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Biomedical subjects

K Swedberg

Publications and source records attributed to K Swedberg.

At least 109 records · Page 6Linked to original sources
PubMed1994

Left ventricular remodelling, neurohormonal activation and early treatment with enalapril (CONSENSUS II) following myocardial infarction.

The effects of angiotensin converting enzyme (ACE) inhibitors on mortality following acute myocardial infarction (MI) has recently been studied in several clinical trials. The rationale for the use of these drugs following an injury to the myocardium is largely based on their ability to attenuate left ventricular volume expansion and modulate neurohormonal activation. Left ventricular dilatation following MI is due to complex structural changes in the infarcted myocardium as well as alterations in the non-infarcted contractile myocardium. The magnitude of this remodelling is associated with adverse prognosis. Neurohormonal systems are activated in the early phase of acute MI. Prolonged neurohormonal activation mainly occurs among patients with marked left ventricular dysfunction. The CONSENSUS II trial examined the effects on mortality of the ACE inhibitor enalapril, when initiated within 24 h from the onset of the infarct and continued for 6 months. There were 6090 patients randomly assigned to placebo (n = 3046) or enalapril (n = 3044). At the end of the trial, 598 patients had died: 286 (9.4%) in the placebo group and 312 (10.2%) in the enalapril group (P = 0.26). These results are in contrast to some other studies in which mortality was reduced by ACE inhibitor therapy post-MI. It is considered likely that the positive effects of ACE inhibitors following MI are confined mainly to patients with marked left ventricular dysfunction and prolonged neurohormonal activation.

Aged↗
PubMed1994

Declining hospital mortality in acute myocardial infarction.

Beta-blockers, nitrates, aspirin and thrombolytic drugs have each separately been shown to reduce mortality in acute myocardial infarction, but the effect of these treatments combined during routine coronary care has not been assessed. The coronary care unit at Ostra Hospital services a stable community of 250,000 inhabitants. Since 1984 all patients have been entered into a computerized database. In addition, information on age, sex, discharge diagnosis and hospital outcome is also available for patients admitted between 1979 and 1983. In 1984, routine treatment with intravenous beta-blockers was introduced, to be followed in 1986 by intravenous nitroglycerin and in 1988 by aspirin in all patients without contraindications. Since 1988, intravenous thrombolytic treatment has been also given routinely to all patients with ST-elevation and chest pain < 6 h. Despite a similar number of patients and an increasing median age, the in-hospital mortality has declined from 18.5% in 1979 to 11.8% in 1990 (P < 0.01). It is concluded that mortality from acute myocardial infarction has declined by almost 40% since 1979. This reduction cannot be explained by a single major therapeutic intervention but may be attributed to the combined use of multi-lead monitoring, early use of beta-blockers, nitroglycerin, aspirin and thrombolytic agents.

Adrenergic beta-Antagonists↗
PubMed1994

Absence of effect on exercise capacity of 12-weeks treatment with ramipril in patients with moderate congestive heart failure. Ramipril Study Group.

Pharmacological therapy in cases of chronic congestive heart failure (CHF) is usually evaluated by maximal exercise time. To assess the effect of an angiotensin converting enzyme inhibitor, ramipril, 223 patients with moderate CHF were studied in 24 centres in four Nordic countries in a randomized, double-blind, placebo-controlled, parallel group design. The study drug was titrated from 1.25 mg to a maximum of 10 mg once daily (o.d) over a period of 4 weeks (mean dose 8 mg). A symptom-limited bicycle exercise test, starting at 30 watts and increasing by 10 watts.min-1, was used to evaluate exercise capacity. Reproducible tests were required at baseline, and the test was repeated after 4, 8 and 12 weeks of treatment. Seven deaths were recorded in the placebo group and one death in the ramipril group. A total of 195 patients completed 12 weeks of treatment (placebo group n = 91, ramipril group n = 104). The groups had similar baseline characteristics. Maximal exercise time was increased by mean (SD) 35 s (9) and 41 s (8) in the placebo and ramipril groups, respectively. The adjusted difference between the groups at 12 weeks was 9 s (12) (ns). A significant decrease in blood pressure and rate-pressure product at rest and at end of exercise was obtained by ramipril as compared with placebo. Significantly fewer patients deteriorated in NYHA class from baseline to 12 weeks of ramipril treatment compared to placebo (P = 0.012). Concomitant medication for CHF increased significantly in the placebo group as compared with ramipril-treated patients (P = 0.003).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Output, Low↗
PubMed1994

Effects of ramipril on the neurohormonal response to exercise in patients with mild or moderate congestive heart failure.

