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- HEDNER, J, et al.
(author)
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Reduction in sympathetic activity after long-term CPAP treatment in sleep apnoea: cardiovascular implications
- 1995
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In: The European respiratory journal. - : European Respiratory Society (ERS). - 0903-1936 .- 1399-3003. ; 8:2, s. 222-229
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Journal article (peer-reviewed)abstract
- Twelve patients with severe obstructive sleep apnoea were included in an open, long-term, prospective, follow-up study addressing the effects of nasal continuous positive airway pressure (CPAP) on sympathetic activity, cardiac structure and blood pressure. Plasma norepinephrine (P-NE) (daytime at rest), daytime and night-time urinary excretion of NE (U-NE), vanylmandelic acid and metanephrines, together with 24 h noninvasive blood pressure (BP) recording and Doppler-echocardiography, were assessed before and after a mean of 20.5 (range 14-26) months of CPAP. Average self-reported use of CPAP was 89% (range 65-100%) of time spent in bed. Resting daytime P-NE ranged 0.35-0.83 ng.ml-1, which is elevated compared to healthy controls. Only night-time U-NE, mean daytime BP and average 24 h BP were related to severity of OSA. Night-time metanephrine was related to daytime and night-time diastolic, as well as night-time systolic, BP. Left ventricular mass index (LVMI) at baseline was correlated to daytime systolic BP and P-NE. Long-term CPAP treatment reduced biochemical markers of sympathetic activity. P-NE decreased by approximately 50%, and daytime and night-time vanylmandelic acid and metanephrine by 32-54%. In contrast, there were no overall reductions in BP or LVMI. It is concluded that obstructive sleep apnoea is associated with high sympathetic activity both during sleep and waking periods. Urinary metanephrine excretion seemed to reflect blood pressure, but neither daytime nor night-time catecholamine excretion was directly related to disease severity in patients with severe obstructive sleep apnoea.(ABSTRACT TRUNCATED AT 250 WORDS)
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- Everts, B, et al.
(author)
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A comparison of metoprolol and morphine in the treatment of chest pain in patients with suspected acute myocardial infarction--the MEMO study
- 1998
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In: Journal of Internal Medicine. - : Wiley-Blackwell Publishing Ltd. - 0954-6820 .- 1365-2796. ; 245:2, s. 133-141
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Journal article (peer-reviewed)abstract
- Objectives. To compare the analgesic effect of metoprolol and morphine in patients with chest pain due to suspected or definite acute myocardial infarction after initial treatment with intravenous metoprolol. Design. All patients, regardless of age, admitted to the coronary care unit at Uddevalla Central Hospital due to suspected acute myocardial infarction were evaluated for inclusion in the MEMO study (metoprolol–morphine). The effects on chest pain and side-effects of the two treatments were followed during 24 h. Pain was assessed by a numerical rating scale. Results. A total of 265 patients were randomized in this prospective double-blind study and 59% developed a confirmed acute myocardial infarction. In both treatment groups, there were rapid reductions of pain intensity. However, in the patient group treated with morphine, there was a more pronounced pain relief during the first 80 min after start of double-blind treatment. The side-effects were few and were those expected from each therapeutic regimen. During the first 24 h, nausea requiring anti-emetics was more common in the morphine-treated patients. Conclusion. In suspected acute myocardial infarction, if chest pain persists after intravenous beta-adrenergic blockade treatment, standard doses of an opioid analgesic such as morphine will offer better pain relief than increased dosages of metoprolol.
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- Everts, B, et al.
