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Biomedical subjects

J Kjekshus

Publications and source records attributed to J Kjekshus.

At least 145 records · Page 8Linked to original sources
PubMed1985

The importance of pre- and postinfarction angina on timolol-related reduction in mortality and reinfarction.

The importance of a history of angina pectoris on long-term timolol treatment after myocardial infarction was studied with respect to mortality and reinfarction. The analyses were performed retrospectively using cohorts from the Norwegian timolol multicenter study. In patients without angina pectoris prior to the infarction, timolol treatment reduced mortality by 61% and the occurrence of first nonfatal reinfarction by 16.9% as compared with placebo. Patients with preinfarction angina had a reduction in mortality of 21.8% and in first nonfatal reinfarction of 48.6%. The frequency of angina pectoris increased from 38% in both treatment groups before the infarction to 59% in the placebo group and 52% in the timolol group the first 6 months after the infarction. In patients without postinfarction angina pectoris, timolol treatment reduced mortality by 30.7% and the number of first nonfatal reinfarctions by 22.7%. The reductions in mortality and reinfarction in patients with postinfarction angina were 43.8% and 38.5%, respectively. Thus, the decision for timolol treatment after myocardial infarction should not be dependent on pre- and postinfarction angina.

Angina Pectoris↗
PubMed1985

Course of chest pain and its relation to CK release and ST/QRS vector changes in patients with acute myocardial infarction randomized to treatment with intravenous timolol or placebo.

Assessments of hourly pain scores (0 to 4) were made in 135 patients during the initial 24 hours after admission to the hospital. The duration of chest pain and the cumulative pain score obtained by adding the pain scores hour by hour were compared to ST and QRS vector changes and CK release. The cumulative pain score over a 24-hour period after admission correlated to the maximal QRS vector difference (r = 0.51) and the cumulative CK release (r = 0.58). The time until patients had complete relief of pain was closely related to the time during which QRS vector changes were seen to continue (r = 0.73). No corresponding correlation was found between pain duration and CK release time (r = 0.24). The ST decline time correlated to the duration of the first uninterrupted episode of chest pain in the placebo group only (r = 0.50). Pain duration showed no correlation to our indices of infarct size. There was a recurrence of pain in 41% of the patients, of whom 36% had a time-associated further increase of the ST vector magnitude. We conclude that chest pain is an important clinical symptom that signals ongoing necrosis. Furthermore, assessments of a "soft" parameter, such as the cumulative pain score, can add valuable information concerning the severity of myocardial damage.

Adult↗
PubMed1985

Timolol maleate and HDL cholesterol after myocardial infarction.

The influence of long-term timolol treatment on plasma lipids was analysed in cohorts of the Norwegian timolol multicentre study. The prognostic importance of high-density lipoprotein (HDL) cholesterol concentration after myocardial infarction was also examined. One year timolol treatment was related to a significant reduction in HDL cholesterol levels, from 1.32 mmol l-1 to 1.26 mmol l-1 (P less than 0.05). After one year the HDL cholesterol levels were significantly lower in the timolol treated patients (1.26 mmol l-1) than in the placebo treated patients (1.32 mmol l-1, P less than 0.01). However, the HDL cholesterol values after myocardial infarction had no prognostic importance, and in the placebo group total mortality was the same in patients with low HDL cholesterol (less than 1.25 mmol l-1) and high HDL cholesterol (greater than or equal to 1.25 mmol l-1), respectively 15.0% and 14.8%. Timolol treatment was related to a reduction in mortality both in patients with low (24%, NS) and with high (43%, P less than 0.05) HDL cholesterol levels. Thus, any deleterious effects of timolol on serum lipids did not attenuate its protective effect on the damaged myocardium.

Cholesterol↗
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

Timolol-related reduction in mortality and reinfarction in diabetic patients surviving acute myocardial infarction.

