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Biomedical subjects

K A Johannessen

Publications and source records attributed to K A Johannessen.

25 records · Page 2Linked to original sources
PubMed1985

Usefulness of high-dose anticoagulants in preventing left ventricular thrombus in acute myocardial infarction.

Fifty-three patients with a suspected first anterior wall acute myocardial infarction (AMI) were randomized to intervention with intravenous heparin followed by oral warfarin (26 patients) or matching placebo (27 patients). The regimen was started within 12 hours after the onset of AMI. Anticoagulation was maintained at a therapeutic level (for heparin, activated partial thromboplastin time 70 to 140 seconds; for warfarin, thrombotest 5 to 10%) for 10 days, and no bleeding episodes occurred. The baseline characteristics of the 2 study groups were well matched. In 7 patients in the placebo group and in none in the anticoagulant group, left ventricular thrombus developed during the study, as detected by serial 2-dimensional echocardiography. Early intervention with high-dose anticoagulant drugs may prevent the development of left ventricular thrombus in anterior wall AMI.

Aged↗
PubMed1985

Circulating catecholamine and potassium concentrations early in acute myocardial infarction: effect of intervention with timolol.

In a prospective study, 20 patients with a first acute myocardial infarction and no current treatment with diuretics or cardioactive drugs were randomized to treatment with intravenous timolol (10 patients) or placebo (10 patients). Plasma adrenaline, noradrenaline, and serum potassium were estimated at baseline (mean +/- SD 3.6 +/- 0.8 hours after the onset of the infarction) and 4 hours after the start of treatment. The patient selection criteria embraced a low-risk study population. Before treatment, the serum potassium concentrations correlated inversely with plasma adrenaline but not with plasma noradrenaline concentrations. A rise of serum potassium (mean +/- SD mmol/L) from 4.1 +/- 0.3 to 4.4 +/- 0.4 (p less than 0.05) in the placebo group and from 4.0 +/- 0.4 to 4.5 +/- 0.5 (p less than 0.05) in the timolol group was in multivariate analysis associated with infarct size, estimated as cumulative creatine kinase release, in the placebo group, and with the mean individual plasma adrenaline concentrations in the timolol group. By reversing the effect of adrenaline from a decrease to an increase in the serum potassium concentrations, timolol changes the relationships between circulating adrenaline, potassium, and infarct size.

Aged↗
PubMed1985

Effect of timolol on changes in serum potassium concentration during acute myocardial infarction.

One hundred and six patients with acute myocardial infarction admitted to hospital within four hours after the onset of symptoms were randomised to treatment with intravenous timolol (54 patients) or placebo (52 patients). Serum potassium concentrations were estimated at frequent intervals during the first 24 hours of admission. Patients in both treatment groups, who did not receive subsequent diuretic treatment, had a transient rise in serum potassium concentration, which was maximal after four hours. This rise was abolished by diuretic treatment in the placebo group but not in the timolol group, in which there was a pronounced and prolonged rise in serum potassium concentration. The change in serum potassium concentration in the first four hours after admission correlated with cumulative creatine kinase release in the placebo group, but not in the timolol group. Hypokalaemia (serum potassium concentration less than or equal to 3.5 mmol/l) occurred in 15 (28.8%) patients in the placebo group and in seven (13%) in the timolol group and was independent of infarct size. The frequency of hyperkalaemia was not increased in the timolol group. By increasing the serum potassium concentration and preventing hypokalaemia, the use of intravenous timolol early in acute myocardial infarction may have important clinical effects in addition to reducing infarct size.

Clinical Trials as Topic↗
PubMed1985

Serum potassium concentration as a risk factor of ventricular arrhythmias early in acute myocardial infarction.

Sixty patients with a first acute myocardial infarction and no current treatment with cardioactive drugs were included in a prospective study of the relationship between serum potassium concentration and the early occurrence of ventricular tachycardia and premature ventricular contractions (PVCs). Serum potassium level (range 2.5 to 5 mmol/liter) was estimated 3.8 +/- 2.5 hr (mean +/- SD) after the onset of the infarction, and Holter monitoring was performed during the subsequent 12 hr. In multivariate analysis, serum potassium level was negatively and age positively related to ventricular tachycardia. Among the subclasses of PVCs (frequent unifocal, multifocal, couplets, bigeminy), serum potassium concentration was negatively related to the frequent unifocal subclass; hypertension was related to couplets and to the presence of any of the subclasses, and serum aspartate aminotransferase concentration was related to multifocal PVCs. Heart failure leading to death was related to all subclasses of PVC. Serum potassium concentration is an independent inverse predictor of the occurrence of ventricular tachycardia and frequent unifocal PVCs early in acute myocardial infarction.

Aged↗
PubMed1984

Left ventricular thrombosis and cerebrovascular accident in acute myocardial infarction.

In a prospective study of 90 consecutive patients with acute myocardial infarction, 15 (28.3%) of 53 patients with an anterior wall infarction developed a left ventricular thrombosis diagnosed by cross sectional echocardiography. Patients received anticoagulants only after a left ventricular thrombosis had been diagnosed. Twenty eight patients had an inferior infarction, but none of these had a left ventricular thrombosis. Five (5.5%) of the 90 patients suffered a cerebrovascular accident, and all had an anterior wall infarction. In four of these five patients a left ventricular thrombosis was confirmed by echocardiography before the cerebrovascular accident. All patients with left ventricular thrombosis had apical akinesis. The incidence of a thrombosis did not differ in patients with a first anterior myocardial infarction and with reinfarctions. Among the 40 patients with a first anterior wall infarction, 12 with a thrombosis had a significantly higher incidence of enlarged heart on chest radiographs and significantly higher serum aspartate aminotransferase enzyme activity than those without. Thus patients with a large anterior wall infarction and with akinesis in the apical region are at high risk of developing a left ventricular thrombosis, which may be a source of peripheral emboli. Left ventricular thrombosis appears to be rare with infarctions in other locations.

Aspartate Aminotransferases↗