PubMed Health⌕ Search

Biomedical subjects

A Sigurdsson

Publications and source records attributed to A Sigurdsson.

52 records · Page 3Linked 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

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↗
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↗
PubMed1992

Intracanal placement of Ca(OH)2: a comparison of techniques.

Ten extracted human maxillary first molars were selected with a variety of root curvatures. The distofacial roots were resected and the mesiofacial canals were instrumented to a size #25 K file. Three techniques were used to introduce Ca(OH)2 paste into the instrumented canals. These techniques were evaluated for their ability to carry the Ca(OH)2 to working length and also to produce a dense fill. The Lentulo spiral was most effective in carrying the paste to working length. The Lentulo spiral also produced the highest quality fill. The Calasept injection system followed by a #25 finger plugger was the second most effective technique. Counterclockwise rotation of a #25 K file was the least effective of the techniques tested.

Calcium Hydroxide↗
PubMed1991

Enalaprilat in acute myocardial infarction: tolerability and effects on the renin-angiotensin system.

We treated 48 patients with intravenous enalaprilat within 24 hours from the onset of acute myocardial infarction. Concomitant therapy included thrombolytic treatment (29), intravenous metoprolol (34), intravenous nitroglycerin (16) and intravenous furosemide (15). The first 40 patients included had systolic blood pressure at baseline greater than or equal to 110 mmHg. Intravenous bolus injections of 0.2-1.2 mg (mean 1.0 mg) enalaprilat in one hour were given to 20 patients and an intravenous infusion of 1 mg over two hours was administered to another 20 patients, as well as to a separate group of 8 patients with systolic blood pressure between 100-109 mmHg at baseline. The infusion was stopped in five cases when the systolic blood pressure fell below 100 and 90 mmHg, respectively, in the two infusion groups. No hypotensive reactions were symptomatic. Blood pressure decreased from a mean of 134/82, 131/79 and 106/72 mmHg to a minimum of 117/71, 118/73 and 97/63 mmHg, respectively, in the three groups. Almost complete suppression of plasma angiotensin converting enzyme activity was achieved within 30 minutes. No significant changes were found in plasma levels of angiotensin II, renin activity or atrial natriuretic peptide between baseline and 24 hours. Treatment was continued with oral enalapril 2.5-10 mg/day, which was generally well tolerated. We conclude that intravenous and oral enalapril added to conventional therapy in the early phase of acute myocardial infarction is well tolerated in selected patients, but should be carefully titrated.

Aged↗
PubMed1975

Benign cementoblastoma (true cementoma).

Benign cementoblastoma is a rare benign odontogenic tumor of mesenchymal origin. As only a few documented cases have been reported in the literature, the clinical and histologic criteria for identifying this type of tumor are still uncertain. Thus, problems of differential diagnosis warrant the present report of a case of benign cementoblastoma in the mandible of a 27-year-old man.

Adult↗
PubMedDate not supplied

Relationship between pain sensitivity and resting arterial blood pressure in patients with painful temporomandibular disorders.

OBJECTIVE: Patients experiencing temporomandibular disorders (TMD) show greater sensitivity to painful stimuli than age- and gender-matched control subjects. This enhanced pain sensitivity may result, at least in part, from an alteration in pain regulatory systems that are influenced by resting arterial blood pressure. In this study, we examined the relationship between resting systolic blood pressure and pain perception in 64 female TMD and 23 age-matched pain-free female subjects. METHOD: Resting arterial blood pressure and measures of thermal and ischemic pain threshold and tolerance were determined for each participant. Subjective ratings of thermal pain evoked by suprathreshold noxious thermal stimuli (45-49 degrees C) using a magnitude matching procedure were also obtained for both groups. RESULTS: TMD patients had lower thermal and ischemic pain thresholds and tolerances than pain-free subjects (ps < .05). Both groups provided equivalent intensity ratings to suprathreshold noxious thermal stimuli. A median split of each group based on resting systolic blood pressure revealed an influence of blood pressure on both thermal and ischemic pain perception for the Pain-Free group. The Pain-Free high resting blood pressure subgroup had higher thermal pain tolerances, higher ischemic pain thresholds, and provided lower magnitude estimates of the intensity of graded heat pulses compared with the Pain-Free low blood pressure subgroup. A trend toward a significant effect of blood pressure level on ischemic pain tolerance was also observed for the Pain-Free group. In contrast to the Pain-Free group, blood pressure level did not influence ischemic or thermal pain perception for TMD patients. Similar to the lack of effect of resting blood pressure on experimental pain perception in TMD patients, resting blood pressure was not related to measures of clinical orofacial pain in TMD patients. CONCLUSIONS: These findings confirm our previous findings that TMD patients are more sensitive to noxious stimuli and suggest that painful TMD may result, at least in part, from an impairment in central pain regulatory systems that are influenced by resting arterial blood pressure.

Adult↗
PubMedDate not supplied

Loss of heterozygosity at chromosome 7q in human breast cancer: association with clinical variables.

In this study 238 human primary breast cancers were analysed with 9 polymorphic microsatellite markers specific to region 7q21-q35 on chromosome 7. LOH was observed at one or more marker in 82 cases or (34%). The deletions were evenly distributed throughout the region. Patients were divided into two groups according to whether LOH was observed in their tumours or not, and tested for association with overall survival, the clinicopathological features: steroid receptor content, tumour size, node status, DNA ploidy and S-phase fraction, and LOH at other chromosomal regions. An association was found between 7q LOH and high S-phase fraction. An association was found between LOH at 7q and LOH at 1p, 3p, 9p, 13q and 17q. These results suggest the location of a putative tumour suppressor gene at chromosome 7q21-q35 that, in combination with other deletions, might enhance tumour growth.

Breast Neoplasms↗
PubMedDate not supplied

High frequency of LOH at chromosome 18q in human breast cancer: association with high S-phase fraction and low progesterone receptor content.

Human primary breast cancers were analysed for somatic loss of heterozygosity (LOH) at chromosome 18 with 15 polymorphic microsatellite markers. LOH was observed in 148 of the 228 cases analyzed, (65%). Three smallest common deletion regions (SCDR) were detected on the long arm of chromosome 18. The marker D18S51 at the region 18q22 showed the highest LOH (42%). Tumors with and without LOH at 18q were tested for association with clinico-pathological features of the tumors, such as estrogen and progesterone receptor content, age at diagnosis, tumor size, node status, histological type, S-phase fraction, DNA ploidy and LOH at other chromosomal regions. A significant association was found between LOH at 18q and high S-phase fraction (99.9% confidence interval) and low progesterone receptor content (99% confidence interval). Furthermore, an association was found between LOH at 18q and LOH at 1p, 7q, 9p, 13q and 17q. We conclude that there are three separate LOH target regions at chromosome 18q, and that inactivation of one or more genes at these regions might be important for human breast carcinogenesis.

Breast Neoplasms↗