in the placebo group were withdrawn because of hypotension and/or bradycardia. None was withdrawn because of congestive heart failure or A-V block. It is concluded that the combination of nifedipine and metoprolol seems to be a relatively well-tolerated combination in acute myocardial infarction.

Adult↗