Static measurements of plasma neurohormones at rest may not be adequate to detect alterations in cardiovascular control mechanisms in congestive heart failure (CHF). Therefore, it is of interest to study neurohormonal activation during different physiological conditions. Plasma neurohormones were measured in 54 patients on diuretic therapy for mild or moderate CHF. Samples were taken at rest and immediately after maximal bicycle exercise, before and after 12 weeks of treatment with ramipril or placebo. There was a strong correlation between the plasma levels of each hormone before and after exercise. An inverse correlation existed at baseline between exercise duration and angiotensin II levels after maximal exercise (r = -0.30, P = 0.03), but not at rest. Plasma levels of angiotensin II, aldosterone, atrial natriuretic peptide (ANP) and noradrenaline were increased after maximal exercise compared to rest. Plasma angiotensin converting enzyme activity and ANP were reduced by ramipril compared to placebo, both at rest and after exercise, but levels of angiotensin II, aldosterone and nordrenaline were not significantly affected. Thus, exercise consistently activates neurohormonal systems in patients with CHF. Patients with the lowest exercise duration had the highest angiotensin II levels after exercise. Measurements of plasma neurohormones after maximal exercise provide limited additional value to measurements at rest.

Aged↗
PubMed1994

Response of plasma neuropeptide Y and noradrenaline to dynamic exercise and ramipril treatment in patients with congestive heart failure.

Forty-two patients with congestive heart failure were studied in order to clarify whether the plasma level of neuropeptide Y-like immunoreactivity (NPY-LI) rises in parallel with plasma noradrenaline (NA) during physical exercise in congestive heart failure (CHF). All patients were studied in a randomized placebo-controlled trial with the ACE-inhibitor ramipril during 12 weeks to determine whether ACE-inhibition alters the response of plasma NPY-LI to exercise. The patients were treated with diuretics and had stable congestive heart failure (NYHA classes II-III). Plasma NPY-LI was 50 +/- 5 pmol l-1 (mean +/- standard error of the mean) at rest and 60 +/- 6 pmol l-1 at the end of exercise at baseline (P < 0.01). The corresponding values for plasma NA were 2.8 +/- 0.2 nmol l-1 and 15.3 +/- 1.2 nmol l-1 (P < 0.001). Before ACE-inhibition, there was a correlation between high NPY-LI and NA values after exercise. After treatment with ramipril or placebo for 12 weeks, there was no difference in plasma NPY-LI and NA at rest or after exercise between the two treatment groups. The maximal exercise time was unchanged. It is concluded that plasma NPY-LI and NA were elevated at rest in CHF. The additional rise of plasma NPY-LI and NA after exercise was attenuated in CHF compared to healthy individuals. ACE-inhibition with ramipril did not alter plasma NPY-LI or NA at rest or after exercise compared to placebo.

Aged↗
PubMed1994

Neurohormonal activation in patients with mild or moderately severe congestive heart failure and effects of ramipril. The Ramipril Trial Study Group.

