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Biomedical subjects

T Gundersen

Publications and source records attributed to T Gundersen.

At least 37 records · Page 2Linked to original sources
PubMed1987

Tolerability and antiarrhythmic efficacy of disopyramide compared to lignocaine in selected patients with suspected acute myocardial infarction.

In a randomized open study with intravenous lignocaine and disopyramide in patients with suspected acute myocardial infarction and ventricular premature contractions the occurrence of cardiac events, adverse reactions, withdrawals and arrhythmias were compared. Of the total 68 patients included in the study, 33 were randomized to disopyramide and 35 to lignocaine treatment. The treatment was given for 24 hours or until withdrawal due to occurrence of serious cardiac events or side-effects possibly related to the drugs. Sustained ventricular tachycardia occurred in one patient in each treatment group. 15 per cent of the patients treated with disopyramide and 14 per cent of the patients treated with lignocaine were withdrawn because of adverse reactions. Withdrawals due to depressed left ventricular function and sinoatrial and atrioventricular conduction disturbances were not different in the two treatment groups. However, more patients treated with lignocaine had supraventricular arrhythmias compared to disopyramide. Significantly more patients treated with disopyramide obtained complete abolition of premature ventricular contractions on Holter recordings compared to lignocaine treatment (P less than 0.001). The results indicate that disopyramide and lignocaine can be used alternatively in the treatment of ventricular arrhythmias in patients with suspected acute myocardial infarction.

Adrenergic beta-Antagonists↗
PubMed1986

Effect of timolol on mortality and reinfarction after acute myocardial infarction: prognostic importance of heart rate at rest.

Long-term timolol treatment after acute myocardial infarction is associated with a significant reduction in mortality and nonfatal reinfarction. To evaluate whether the reduction in mortality and morbidity is exclusively or partly dependent on a reduction in heart rate (HR), cardiac events in the Norwegian Timolol Multicenter Study were analyzed according to resting HR at baseline and at 1 month of follow-up Resting HR at baseline was a significant predictor of total death and all events (total death plus nonfatal reinfarction) both in placebo- and in timolol-treated patients. In the placebo group the median resting HR was unchanged from baseline to 1 month control (72 beats/min), but was reduced from 72 beats/min to 56 beats/min in the timolol group. Resting HR during follow-up remained a significant predictor of total death. Further, mortality at a given HR during treatment was not markedly different whether the HR was spontaneous or caused by timolol. Timolol treatment was related to a significant reduction in mortality, and this study suggests that the major effect of timolol treatment on mortality after acute myocardial infarction may be attributed to the reduction in HR. Timolol treatment was also associated with an overall reduction in nonfatal reinfarction. However, nonfatal reinfarction was inversely related to resting HR during follow-up, indicating that although coronary artery occlusion in low-risk patients may cause nonfatal reinfarction, the outcome in high-risk patients is more likely to be death. When analyzing mortality and nonfatal reinfarction combined, timolol treatment was related to a reduction in cardiac events at any given HR, suggesting that factors in addition to HR reduction are important in the protective effects of timolol.

Clinical Trials as Topic↗
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

Secondary prevention after myocardial infarction: subgroup analysis of patients at risk in the Norwegian Timolol Multicenter Study.

Timolol treatment after myocardial infarction is generally related to a significant reduction in both mortality and reinfarction compared with placebo. Retrospective analyses of the timolol study are performed on subgroups of patients with a high placebo mortality. The present study shows that these patients are target groups for secondary prevention, as they benefit most from timolol treatment after myocardial infarction. In patients 65-75 years of age, the number of cardiac deaths and reinfarctions prevented by timolol treatment is twice as high as that of patients below 65 years of age. Timolol treatment is well tolerated in the older age group and the contraindications for timolol treatment are independent of age up to 75 years. The reduction in mortality and reinfarction is independent of heart size at baseline. However, in patients with cardiomegaly and compensated heart failure on treatment with digitalis and diuretics, timolol treatment may be of special importance because of the very high incidence of cardiac death in this group of patients. In patients with compensated heart failure on treatment with digitalis and diuretics, timolol treatment does not precipitate heart failure. Patients with stable diabetes mellitus basically behave like nondiabetic patients regarding inclusion rate, side effects, and timolol-related reduction in mortality and reinfarction. Decisions concerning secondary prevention with timolol should be independent of preinfarction and postinfarction angina. In conclusion, 70-80% of all the patients below 75 years of age surviving myocardial infarction, without contraindication to beta-blocker treatment, can be treated with timolol 10 mg twice daily to reduce mortality and reinfarction. In contrast to previous routines, secondary prevention with beta blockers should be especially directed to high-risk patients.

