Search PubMed⌕ Search

Biomedical subjects

K Swedberg

Publications and source records attributed to K Swedberg.

At least 145 records · Page 8Linked to original sources
PubMed1991

Effect of early intravenous rt-PA on infarct size estimated from serum enzyme activity: results from the TEAHAT Study.

In 319 patients who participated in a double-blind trial to evaluate the effect of early rt-PA administration compared to placebo in suspected acute myocardial infarction, infarct size was assessed from analyses of serum activity of lactate dehydrogenase isoenzyme 1 (LD 1). Treatment was always started less than 3 h after the onset of symptoms, with one-third of the patients' treatment being initiated outside the hospital. The maximum activity of LD 1 was reduced by 32%, from 13.3 mu kat l-1 in placebo to 9.0 mu kat l-1 in rt-PA treated patients (P = 0.001). A reduction in LD-1 activity after rt-PA treatment was restricted to patients with ST-elevation in the initial electrocardiogram, and was more pronounced in patients with previous ischaemic heart disease, above median age, and in those with a shorter delay in initiation of treatment. We conclude that very early intravenous treatment with rt-PA limits indirect signs of infarct size. The effect appears to be restricted to patients with ST-segment elevation in their initial electrocardiogram.

Ambulatory Care↗
PubMed1991

Prehospital thrombolysis in suspected acute myocardial infarction: results from the TEAHAT Study.

In a randomized, double-blind study, rt-PA vs. placebo treatment in early suspected acute myocardial infarction (AMI) was evaluated in patients both in hospital and prehospitally. The inclusion criteria were as follows: (a) age less than 75 years; and (b) chest pain indicative of AMI, of no longer than 2.75 h duration before first examination. In the prehospital setting a mobile coronary-care unit, accompanied by a cardiologist, was sent out by the ambulance services to 350 patients, of whom 205 (59%) were classified as non-eligible when examined by the cardiologist. Of the 145 patients who fulfilled the inclusion criteria, 44 were excluded due to contraindications to thrombolytic treatment. Thus 101 patients were randomized to blinded treatment outside hospital. The median time interval between onset of pain and treatment was 75 min, 45 min less than for those subjects who were randomized in hospital. The prevalence of confirmed AMI was 42% in the prehospital group, compared to 66% in the hospital group. Bleeding and cardiac complications for prehospital treatment were few, and similar to those for hospital treatment. In conclusion, prehospital thrombolysis was feasible, and delay times prior to treatment were significantly reduced. However, the specificity and diagnostic accuracy were lower than those achieved with in-hospital therapy.

Aged↗
PubMed1991

Early treatment with thrombolysis and beta-blockade in suspected acute myocardial infarction: results from the TEAHAT Study.

Independent trials of early administration of beta-blockers and thrombolytic agents have shown beneficial effects on both short- and long-term prognoses in acute myocardial infarction (AMI). The effects of a combination of the two strategies have not been thoroughly documented. Three hundred and fifty-two patients, of less than 75 years of age, with chest pain indicative of AMI, and onset less than 2 h and 45 min before first examination, were randomized to treatment with rt-PA or placebo. All patients without contraindication were given intravenous metoprolol 15 mg acutely and then 200 mg orally daily. Treatment was started either at the prehospital stage or in hospital. Thirty-seven per cent of patients had contraindications to beta-blockade, the most frequent of which were heart rate less than 60 beats min-1 and hypotension. The remaining 63% were given intravenous beta-blockade. No side-effects of metoprolol, alone or in combination with rt-PA, were observed during the prehospital phase. Overall, toleration of the treatment was good. Reduction in enzymatically estimated infarct size by rt-PA was more pronounced in patients who were also treated with metoprolol (41%, P less than 0.001) than in those with contraindications to beta-blockade (15%, NS). Patients who were also treated with metoprolol also had a lower incidence of Q-wave infarctions, congestive heart failure and ventricular fibrillation than those who were not given intravenous beta-blockade. In conclusion, toleration of intravenous administration of rt-PA and metoprolol was good, and this was also the case in the prehospital phase.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

Mortality and morbidity 1 year after early thrombolysis in suspected AMI: results from the TEAHAT Study.

