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Biomedical subjects

A Hjalmarson

Publications and source records attributed to A Hjalmarson.

At least 217 records · Page 12Linked to original sources
PubMed1986

Experiences from the use of twenty-four precordial chest leads in suspected acute myocardial infarction.

In 671 patients with suspected acute myocardial infarction (MI) and no previous MI, precordial mapping with a grid containing 24 chest leads was performed within a few hours (mean = 4.8 hours; range 0-42 hours) after arrival in hospital and four days later. In 76% of the patients the criteria for definite MI, based on serum enzymes and a 12 lead standard electrocardiogram, were fulfilled. Among patients classified as having no definite MI, 2% had abnormal Q-waves on mapping on the fourth day; among patients classified as having a subendocardial MI (no abnormal Q-waves in the 12 standard leads), 7% had abnormal Q-waves on mapping on the fourth day. In patients who subsequently developed anterior MI, changes in the sum of Q-waves and the sum of R-waves were observed for more than 12 hours after onset of pain. ST-elevations defined from a normal population were seen in the initial recording in 60% of patients with anterior MI. Among those in whom the first recording was performed less than or equal to 4 hours after onset of pain, ST elevation was initially seen in 72%. A positive correlation was observed between the initial ST elevation and severity of chest pain, incidence of congestive heart failure and two-year mortality rate. We thus conclude that some further information regarding presence of Q-waves can be obtained in about 5% of patients with suspected acute MI from an increased number of precordial leads.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical Trials as Topic↗
PubMed1986

Muscarinic receptors in mammalian myocardium: effects of atrial and ventricular receptors on phosphatidylinositol metabolism and adenylate cyclase.

Cat myocardium was used to investigate muscarinic receptor function in atria and ventricles. Carbachol and oxotremorine were used to determine agonist binding to the muscarinic receptors. It was found that carbachol was bound with almost the same characteristics in atria (KdH 1 microM; KdL 150 microM) as in ventricles (KdH 3 microM; KdL 150 microM). However, in the presence of guanylylimidodiphosphate Gpp(NH)p a difference was apparent so that the ventricular curve was shifted to a majority of low affinity sites whereas in atria two affinity sites remained even if the guanine nucleotide concentration was increased to 10 mM. Oxotremorine was bound with almost equal affinity in both atria and ventricles. The addition of Gpp(NH)p left all the receptors in the low affinity state irrespective of receptor localisation. The two agonists were also used to determine inhibition of adenylate cyclase activity. It was shown that the magnitude of adenylate cyclase inhibition was more pronounced in ventricles than in atria whether it was induced by oxotremorine or carbachol. When the effects of muscarinic agonists were determined on phosphatidylinositol metabolism it was shown that carbachol mediated a greater effect in atria than in ventricles. Almost no effect was seen with oxotremorine on phosphatidylinositol breakdown. Pirenzipine binding showed the presence of M1 receptors both in atria and ventricles. On the basis of diversity of muscarinic agonists on function and receptor occupancy it is suggested that heterogeneity exists for muscarinic receptors in both atria and ventricles.

Adenosine Triphosphate↗
PubMed1986

The role of beta blockade in the limitation of infarct development.

This review article deals with the role of beta blockade in the limitation of infarct development. A large number of studies have reported that early administration of beta blockers limits infarct size in animals. In a few, however, these results were not reconfirmed. In man, several large randomized trials have shown that early administration of beta blockade limits infarct development judged from serum enzyme activity and ECG recordings. Delay time between the onset of symptoms and start of treatment is of major importance. It appears as though patients with a higher initial rate pressure product respond most favourably. Although these results are encouraging, the role of infarct limitation in relation to effects on early mortality, chest pain and arrhythmias have not been clearly defined.

Adrenergic beta-Antagonists↗
PubMed1986

Central haemodynamic effects of metoprolol early in acute myocardial infarction. A placebo controlled randomized study of patients with low heart rate.