Clinical Trials as Topic↗
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

Frequency characteristics of the middle ear.

For 68 temporal bones, frequency curves for the round window volume displacement have been measured for a constant sound pressure at the eardrum. Phase curves were measured for 33 of the specimens. The levels averaged amplitude curve is approximately flat below 1 kHz, where the round window volume displacement per unit sound pressure at the eardrum is 6.8 X 10(-5) mm3/Pa, and falls off by about 15 dB/oct at higher frequencies. For the 20 ears having the largest sound transmission magnitude at low frequencies, the corresponding amplitude curve is displaced about 5 dB towards higher levels. The phase of the round window volume displacement lags the eardrum sound pressure phase. In average for 33 temporal bones, the phase lag increases from zero at the lowest frequencies to pi near 2 kHz and to about 1.5 pi at 10 kHz.

Acoustics↗
PubMed1985

Effect of smoking habits and timolol treatment on mortality and reinfarction in patients surviving acute myocardial infarction.

The Norwegian Multicenter Group Study noted the effect of smoking habits before and after myocardial infarction and their relation to mortality and reinfarction rate after treatment with timolol in patients surviving acute myocardial infarction. The mean follow up period was 17.3 (range 12-33) months. No relation was found between initial smoking habits and risk category after infarction or between initial smoking habits and later outcome. At the time of their first infarct smokers were seven years younger than non-smokers. One moth after infarction nearly 60% of the smokers had stopped smoking completely. A significantly lower incidence of early cardiac death and lower total mortality was found in patients treated with timolol in both those who continued smoking and in the combined non-smoking groups and a significantly lower reinfarction rate among non-smokers. Cessation of smoking alone was associated with a reduced reinfarction rate by 45% but a non-significant reduction in mortality by 26%. It is concluded that treatment with timolol and cessation of smoking have an additive effect in reducing mortality and reinfarction rate after myocardial infarction.

Aged↗
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

Ventilating tubes in the middle ear. Long-term observations.

This follow-up study is of the same patients we studied in 1976. Then we thought the results were unsatisfactory in 20.9% of the ears treated with ventilating tubes. The hearing losses varied from 25 to 60 dB and chronic otitis media developed in 7.7% of the cases. We think the results of treatment with ventilating tubes in chronic serous otitis media are not good enough. This study shows that there has been an increase in the number of patients with permanent hearing loss and chronic otitis media than in the first study.

Adolescent↗
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

Changes in heart size during long-term timolol treatment after myocardial infarction.

The effect of long-term timolol treatment on heart size after myocardial infarction was evaluated by X-ray in a double-blind study including 241 patients (placebo 126, timolol 115). The follow-up period was 12 months. The timolol-treated patients showed a small but significant increase in heart size from baseline in contrast to a decrease in the placebo group. These differences may be caused by timolol-induced bradycardia and a compensatory increase in end-diastolic volume. The timolol-related increase in heart size was observed only in patients with normal and borderline heart size. In patients with cardiomegaly, the increase in heart size was similar in both groups. After re-infarction, heart size increased in the placebo group and remained unchanged in the timolol group.

Adult↗
PubMed1984

Acute and long-term response to enalapril in congestive failure.

Enalapril, a novel long acting angiotensin converting enzyme (ACE) inhibitor, was given orally to 12 patients with chronic heart failure (NYHA functional class III and IV) and cardiomegaly. The optimal dose averaged 17 mg given once-daily. Heart rate, systemic arterial blood pressure, pulmonary arterial pressure, right and left ventricular filling pressures and cardiac index were monitored during dose efficacy titration. Eleven patients were recatheterised 3 months later. After stabilisation of cardiac filling pressures, all patients had left ventricular filling pressures in excess of 20 mmHg. Enalapril increased cardiac index acutely by 34% but at 12 weeks follow-up, cardiac index was not different from control levels. Left ventricular filling pressure was reduced acutely by 36% and by 41% at 3 months. Heart rate, systemic arterial and right atrial pressures and plasma concentrations of aldosterone were reduced during the observation period. ACE activity was inhibited at the time of peak haemodynamic effect from 25.3 +/- 9.8 to 4.9 +/- 3.4 U/ml (P less than 0.01). Renin was markedly elevated. These changes were accompanied by marked and sustained clinical improvement and subjective well-being.

Aged↗