We randomized 352 patients with suspected acute myocardial infarction (AMI) to treatment with rt-PA (n = 177) or placebo (n = 175). Patients were eligible if evaluated within 2 h and 45 min from onset of chest pain, and if aged less than 75 years. There were no ECG criteria for inclusion. A mobile coronary-care unit with a cardiologist present was used to initiate treatment at home in 29% of cases. During 1 year of follow-up the mortality in patients treated with rt-PA was 10.2%, as compared with 14.3% in patients the initial ECG, the mortality during the first year was 8% in the rt-PA group vs. 18% in the placebo group (P less than 0.05). Among patients without ST-elevation the mortality was 9% for the rt-PA group vs. 12% for the placebo group (NS). Requirement for rehospitalization, symptoms of angina pectoris and congestive heart failure, time of return to work and requirement for various medications did not differ significantly between the two groups, regardless of the initial ECG pattern.

Aged↗
PubMed1991

Effect of ACE-inhibition on renal function in severe congestive heart failure.

The long-term prognosis in severe congestive heart failure is very poor. Therapeutic regimens, in order to improve prognosis, should directly or indirectly influence the compensatory systems that are activated, ACE-inhibitor therapy has emerged as an important regimen in this context. In the CONSENSUS-trial (3), we could demonstrate that the addition of enalapril to conventional therapy in severe CHF significantly improved survival. The experience from this study forms the background for the recommendations in this work. 253 patients with severe heart failure (New York Heart Association (NYHA) Classification functional class IV) were randomized at 35 Scandinavian centers to placebo (n = 126) or enalapril (n = 127), in addition to their conventional therapy. The treatment dose of enalapril varied between 2.5 and 40 mg daily (man 18.3 mg). Blood samples for measurement of serum electrolytes and serum creatinine were taken repeatedly during follow-up. There seems to be about a 10% increase in creatinine within 2 weeks of initiating enalapril therapy. This increase seems to be independent of baseline creatinine level. Adverse experience regarding serum creatinine was reported in 22 placebo-treated patients and in 51 patients in the enalapril group. This reporting was based upon the investigators' feelings of significant importance of the observation and not on symptomatology. This was the main reason for permanent withdrawal in 2 and 7 patients, respectively. During initiation of enalapril therapy the blood pressure response is important after the very first dose, but for renal function the response may not appear until several days later. However, in most patients there are no problems with starting enalapril.(ABSTRACT TRUNCATED AT 250 WORDS)

Combined Modality Therapy↗
PubMed1990

Effects of enalapril and neuroendocrine activation on prognosis in severe congestive heart failure (follow-up of the CONSENSUS trial). CONSENSUS Trial Study Group.

This study enrolled 253 patients with severe heart failure (New York Heart Association functional class IV) from 35 centers in Scandinavia, randomly assigned to treatment with placebo or enalapril, in addition to their usual treatment for heart failure. After an initial titration period, the daily doses of enalapril ranged from 2.5 to 40 mg. At the end of the trial, 46% of the placebo-treated patients and 61% of the enalapril-treated patients were alive (p = 0.003); the survival figures at 8 months after completion of the trial were 32 and 48%, respectively (p = 0.001); and 21 and 30%, respectively (p = 0.006) at the 2-year follow-up. In the placebo group, there was a significant positive association between mortality and baseline levels of norepinephrine, epinephrine, angiotensin II, aldosterone and atrial natriuretic peptide; no such association was found in the enalapril-treated patients. The results suggest that the effects of enalapril on mortality are related to a counteraction of the neuroendocrine activation in general and to the renin-angiotensin system in particular.

Enalapril↗
PubMed1990

Pharmacokinetic and pharmacodynamic properties of atenolol in acute myocardial infarction.