OBJECTIVES: To describe neurohormonal activation in patients with mild or moderate heart failure and how it may be modified by treatment with ramipril. SETTING: Cardiology departments at 24 hospitals in Denmark, Finland, Norway, and Sweden. PATIENTS: 223 patients with mild or moderately severe congestive heart failure who were taking diuretics with or without digitalis. DESIGN: Randomised, double bind, multicentre, placebo controlled comparison of ramipril and placebo. Venous blood samples were drawn at rest, before blind treatment, and after 12 weeks of treatment with the study drug. A probability prediction score for mortality derived by stepwise linear discriminant from neurohormone data in the first cooperative north Scandinavian enalapril survival study (CONSENSUS I) was used to assess combined activity of the different neurohormonal systems. RESULTS: Plasma concentrations of atrial natriuretic peptide were raised at baseline but angiotensin II, aldosterone, and noradrenaline concentrations were within normal limits. There was, however, a wide interindividual variation. Plasma noradrenaline concentration and prediction score were higher among patients with class III congestive heart failure according to the New York Heart Association's classification than among patients with class II congestive heart failure (P < 0.05). There was a modest but significant inverse correlation between exercise duration at baseline and plasma noradrenaline concentration (r = -0.21, P = 0.0023), aldosterone concentration (r = -0.14, P = 0.04), and prediction score (r = -0.24, P = 0.0004). Prediction score at baseline was significantly higher among those who died (n = 10) than among survivors (P = 0.03). Angiotensin converting enzyme activity was suppressed and plasma concentrations of aldosterone and atrial natriuretic peptide were reduced after 12 weeks of treatment with ramipril compared with placebo. In patients with the most pronounced neurohormonal activation at baseline (highest third of noradrenaline concentration or prediction score), noradrenaline concentration and prediction score were significantly lower after 12 weeks of taking ramipril compared with placebo. Patients with a prediction score in the highest third at baseline had a higher heart rate than to those in the lowest third (P = 0.003). CONCLUSIONS: Neurohormonal activation is associated with the degree of symptoms and the severity of disease in mild or moderately severe congestive heart failure. Treatment with ramipril attenuates neurohormonal activation. This effect is most pronounced among patients with the highest circulating concentrations of neurohormones before the start of treatment.

Adult↗
PubMed1994

Patient characteristics in cases of chronic severe heart failure with different degrees of left ventricular systolic dysfunction.

It has not been determined previously whether patients with severe chronic congestive heart failure differ in demographic characteristics with respect to left ventricular systolic dysfunction (LVD). In patients with severe chronic congestive heart failure in NYHA IV, an optional protocol in the CONSENSUS-I trial was designed to ascertain whether there were any differences in patient characteristics regarding the degree of LVD defined as left ventricular fractional shortening (FS). A subgroup of 54 patients from the CONSENSUS-I trial were evaluated with M-mode echocardiography. Patients with FS above median (14%) were older (74 +/- 7 vs. 68 +/- 7, p < 0.01), more often female (48 vs. 15%, p < 0.05) and had lower heart rates (77 +/- 15 vs. 95 +/- 17, p < 0.01). Analysis of the 2-year follow-up from the end of the trial was also performed. In the placebo group, patients with FS > 14% had significantly better prognosis than patients with FS < 14%. In the enalapril-treated group no such difference in survival was seen. The difference between the original treatment groups remained, despite the fact that treatment with enalapril was then made available to all surviving patients. In conclusion, patients with advanced chronic congestive heart failure and less severe LVD have different demographic characteristics than patients with more severe LVD. In the placebo group, but not in the enalapril group, prognosis was better in patients with less severe LVD.

Aged↗
PubMed1994

Exercise testing in heart failure. A critical review.

Exercise intolerance is one of the primary characteristics of chronic congestive heart failure (CHF). Therefore, exercise testing has been widely used in the assessment of CHF patients, both to define the severity of the disease and to assess the efficacy of pharmaceutical agents in clinical trials. A number of different exercise tests can be used, although maximal exercise testing is the most common. Maximal exercise capacity can be determined by measuring exercise duration during incremental exercise, or maximal oxygen (O2) consumption, or it can be estimated by anaerobic threshold. While baseline exercise testing in CHF patients accurately identifies and quantifies cardiac failure and determines prognosis, it is of limited value in assessing changes that occur as a result of drug therapy. A key drawback of exercise testing as a measurement of drug effect is the fact that exercise changes produced by drug intervention do not correlate well with changes in the mortality rate. Several examples of the lack of correlation between exercise testing and mortality rates have been observed in clinical trials with angiotensin converting enzyme (ACE) inhibitors and vasodilators. ACE inhibitors have a modest effect on maximal exercise capacity but they improve survival. It is thought that neuroendocrine activation more closely reflects mortality rates and also the changes in survival observed with pharmacological intervention compared with other modes of evaluation.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Beneficial effects of metoprolol in idiopathic dilated cardiomyopathy. Metoprolol in Dilated Cardiomyopathy (MDC) Trial Study Group.