The long-term effect of timolol treatment (20 mg daily) on mortality and reinfarction was evaluated in 99 diabetic patients (placebo 46, timolol 53) surviving acute myocardial infarction. During the follow-up period of mean 17 months (12-33 months) there were 13 cardiac deaths in the placebo group and 5 in the timolol group, a reduction of 66.6% (p less than 0.05). The number of non-fatal reinfarctions was 10 in the placebo group and 2 in the timolol group, a reduction of 82.7% (p less than 0.05). The timolol treatment was well tolerated. However, in patients not suffering from diabetes mellitus, long-term timolol treatment was related to a slight increase in new onset diabetes mellitus and in fasting blood sugar levels.

Blood Glucose↗
PubMed1984

A double-blind, crossover comparison of flecainide acetate and disopyramide phosphate in the treatment of ventricular premature complexes.

The efficacy and safety of flecainide, 200 mg twice daily, was compared with disopyramide, 150 mg 4 times daily, in a randomized, double-blind, crossover study in 25 patients (19 men and 6 women, aged 20 to 71 years, mean 52.5) with more than 1,000 ventricular premature complexes (VPCs) in a pretrial 24-hour Holter monitoring screen. Each 14-day active treatment period was preceded and followed by a 7-day placebo period. Ambulatory ECGs were recorded at the end of each study week and analyzed blindly. Average VPCs recorded during each of the 2 active periods were compared with average VPCs in the placebo periods. Twenty-two of 25 patients attained therapeutic plasma levels of both drugs. The occurrence of VPCs was significantly less during flecainide than during disopyramide treatment, 92 and 39%, respectively (p less than 0.01). Complex arrhythmic events were significantly more suppressed with flecainide than with disopyramide. No difference was observed between the 2 drugs in the incidence or severity of reported side effects. PQ, QRS and QT intervals increased beyond normal limits on both drugs in some patients, significantly more with flecainide than with disopyramide. The JT interval did not change or decrease; hence, all changes in the QT interval were attributable to a widening of the QRS complex. Neither drug showed any significant effect on blood pressure or heart rate. Flecainide may be a well-tolerated and valuable alternative to currently available antiarrhythmic agents.

Adult↗
PubMed1984

Acute and chronic hemodynamic effects of enalapril (MK-421) in congestive heart failure.

Enalapril, a new long-acting angiotensin-converting enzyme inhibitor, was administered orally to 12 patients with stable congestive cardiac failure, NYHA function class III-IV. Acute and chronic hemodynamic effects were evaluated in addition to clinical response. The results of this open pilot study indicated marked reduction of pulmonary capillary wedge pressure from 21.8 +/- 5.9 mm Hg (mean +/- 1 SD) to 13.3 +/- 4.5 mm Hg (P less than 0.01) and peripheral resistance from 1837 +/- 860 dynes X sec-1 X cm-5 to 1063 +/- 584 dynes X sec-1 X cm-5 at 6 hr (P less than 0.01). Well-tolerated hypotension with mean arterial pressure from 88.0 +/- 11.6 mm Hg to 73.1 +/- 11.7 mm Hg at 6 hr (P less than 0.01) was recorded. No significant increase in cardiac output was observed. Angiotensin-converting enzyme activity was powerfully inhibited at the time of peak hemodynamic effect from 25.3 +/- 9.8 U/ml to 4.9 +/- 3.4 U/ml (P less than 0.01) and sustained, but attenuated reduction at 24 hr (8.7 +/- 4.7 U/ml) was observed. All patients reported subjective improvement and this clinical improvement has been sustained during follow-up from 19 to 21 months although baseline hemodynamic parameters at chronic re-catheterization did not demonstrate significant improvement. The pharmacodynamics and toxicity of enalapril as compared to captopril are discussed. The long half-life, low toxicity and gradual onset of action are seen as representing a clinical advantage with regard to patient therapy.

Aged↗
PubMed1984

Cardiovascular responses to face immersion and apnea during steady state muscle exercise. A heart catheterization study on humans.