A commonly used combined intravenous (i.v.) and oral dose regimen of atenolol was evaluated in 21 patients with acute myocardial infarction (MI). Atenolol 5-10 mg was administered i.v. and was followed by 50 mg twice daily during the first 24 h. Starting on the second day, 100 mg was administered as a single dose. Dose adjustments were made as necessary. The i.v. dose resulted in a rapid plasma peak concentration, but absorption of the first oral dose appeared to be delayed. The half-life (t1/2) was significantly prolonged on day 2 as compared with day 6, but the tmax, Cmax, and area under the curve (AUC) were all comparable to what has been reported in patients without MI. The change in heart rate (HR) or blood pressure (BP) was not related to the initial plasma level of atenolol. The interindividual variation was large, but most patients obtained plasma levels of atenolol which in studies of other diseases have been shown to be effective.

Adult↗
PubMed1990

Hormones regulating cardiovascular function in patients with severe congestive heart failure and their relation to mortality. CONSENSUS Trial Study Group.

There is a varying hormonal activation in heart failure. To be able to evaluate this activation and relate it to prognosis, we took blood samples at baseline and after 6 weeks from 239 patients with severe heart failure (all in New York Heart Association class IV) randomized to additional treatment with enalapril or placebo. In this study (CONSENSUS), which has previously been reported, there was a significant reduction in mortality among patients treated with enalapril. The present data show in the placebo group a significant positive relation between mortality and levels of angiotensin II (p less than 0.05), aldosterone (p = 0.003), noradrenaline (p less than 0.001), adrenaline (p = 0.001), and atrial natriuretic factor (p = 0.003). A similar relation was not observed among the patients treated with enalapril. Significant reductions in mortality in the groups of patients treated with enalapril were consistently found among patients with baseline hormone levels above median values. There were significant reductions in hormone levels from baseline to 6 weeks in the group of patients treated with enalapril for all hormones except adrenaline. There were no correlations between these changes in hormone levels. Summarily, there is a pronounced but variable neurohormonal activation in heart failure even in patients with similar clinical findings. This activation is reduced by enalapril therapy. The results suggest that the effect of enalapril on mortality is related to hormonal activation in general and the renin-angiotensin system in particular.

Aged↗
PubMed1990

Effect of enalapril on mortality in congestive heart failure. Follow-up survival data from the CONSENSUS trial.

The CONSENSUS trial, which compared the effects of enalapril and placebo on survival in severe heart failure, had a limited blinded treatment period. Follow-up for 8.5 months from the end of blinded therapy was performed. Enalapril therapy was encouraged in all patients during follow-up. Of the 135 surviving patients, 58 had previously been allocated placebo and 77 had been allocated enalapril. The follow-up mortality rates in those receiving enalapril were 18 (31%) and 16 (21%), respectively. Mortality was markedly lower in patients treated with enalapril than in those not started on the drug (16% vs 61%). The follow-up data strongly support the original CONSENSUS data regarding reduction of mortality in severe heart failure after the addition of enalapril.

Enalapril↗
PubMed1990

[ACE inhibitors in the treatment of heart failure].

Cardiac insufficiency is a clinical syndrome which presents several distinctive findings but is nevertheless difficult to define both clinically and in the scientific literature. In this article we maintain that cardiac insufficiency is a clinical condition characterized by symptomatic fluid retention on a cardiac basis, combined with signs of impaired pumping in the form of reduced capacity and/or other organic effects such as reduced renal function. The renin-angiotensin system is of cardinal importance once cardiac insufficiency is established and ACE inhibition is of essential significance for the treatment. It is not yet clear whether it is possible to prevent the onset of cardiac insufficiency in patients at high risk thereof. Current studies may answer this question.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

Enalapril for congestive heart failure.