The central haemodynamic effects of metoprolol in patients with acute myocardial infarction and with heart rate less than or equal to 65 beats min-1 have been investigated in a randomized double-blind trial. The aim was to study the tolerance in this selected patient group and to assess possible differences in haemodynamic response amongst patients with initially higher heart rates. Exclusion criteria were: treatment with beta blockers; heart rate greater than 65 beats min-1; systolic blood pressure less than 110 mmHg; and physical signs of serious heart failure. Following pulmonary artery catheterization, 22 patients were randomized to metoprolol 15 mg i.v. + 50 mg q.i.d. orally (N = 12) or placebo (N = 10). Central pressures and cardiac output were recorded before and during the 24 hours after drug administration. There was a significant fall in heart rate, cardiac index, rate pressure product and stroke work index of 10-20% in the metoprolol, compared with the placebo group. The differences were most pronounced immediately after the metoprolol injection. The pulmonary artery capillary wedge pressure was not significantly changed. The overall haemodynamic response to metoprolol was similar to that reported in patients with acute myocardial infarction and heart rate above 65 beats min-1. Tolerance was good.

Aged↗
PubMed1986

Central haemodynamics in acute myocardial infarction in relation to mortality and peak enzyme activity.

The relation of central haemodynamic changes to subsequent mortality and peak enzyme activity was investigated in 190 patients with acute myocardial infarction. The mean delay time from onset of symptoms to the haemodynamic study was 7.2 hours. Major exclusion criteria were heart rate less than 65 beats min-1, systolic blood pressure less than 105 mmHg and lung rales to a distance of greater than 10 cm above the lung bases. Nine patients (4.7%) died within 15 days and 16 patients (8.4%) within 90 days after the infarction. Compared to survivors, non-survivors were characterized by baseline depression of cardiac index, stroke volume index and left ventricular stroke work index, while pulmonary capillary wedge pressure and peripheral resistance were increased. However, a wide overlap between survivors and non-survivors makes the predictive value low in the individual patient. Peak serum aspartate aminotransferase (S-ASAT) activity was weakly related to baseline pulmonary capillary wedge pressure (r = 0.28; P less than 0.001) and stroke volume index (r = -0.22; P less than 0.01). The correlation to pulmonary capillary wedge pressure was only found in anterior (r = 0.34) infarcts. Peak serum lactate dehydrogenase (LD1) was not correlated with baseline haemodynamics.

Aged↗
PubMed1986

Effect of long term treatment with metoprolol and sotalol on ventricular repolarisation measured by use of transoesophageal atrial pacing.

The effects of long term (4 weeks) treatment with oral metoprolol (100 mg twice daily) and sotalol (160 mg twice daily) on ventricular repolarisation time were compared in a double blind crossover study in 20 patients post-infarction. For QT interval studies transoesophageal atrial pacing was performed at a cycle length of 800 ms. Sotalol prolonged the QT interval by 5-7% compared with metoprolol. The prolongation reflects a change in the repolarisation time because there was no change in the QS interval. Measurements of heart rate at rest and during bicycle exercise indicated that metoprolol and sotalol in the doses selected were equipotent as beta blockers. Transoesophageal atrial pacing is a simple non-invasive method with few and mild side effects that is well suited to drug studies.

Aged↗
PubMed1986

Variability, prediction and prognostic significance of chest pain in acute myocardial infarction.

The variability of chest pain is described in 389 patients with acute myocardial infarction. Whereas 17% were free from severe pain after arrival in hospital, 11% required more than 10 analgesic injections. In 27% of the series analgesics were given more than 24 h after arrival in hospital. Predictors for the severity of chest pain were the rate-pressure product and degree of chest pain soon after arrival in hospital as well as electrocardiographic signs of myocardial infarction at entry. Patients with more severe chest pain had a higher 2-year mortality rate and a higher incidence of ventricular fibrillation and congestive heart failure during hospitalization.

Analgesia↗
PubMed1986

Relationship between serum enzyme activity in acute myocardial infarction and morbidity during a 2-year follow-up.

In 585 patients with a first myocardial infarction the enzymatically estimated infarct size was related to the clinical course during a 2-year follow-up. Infarct size was estimated from maximum heat-stable lactate dehydrogenase activity. A higher maximum serum activity was associated with a higher mortality rate, more treatment with diuretics, digitalis and antiarrhythmics and a lower frequency of return to work. Patients with smaller infarcts according to maximum serum activity, however, had a higher incidence of angina pectoris and a higher reinfarction rate. We conclude that although there is a strong association between serum enzyme activity and mortality during a 2-year follow-up, the relation with morbidity appears to be more complex.

Adult↗
PubMed1986

Felodipine-induced dilatation of epicardial coronary arteries. A randomized, double-blind study.