The cardiovascular adjustments to face immersion and apnea (FIA) in human beings during steady-state muscle exercise (163 and 98 watt) have been investigated. Using a triple lumen flow directed catheter inserted into the pulmonary artery we were able to measure cardiac output (CO) by thermodilution technique, pulmonary arterial pressure (PPA) right atrial pressure (PRA) and left ventricular filling pressure (PAD). Phasic arterial blood pressure (BP) was measured via a cannula in the radial artery. A 12 lead ECG was recorded continuously. FIA caused an immediate rise in BP (median 61%), the highest level being 25.33 kPa. CO during the last half of FIA was reduced by 49% (range 46-59, n = 7) systemic vascular resistance increased by median 200% (range 111-280). Myocardial oxygen demand determined by the heart rate pressure double product fell from median 33.6 to 16.8 (163 W) and 28.5 to 19.1 (98 W) given as beats/min X kPa X 10(2). Mean reduction was by 42%. PPA and PRA immediately increased and remained constant until a further pronounced increase was seen towards the end of FIA when pulmonary vascular resistance (PVR) went up. PACO2 and PAO2 at the end of 30 sec FIA (163 W) was 10.0 and 5.6 kPa, respectively, values which expectedly would cause pulmonary vasoconstriction. Our findings demonstrate that humans are able to make principally the same cardiovascular adjustments to diving as aquatic mammals, although the response patterns are slower and less efficient.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Effect of ACE-Inhibition on regional blood flow during acute left ventricular failure in the dog. Preliminary report.

Acute left ventricular failure was induced in 7 anaesthetized dogs by embolization of the left coronary circulation with 57 micron plastic microspheres. The dogs were then subjected to ACE-inhibition with enalapril. In addition to hemodynamic measurements, tissue blood flow was measured with the radioactive microsphere method. Preliminary results are presented, showing the vasodilatory effects of enalapril to be greatest in stomach, muscle and brain while possibly compromising the renal circulation.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1983

Quantitative assessment of myocardial ischemia and necrosis by continuous vectorcardiography and measurement of creatine kinase release in patients.

The accuracy of the use of the maximal QRS vector difference to estimate myocardial infarct size irrespective of infarct location was compared with that of measurement of cumulative creatine kinase (CK) release. Sixty patients with acute myocardial infarction and a history of symptoms of less than 4 hr duration were followed for 24 to 72 hr with orthogonal vectorcardiography and CK release analysis. Spatial QRS vector differences were calculated between the first QRS complex recorded and subsequent QRS complexes at timed intervals. The QRS vector difference increased rapidly and reached a plateau at an average 12.1 hr after onset of symptoms, as compared with 34.0 hr for the cumulated CK release. In 42% of the patients a stepwise progression of infarct evolution was observed. Irrespective of infarct location the maximal spatial ST vector magnitude was related to the ultimate QRS vector difference (r = .80) and to the cumulative amount of CK released (r = .64). Furthermore, maximal QRS vector difference correlated well with the maximal cumulative CK release (r = .64) Ten patients had possible infarct expansion, as indicated by recurrent QRS changes without concomitant CK release. Fifteen patients had infarct extension that was indicated by secondary CK release and that in seven patients was associated with further QRS changes. Infarct extension caused an approximate 25% increase in infarct size. Spatial ST vector magnitude, QRS vector difference, and cumulative CK release are complementary measures in the quantification of evolving myocardial injury after acute coronary occlusion and in the determination of sequels to therapeutic interventions.

Adult↗
PubMed1982

Effects of red rest and prazosin in congestive heart failure.

Twelve patients with congestive heart failure were monitored with invasive and noninvasive techniques to evaluate the effect of vasodilator treatment. During the 18 hours of strict bed rest before administration of prazosin, the hemodynamics improved substantially while only small and transient heModynamic changes were observed after introduction of prazosin. At 6 weeks' control the effect of vasodilator treatment with prazosin, 3 mg x 4, was lost. The beneficial results often credited to vasodilators in studies on congestive heart failure might in part be due to the concomitant bed rest introduced during the monitoring of the patients.

Adult↗
PubMed1982

Timolol-related reduction in mortality and reinfarction in patients ages 65-75 years surviving acute myocardial infarction. Prepared for the Norwegian Multicentre Study Group.