(author)
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Effects and pharmacokinetics of high dose metoprolol on chest pain in patients with suspected or definite acute myocardial infarction
- 1997
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In: European Journal of Clinical Pharmacology. - : Springer. - 0031-6970 .- 1432-1041. ; 53:1, s. 23-31
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Journal article (peer-reviewed)abstract
- OBJECTIVE: Pain intensity and the plasma concentrations of metoprolol and its major metabolite alpha-hydroxymetoprolol as well as noradrenaline (NA), adrenaline (A) and neuropeptide Y (NPY) were determined in patients with pain due to definite or suspected acute myocardial infarction (AMI) after graded metoprolol infusion. Pain intensity and metoprolol kinetics were assessed over 8 h. METHODS: Twenty-seven patients of either sex, aged 48-84 years with ongoing chest pain upon arrival to the Coronary Care Unit (CCU) were subdivided into two groups: (1) patients with ECG signs of threatening transmural myocardial damage (n = 15); and (2) patients without such ECG signs (n = 12). Pain intensity was assessed by a numerical rating scale (NRS) and venous blood was obtained for determination of plasma catecholamine and NPY concentrations. A continuous infusion of metoprolol (3 mg.min-1 i.v) was started and serial blood samples for plasma catecholamines, NPY as well as metoprolol and its major metabolite alpha-hydroxymetoprolol were obtained from the contralateral arm. RESULTS: Initial pain intensity was 5.9 (arbitrary units) and 5.4 in the groups with and without signs of transmural myocardial damage, respectively. One third of the patients with ST changes reported full pain relief (NRS = 0) within 70 min after starting metoprolol infusion (accumulated dose, 15-180 mg). Among the patients without ST changes upon arrival, full pain relief was obtained in 70% (accumulated dose, 30-120 mg). There was a dose-dependent relation between accumulated metoprolol dose and pain relief. The diagnosis of acute myocardial infarction (AMI) was confirmed in all 15 patients with ECG signs on arrival of transmural myocardial damage. The mean metoprolol dose in this group was 91(12) mg. The mean metoprolol dose in the 12 patients without ST changes was 64(8) mg. In all, seven of these patients developed definite AMI. The terminal half-life of unchanged metoprolol ranged from 2.5 to 8.5 h in group 1 and from 2.2 to 5.2 h in group 2. In group 1, metoprolol half-life was 4.5 h and total plasma clearance (CL) 54.1 1.h-1. In group 2, the metoprolol half-life was 3.7 h and total plasma clearance 75.4 1.h-1. There was a significant difference in clearance between the groups. After the intravenous metoprolol infusion, alpha-hydroxymetoprolol concentrations increased gradually. In groups 1 and 2, maximal concentrations in plasma (Cmax) were 143 and 135 nmol.1(-1) for alpha-hydroxymetoprolol and 2830 and 1653 nmol.1(-1) for metoprolol, respectively. Plasma NA or NPY did not differ between the groups. In contrast, plasma A was significantly higher during the initial 90 min of observation in patients with ECG signs of transmural myocardial damage. CONCLUSION: High-dose intravenous metoprolol was well tolerated in patients with suspected AMI. There was a more rapid and almost complete pain relief in patients without signs of transmural ischaemia compared with the patients with ECG signs of transmural AMI at arrival. In the later group of patients, plasma clearance of metoprolol was significantly reduced.
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- Everts, B, et al.
(author)
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Pain recollection after chest pain of cardiac origin
- 1999
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In: Cardiology. - : S. Karger AG. - 0008-6312 .- 1421-9751. ; 92:2, s. 115-120
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Journal article (peer-reviewed)abstract
- Memory for pain is an important research and clinical issue since patients ability to accurately recall pain plays a prominent role in medical practice. The purpose of this prospective study was to find out if patients, with an episode of chest pain due to suspected acute myocardial infarction could accurately retrieve the pain initially experienced at home and during the first day of hospitalization after 6 months. A total of 177 patients were included in this analysis. The patients rated their experience of pain on a numerical rating scale. The maximal pain at home was retrospectively assessed, thereafter pain assessments were made at several points of time after admission. After 6 months they were asked to recall the intensity of pain and once again rate it on the numerical rating scale. The results from the initial and 6-month registrations were compared. In general, patients rated their maximal intensity of chest pain as being higher at the 6-month recollection as compared with the assessments made during the initial hospitalization. In particular, in patients with a high level of emotional distress, there was a systematic overestimation of the pain intensity at recall.
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