Dilatation of large coronary arteries is of potential value in the treatment of angina pectoris. In this double-blind study, the acute effect of felodipine or placebo on coronary artery dilatation was studied in patients with severe angina pectoris with the aid of coronary arteriography. There were two parallel groups, one with 9 patients who received felodipine, the other with 12 patients who received placebo. Measurements of vessel diameters were performed at a proximal position of the affected artery, at the site of the stenosis, and distal to the lesion. The mean plasma felodipine concentration was 17+/-6 nmol/l. The systolic blood pressure was reduced from 156+/-15 to 145+/-13 mm Hg after felodipine (p less than 0.05), but was unaffected by placebo. The heart rate and arterial catecholamine levels were basically unchanged in both groups of patients. The proximal arterial segment was dilated 7% after felodipine (p = 0.05), the stenosis area 9% (N.S.) and the distal part of the vessel 7% (p less than 0.05). There were no changes in coronary diameters in the placebo group. In conclusion, felodipine dilates large coronary arteries, and this mode of action may be valuable in the treatment of patients with coronary artery disease, especially in cases where coronary spasm is a prominent feature.

Adult↗
PubMed1985

Hemodynamic effects of metoprolol in acute myocardial infarction. A randomized, placebo-controlled multicenter study.

The central hemodynamic effects of metoprolol in acute myocardial infarction have been studied in a multicenter, double-blind, randomized trial. One hundred and ninety patients with acute myocardial infarction not previously on beta blockers with heart rate greater than 65 beats/min and blood pressure greater than 105 mm Hg and without clinical signs of serious heart failure were included. After insertion of a pulmonary artery catheter, patients were randomized to metoprolol, 15 mg intravenously, and 50 mg 4 times a day orally (n = 95) or placebo (n = 95) with a mean delay of 7.2 hours. Hemodynamic measurements were made at baseline and repeatedly during 24 hours. Heart rate, systolic blood pressure and cardiac index were all immediately reduced by 10 to 20% in the metoprolol group and the difference compared with placebo was maintained throughout the 24 hours (p less than 0.001). Pulmonary capillary wedge pressure (PCWP) in the metoprolol group increased from 13.7 +/- 6.7 to a peak of 15.5 +/- 5.5 mm Hg 30 minutes after injection. The difference compared with placebo was maintained for 8 hours (p less than 0.01). This increase was seen only in the patient group with initial PCWP below the median of 13 mm Hg. In patients with initial PCWP above the median a continuous decrease was observed in both the placebo and metoprolol groups. Thus high initial PCWP was not associated with intolerance to metoprolol. Based on hemodynamic measurements tolerance to metoprolol was good.

Aged↗
PubMed1985

Astronomical identification of the C3H radical.

The C3H radical, a linear carbon chain with a 2 pi electronic ground state, has been identified in the millimeter-wave spectra of two astronomical sources, IRC +10216 and TMC-1, and conclusively confirmed (accompanying Letter) in a laboratory glow discharge. In IRC +10216 four rotational transitions have been observed, three in the lower fine-structure ladder (2 pi 1/2) and one in the upper (2 pi 3/2), each a resolved or partially resolved lambda-doublet. In TMC-1, both lambda components of the lowest lying 3/2 --> 1/2 transition of the 2 pi 1/2 ladder have been observed, each with well-resolved hfs. In IRC +10216 the excitation of C3H is similar to that of SiCC: the rotational temperature Trot within the 2 pi 1/2 ladder is low (8.5 K), owing to rapid radiative decay, while Trot across the ladders is high (approximately 52 K) because interconnecting far-IR radiative transitions are only weakly permitted. The column density of C3H in IRC +10216 averaged over the estimated source diameter of 84" is 2.8 x 10(13) cm-2, an order of magnitude less than that of C2H and C4H. A determination of the spectroscopic constraints of C3H that permitted the entire radio spectrum of this molecule to be calculated to high accuracy has been derived from analysis of the combined astronomical and laboratory data presented in the accompanying Letter.

Astronomical Phenomena↗
PubMed1985

The relationship between the electrocardiographically estimated infarct size and 1- and 2-year survival in acute myocardial infarction.