In a randomized, double-blind trial, 253 patients with congestive heart failure (New York Heart Association class IV) received either enalapril (n = 127) or placebo (n = 126) in addition to their existing therapeutic regimens (consisting of digitalis, diuretics, and vasodilators other than angiotensin-converting enzyme inhibitors). The study was discontinued prematurely for ethical reasons because of the much lower mortality among the patients receiving enalapril (n = 50) than among those receiving placebo (n = 68) (p less than 0.003). The important reduction in mortality was observed among patients dying from progressive heart failure. Follow-up ranged from 1 day to 20 months (average 188 days). The reduction in mortality was associated with general improvements in the symptoms and signs of left and right ventricular heart failure, reduction of heart size, improvements in New York Heart Association classification, reduction of concurrent cardiovascular medication, and reduction of hospital admissions and days spent in the hospital. The overall withdrawal rate was low, and was comparable in the 2 treatment groups (16%; enalapril, n = 22, placebo, n = 18). Symptomatic hypotension was observed in 17% (n = 21) of the enalapril group vs 0% of the placebo group. Hypotension was the reason for withdrawal of enalapril therapy in 7 patients. After the initial dose of enalapril was reduced to 2.5 mg in high-risk patients, hypotension necessitated withdrawal in only 3.2% of the patients. Hyperkalemia was observed exclusively among patients with concurrent use of potassium-sparing agents.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

Mechanisms for improved survival in heart failure.

The two major causes of death in congestive heart failure (CHF) are progressive heart failure (approximately 60% of cases) and sudden death (30%). Sudden death in CHF is caused primarily by malignant ventricular arrhythmias. The underlying mechanism has yet to be established, but myocardial metabolic factors are probably involved. Although there is a clear association between complex ventricular arrhythmias and left ventricular function, it has not been shown convincingly that antiarrhythmic agents can reduce sudden death in CHF. Progressive deterioration of myocardial function is associated with altered myocardial energy production. Notably, the physiological effects of neuroendocrine activation in chronic CHF may be deleterious to myocardial function. The CONSENSUS study was carried out to evaluate the association between neuroendocrine activation and deterioration of myocardial function using ACE inhibitors. A marked reduction in mortality rate occurred in the enalapril-treated group, where the one-year mortality was reduced by 31%. The reduction in mortality was solely among patients with progressive CHF (a reduction of 50%); there was no difference in the incidence of sudden death. Analysis of blood samples drawn at baseline in the placebo group showed a significant positive correlation between mortality and plasma angiotensin II (P less than 0.05), aldosterone (P = 0.003), noradrenaline (P less than 0.001), adrenal levels (P less than 0.001), and atrial natriuretic peptide (P = 0.003). This was not observed in enalapril-treated patients. The significant reduction in mortality in the enalapril group was found consistently among patients with baseline hormone levels above the median value. In CHF, the underlying disease may induce serious arrhythmias and/or progressive failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1988

Effects of enalapril on mortality in severe congestive heart failure: results of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS).

To evaluate the influence of the angiotensin-converting enzyme inhibitor, enalapril (2.5 to 40 mg/day), on the prognosis of severe congestive heart failure, defined as New York Heart Association functional class IV, a double-blind study was undertaken in which 253 patients were randomized to receive either placebo (n = 126) or enalapril (n = 127) in addition to conventional treatment, including vasodilators. Follow-up averaged 188 days (range 1 day to 20 months). The reduction in crude mortality within 6 months (primary objective) was 40% in the enalapril-treated group (from 44 to 26%, p = 0.002) and within 1 year 31% (p = 0.001). By the end of the study, 68 subjects in the placebo group and 50 in the enalapril group had died--a reduction of 27% (p = 0.003). The entire reduction in total mortality (50%) was found in patients dying from progressive heart failure, whereas no difference was seen in the incidence of sudden cardiac death. There was a significant improvement in New York Heart Association classification in the enalapril group, together with a reduction in heart size and a reduced requirement for other heart failure medication. It is concluded that the addition of enalapril to conventional therapy in patients with severe congestive heart failure can reduce mortality and improve symptoms. The effect seems to be due to a reduction in death from progression of heart failure.

Aged↗