Several small studies have suggested beneficial effects of long-term beta-blocker treatment in idiopathic dilated cardiomyopathy. Our large multicentre study aimed to find out whether metoprolol improves overall survival and morbidity in this disorder. 383 subjects with heart failure from idiopathic dilated cardiomyopathy (ejection fraction < 0.40) were randomly assigned placebo or metoprolol. 94% were in New York Heart Association functional classes II and III, and 80% were receiving background treatment. A test dose of metoprolol (5 mg twice daily) was given for 2-7 days; those tolerating this dose (96%) entered randomisation. Study medication was increased slowly from 10 mg to 100-150 mg daily. There were 34% (95% CI -6 to 62%, p = 0.058) fewer primary endpoints in the metoprolol than the placebo group; 2 and 19 patients, respectively, deteriorated to the point of needing transplantation and 23 and 19 died. The change in ejection fraction from baseline to 12 months was significantly greater with metoprolol than with placebo (0.13 vs 0.06, p < 0.0001). Pulmonary capillary wedge pressure decreased more from baseline to 12 months with metoprolol than with placebo (5 vs 2 mm Hg, p = 0.06). Exercise time at 12 months was significantly greater (p = 0.046) in metoprolol-treated than in placebo-treated patients. In patients with idiopathic dilated cardiomyopathy, treatment with metoprolol prevented clinical deterioration, improved symptoms and cardiac function, and was well tolerated.

Adolescent↗
PubMed1993

Electrocardiographic assessment of infarct size: comparison between QRS scoring of 12-lead electrocardiography and dynamic vectorcardiography.

Myocardial infarct size is one of the most important predictors of prognosis in patients suffering an acute myocardial infarction. It can be assessed by enzymatic and electrocardiographic methods. The present report compares dynamic vectorcardiographic monitoring, serial plasma enzyme activity measurements and QRS scoring according to Palmeri as techniques for infarct size estimation. We report the results from 74 patients with acute myocardial infarction, who participated in a randomized trial of treatment with alteplase. A good correlation was found between myocardial infarct size by estimation from enzymatic measurement and from dynamic vectorcardiography. Dynamic vectorcardiography correlated more closely with enzymatically estimated infarct size in patients with Q-wave infarction, regardless of infarct location, than did QRS scoring of the conventional 12-lead electrocardiogram. Furthermore, dynamic vectorcardiography requires no time-consuming analysis and can be used for on-line monitoring of patients with ongoing infarction to estimate the size of an acute infarction while it is developing.

Clinical Enzyme Tests↗
PubMed1993

Initial experience with beta blockers in dilated cardiomyopathy.

In early 1973, Waagstein administered bolus intravenous injections of practolol and, subsequently, alprenolol, 50 mg twice daily, to reduce the heart rate of a 59-year-old woman with refractory, idiopathic dilated congestive cardiomyopathy (DCCM) and resting tachycardia. The patient's condition improved dramatically and continued to improve during subsequent oral therapy. This experience, combined with increasing interest in the role of beta blockade in myocardial protection, led to investigation of oral practolol, 50-400 mg twice daily, for 2-12 months in 6 additional patients with advanced DCCM. These findings, published in 1975, indicated improved ventricular function for all participants. In a 1980 open-label follow-up study, 28 patients with DCCM received alprenolol, metoprolol, practolol, or propranolol. Treatment was associated with improvements in myocardial function as well as in related symptomatology. These effects were reversed following drug withdrawal. The findings suggested that beta blockers possessed potential value in treatment of idiopathic DCCM.

Adolescent↗
PubMed1993

Short- and long-term neurohormonal activation following acute myocardial infarction.

Plasma levels of atrial natriuretic peptide (ANP), angiotensin II, aldosterone, and catecholamines were followed for 1 month and then for 4 to 6 months in 55 patients with acute myocardial infarction. Plasma hormones were highest within the first 24 hours after the onset of infarction but normalized during the first few days in patients without heart failure. In patients with symptoms of heart failure, angiotensin II and norepinephrine remained elevated for 1 month and ANP remained elevated for 4 to 6 months. During head-up tilt, angiotensin II and norepinephrine increased most in patients with overt heart failure. Among patients with a first myocardial infarction, a positive correlation was found between infarct size and ANP, angiotensin II, and norepinephrine on day 5 to 7 and between infarct size and angiotensin II during head-up tilt at 1 month, and between infarct size and ANP at 1 month. A similar relationship was found when only patients without heart failure were studied. It is concluded that sustained neurohormonal activation after myocardial infarction mainly occurs in patients with clinical heart failure but is related to the magnitude of myocardial damage, even in patients without heart failure. Measurement of neurohormones during head-up tilt may be an additive assessment for the detection of neurohormonal activation.