In 587 patients with acute myocardial infarction (AMI) and no previous MI, electrocardiographically estimated infarct size was related to 1- and 2-year mortality. The overall mortality was higher in patients with transmural MI (Q- or R-wave changes in standard ECG) than in patients with subendocardial infarction (ST-T-wave changes in standard ECG) after 1 year (18.8% compared to 6.5% p less than 0.001) and after 2 years (22.2% compared to 13.8%, p = 0.049). When patients who were alive during primary hospitalization were analyzed separately, slightly higher mortality was found in patients with transmural MI than in subendocardial MI after 1 year (9.6% compared to 4.2%, p = 0.076) while no difference was found after 2 years (13.4% as compared to 11.7%, p greater than 0.2). In a subgroup of patients with anterior MI, precordial mapping with 24 chest leads was analyzed 4 days after arrival in hospital (n = 197). Patients were divided into quartiles according to the sum of R waves, the sum of Q waves, and the number of Q waves. There was a similar overall mortality in each quartile after 1 year and after 2 years regardless of ECG parameters studied. Neither did we find any correlation between the sum of R waves in leads II, III, and aVF on the fourth day in patients with inferior MI and overall 1- or 2-year mortality rate, although there was a trend towards higher mortality with more ECG changes.

Adult↗
PubMed1985

Relationship between electrocardiographically estimated infarct size and morbidity during a two-year follow-up.

In 587 patients with a first myocardial infarction (MI) the electrocardiographically (ECG) estimated infarct size was related to morbidity during a two-year follow-up. Patients with transmural MI (Q- or R-wave changes in standard ECG) were more often treated for heart failure and returned to work less frequently than patients with subendocardial MI (ST-T-wave changes only). There were trends indicating a higher reinfarction rate in patients with subendocardial MI, whereas angina pectoris was observed as frequently in both groups. In a subset of patients with anterior MI, infarct size was estimated from the total Q- and R-wave amplitude in 24 precordial leads 4 days after arrival in hospital. A positive relationship was observed between ECG-estimated infarct size and treatment for heart failure, and patients with smaller infarctions according to ECG criteria returned to work less frequently. A higher reinfarction rate was observed in patients with smaller infarctions. In patients with inferior MI there were mostly weaker correlations between ECG-estimated infarct size (Q- and R-wave changes in leads II, III, and a VF) and morbidity during the two-year follow-up.

Angina Pectoris↗
PubMed1985

Acute haemodynamic effects of felodipine in congestive heart failure.

The haemodynamic effects of felodipine 0.1 mg/kg p.o., a new arteriolar dilator, were studied in 7 patients with severe congestive heart failure of NYHA Class IV (Group A) and in 3 patients in Class II-III (Group B). In Group A, measurements were made before and 1 and 4 h after felodipine administration. There was a substantial fall in systemic arterial pressure, which was not associated with a compensatory tachycardia. In fact, there was a fall in heart rate from 92 to 82 beats/min 1 h after drug administration. The pulmonary capillary wedge pressure was reduced from 22 to 14 mm Hg and the cardiac index and stroke volume index rose significantly. Consequently, there was a marked reduction in systemic vascular resistance. In Group B measurements were performed at rest and during exercise before and 1 h after felodipine. The pulmonary wedge capillary pressure during exercise was lower than in the control situation. Coronary sinus flow was increased and there was a pronounced fall in coronary vascular resistance. The results would suggest that felodipine, by virtue of its ventricular unloading potency, might be a valuable drug in the treatment of congestive heart failure.

Adult↗
PubMed1985

Tolerability to treatment with metoprolol in acute myocardial infarction in relation to age.

A double-blind trial with the beta 1-selective blocker metoprolol in suspected acute myocardial infarction and during 3 months' follow-up included 1395 patients, aged 40-74 years, 698 on metoprolol and 697 on placebo. In order to further evaluate the tolerability to beta-blockade in the elderly, the total series was divided into 2 groups according to median age (61 years) and into quartiles, the lowest quartile (40-57 years) being compared with the highest (67-74 years). The decrease in heart rate and systolic blood pressure after intravenous metoprolol in the acute phase was similar in the elderly and the younger patients. Hypotension was observed more often in the metoprolol-treated than in the placebo-treated younger patients, while no difference was observed in the elderly. Bradycardia was observed more often in the metoprolol group in both age groups, while there was no difference regarding the incidence of congestive heart failure in either the younger or in the elderly patients. The effect on mortality, serious ventricular arrhythmias and chest pain seemed to be similar in different age groups. From the present series we conclude that hemodynamic reactions and tolerability to beta-blockade can be expected to be similar in elderly and younger patients.

Adult↗
PubMed1985

Abnormality of adenylate cyclase regulation in human platelet membranes in renal insufficiency.

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).

Adenylyl Cyclases↗