Long-term treatment with timolol in patients ages 65--75 years who survived myocardial infarction was related to a significant reduction, compared with placebo, in overall mortality (p less than 0.05), total cardiac death (p less than 0.01), sudden death (p less than 0.05) and reinfarction (p less than 0.01). The analyses were based on 732 patients (384 taking placebo and 348 timolol) from a cohort of 1884 patients in the Norwegian multicenter timolol study. The dosage of timolol was 10 mg twice daily and the patients were followed for 12--33 months (mean 17 months). There were 83 deaths in the placebo group and 52 deaths in the timolol group, a reduction of 35.5%. There were 69 initial reinfarctions in the placebo group and 38 in the timolol group, a reduction of 39.2%. There was no difference in the reduction of mortality and reinfarction between patients 65--75 years of age and patients less than 65 years of age. The incidence of side effects, the number of withdrawals and the reasons for withdrawal were similar in older and younger patients. We conclude that age should not be a decision-making factor concerning timolol therapy in postinfarct patients.

Adrenergic beta-Antagonists↗
PubMed1982

Pacing induced angina and platelet reactivity.

Platelet function was studied during pacing-induced angina pectoris in nine patients with coronary heart disease. Blood was sampled via catheters from the coronary sinus and the aorta at rest and during angina. The influence of the sampling procedures on the platelet function was evaluated in blood collected via catheters and via short venflons. The catheter induced pseudopod formation in the platelets. The aggregation response was similar, while platelet retention as measured with Hellem's method for native blood, was slightly lower in blood collected via catheters than via venflons. At rest the maximal rate of primary, ADP-induced aggregation was lower in blood from the coronary sinus than from the aorta, as was the percentage of platelets retained in glass bead columns. The ability of platelets to produce prostaglandin metabolites, estimated from malondialdehyde formation after thrombin stimulation was also moderately, but significantly lower in coronary sinus blood. During pacing-induced angina primary, ADP-induced aggregation and platelet retention values remained significantly lower in blood that had passed the coronary circulation than the aortic blood. There were no differences between aortic or coronary sinus samples collected at rest than during pacing. Unchanged platelet counts indicates that trapping of platelets did not occur. Thus, platelet reactivity was lower in coronary sinus than aortic blood at rest in patients with coronary heart disease, and a moderate pacing-induced angina did not influence this pattern.

Adenosine Diphosphate↗
PubMed1981

Effect of timolol on platelet aggregation in coronary heart disease.

The immediate effect of beta-blockers versus placebo in platelet function was studied in ten healthy men one hour after either 40 mg propranolol, 5 mg timolol or placebo was given. Both beta-blockers had similar platelet effects. They increased the ADP-threshold in a platelet aggregation test and reduced the plasma level of beta-thromboglobulin whereas the primary aggregation remained unchanged. Forty-four patients were given timolol 10 mg twice daily or corresponding placebo medication in a secondary prevention trial after a myocardial infarction. At rest and also immediately after a near maximal exercise test the platelet function was similar on timolol and placebo. During exercise a lower ADP-threshold and a higher plasma level of beta-thromboglobulin was observed irrespective of whether the patients received placebo or timolol. Thus, the acute platelet inhibiting effect of timolol observed after a single dose disappeared during chronic timolol treatment. During 24 hours continuous ambulatory ECG monitoring patients on timolol treatment had significantly less arrhythmias than patients on placebo. A general effect on platelets cannot explain this antiarrhythmic effect of timolol during chronic therapy.

Adult↗
PubMed1981

Effect of timolol on late ventricular arrhythmias after acute myocardial infarction.

This is a subproject of the Norwegian timolol myocardial infarction study carried out at one of the clinical centers. High risk patients surviving either a reinfarction or large initial infarction were randomized to placebo (44 pts) or timolol (37 pts). A 24 hour ECG was obtained the day before randomization (at baseline, 7-28 days after the acute attack) then 3 days, 1 month and 6 months after start of therapy. During this period the number of patients with one or more of ventricular couplets, bigemini, ventricular tachycardia or early cycle premature ventricular contractions (PVC) (i.e. complex ventricular arrhythmias) and the average number of PVC per hour increased significantly in the placebo group but not in the timolol group. The results indicate that there is an increased severity and incidence of ventricular arrhythmias in the first 6 months after myocardial infarction. Timolol effectively inhibited this trend. The importance of timolol as an antiarrhythmic agent may therefore be to prevent subclinical infarction extension and secondary ventricular arrhythmias related to the size of the myocardial damage.

Arrhythmias, Cardiac↗