Adult↗
PubMed1993

Neurohormonal effects of early treatment with enalapril after acute myocardial infarction and the impact on left ventricular remodelling.

Plasma neurohormones were sequentially analysed in 98 patients with acute myocardial infarction randomized to treatment with enalapril or placebo for 4-6 months. Plasma angiotensin converting enzyme activity was rapidly suppressed by enalapril, but unaffected by placebo (P = 0.0001). No significant differences were found in the plasma levels of angiotensin II, aldosterone, atrial natriuretic peptide, noradrenaline, adrenaline or dopamine between the two treatment groups. Among patients with infarct size above median, plasma angiotensin II increased during head-up tilt at one month in the placebo group, but not in the enalapril group. Left ventricular end-diastolic volume (LVEDV) and left ventricular end-systolic volume (LVESV) were evaluated by echocardiography in 28 patients (placebo 15, enalapril 13) and changes in left ventricular volumes between baseline and 4-6 months were calculated. Only in the placebo group was a positive correlation found between plasma levels of noradrenaline at day 5-7 and the subsequent increase in LVEDV (r = 0.78, P = 0.005) and LVESV (r = 0.75, P = 0.008). The same trend was found for angiotensin II, adrenaline and dopamine levels at days 5-7 and the subsequent increase in left ventricular volumes. In the placebo group a negative correlation was found between plasma aldosterone at days 5-7 and the subsequent increase in left ventricular ejection fraction (r = -0.77, P = 0.006) during the study period. Although circulating neurohormones were not significantly influenced by enalapril treatment, it is concluded that enalapril may influence the relationship found between sustained neurohormonal activation and left ventricular remodelling after acute myocardial infarction.

Aldosterone↗
PubMed1993

Acute myocardial infarction: difference in the treatment between men and women.

During the last decade, treatment of myocardial infarction has changed and the prognosis dramatically improved. A sex bias in considering revascularization in men and women with coronary heart disease has been reported. The influence of gender on treatment given to patients with an acute myocardial infarction has not been investigated. From 1989 to 1991 there were 1515 patients with acute myocardial infarction admitted to the coronary care unit at Ostra Hospital; 67% were men. Pharmacological treatment limiting infarct size was given to 60% of all women and to 67% of all men; p < 0.05. In addition, coronary angiography during the hospital stay was performed in 0.2% of all women vs 1.9% of all men; p < 0.05. The prevalence of diabetes, age, symptoms or prehospital delay cannot explain these findings. While a sex bias in referring patients for revascularization has been reported, this report also describes a possible sex bias in the pharmacological treatment of acute myocardial infarction.

Adrenergic beta-Antagonists↗
PubMed1993

Silent myocardial ischemia during coronary angioplasty.

Silent myocardial ischemia is a marker in patients with coronary artery disease identifying those at high risk for subsequent cardiac events. During provoked myocardial ischemia some patients with angina pectoris do not develop chest pain. Are there clinical, angiographic or electrocardiographic differences between patients with chest pain as compared with patients without chest pain during provoked myocardial ischemia? Coronary angioplasty is a well-established method for the treatment of coronary stenosis, but it is also an interesting model for the study of myocardial ischemia as a result of coronary occlusion. We monitored 114 patients with angina pectoris during coronary angioplasty with dynamic, computerized vectorcardiography. During inflation of the balloon 33 of 114 patients had silent ischemia. Patients with silent myocardial ischemia had similar reasons for terminating the preangioplasty exercise test and where on similar anti-ischemic drug regimes. Silent myocardial ischemia was significantly associated with a history of diabetes, presence of collaterals, a history of less severe previous angina and less ST segment changes during angioplasty as compared with patients with painful ischemia. It is suggested that during coronary angioplasty silent ischemia may be caused by a less severe degree of ischemia, possibly as a result of the protective effect of collaterals.

Aged↗