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Biomedical subjects

P Eriksson

Publications and source records attributed to P Eriksson.

At least 19 recordsLinked to original sources

Non-invasive risk stratification within 48 h of hospital admission in patients with unstable coronary disease.

AIMS: In this study we evaluated the prognostic value of three methods of early risk estimation in patients with unstable coronary disease. METHODS AND RESULTS: The methods evaluated were: clinical risk estimation at hospital admission, continuous ST analysis with computerized vectorcardiography for 24 h and serial measurements of creatinine kinase-MB for 48 h. Twenty-seven (14%) of the 195 patients died or had a non-fatal infarction within one year. Clinical risk evaluation correctly identified a subgroup of patients with low risk but did not otherwise predict outcome. Fifty-six (29%) patients had ST vector magnitude episodes on vectorcardiography, 70 (38%) had three or more episodes of ST change vector magnitude and 74 (38%) had a peak creatinine kinase-MB value of 6 microgram.l-1 or more. The even rate for patients with ST vector magnitude episodes (23%) was significantly higher than for those without (10%; P < 0.05). For patients with and without three or more episodes of ST change vector magnitude the event rate was 23% and 9% respectively (P < 0.05) and for patients with and without creatinine kinase-MB > or = 6 microgram.l-1 the event rate was 23% and 8% respectively (P < 0.01). The positive predictive value of having none, either one or both of the ST or creatinine kinase-MB markers positive was incremental. CONCLUSION: Continuous vectorcardiographic monitoring of ischaemia in combination with serial creatinine kinase-MB measurement considerably improves risk stratification in unstable coronary disease.

Adult

Ischemic stroke after acute myocardial infarction. A population-based study.

BACKGROUND AND PURPOSE: Modern treatment may have influenced the risk of stroke after myocardial infarction (MI). The purpose of this study was to examine the incidence of ischemic stroke during the first month after an acute MI in an unselected population, to identify predictors of MI-related stroke, and to investigate the secular trend in MI-related stroke incidence. METHODS: In this case-control study, from a population of approximately 310000 25- to 74-year-old inhabitants, case subjects with a stroke within 1 month after an MI were prospectively recorded in the population-based Northern Sweden MONICA (Monitoring of Trends and Determinants in Cardiovascular Disease) study from 1985 to 1994. The same number of control subjects with an MI but without a stroke were matched for age, sex, and year when MI occurred. RESULTS: One hundred twenty-four case subjects were recorded. Fifty-one percent (63/124) of the strokes occurred within 5 days after onset of MI. The odds ratios (ORs) of an MI-related stroke were for a history of hypertension 1.7 (95% confidence interval [CI], 1.0 to 3.2), previous stroke 2.4 (CI, 1.0 to 6.1), chronic atrial fibrillation 3.0 (CI, 1.1 to 9.2), onset of atrial fibrillation during the hospital stay 3.5 (CI, 1.4 to 10.1), ST-segment elevation 2.4 (CI, 1.4 to 4.6), and anterior infarction 1.5 (CI, 0.9 to 2.6). In a conditional multiple logistic regression model, previous stroke (OR, 2.8; CI, 1.1 to 7.6), chronic atrial fibrillation (OR, 3.8; CI, 1.3 to 11.0), new-onset atrial fibrillation (OR, 4.6; CI, 1.6 to 12.8), and ST-segment elevation (OR, 3.4; CI, 1.6 to 7.4) were independent predictors of stroke. MIs preceding stroke were larger and in 51% were located anteriorly. There was a decrease in the incidence and event rate of MI-related stroke during the study period (P < .01 and P < .05, respectively). CONCLUSIONS: The risk of stroke is highest the first 5 days after MI. Only approximately half of the strokes occurring the first month after an MI are preceded by an anterior MI. The most important predictors of MI-related stroke are atrial fibrillation (chronic or new onset), ST elevation, and a history of a previous stroke. There is a long-term trend toward a lower incidence of MI-related stroke. These findings have important implications concerning both the pathophysiology and prevention of MI-related stroke.

Adult

Reversal of central sleep apnea with oxygen.

OBJECTIVE: To examine the effect of oxygen on apneas and sleep quality in patients with frequent central apneas during sleep. DESIGN/SUBJECTS: Prospective intervention study of 20 consecutive patients with predominant central apnea identified from 570 patients referred for suspected sleep apnea syndrome. Sixteen patients had congestive heart failure and seven of them had a previous stroke. Three of the remaining four patients without heart failure had experienced a previous stroke, and one was being treated with morphine. SETTING: The Department of Pulmonary Medicine at Umeå (Sweden) University Hospital. INTERVENTIONS: The patients were investigated for one night receiving nasal oxygen and one night without it. MEASUREMENTS: Overnight polysomnography with transcutaneous PCO2 and arterial blood gases. RESULTS: Central apneas occurred during Cheyne-Stokes respiration in 18 of 20 patients and two patients had idiopathic central apneas. Without oxygen, the median number of all central apneas and hypopneas was 33.5 (range, 8.0 to 52.0) per hour of sleep. These episodes decreased to 5.0 (range, 0.0 to 31.0)(p < 0.01) during oxygen therapy. In 17 of 20 patients, the frequency of central apneas was reduced by more than 50%. Central apneas were reduced by oxygen irrespective of the presence or absence of heart failure or Cheyne-Stokes respiration. The arousal frequency was reduced during oxygen treatment. Daytime sleepiness, difficulty falling asleep, snoring, and self-scored awakenings were reduced in seven patients who were given nocturnal oxygen at home. Obstructive and mixed apneas were unaffected by oxygen. CONCLUSIONS: Oxygen effectively reduces central sleep apnea in eucapnic patients.

Adult

Autoantibodies and primary Sjögren's syndrome in a hypocitraturic stone population.

Primary Sjögren's syndrome may be complicated by distal renal tubular acidosis (dRTA) and hypocitraturia, which are risk factors for calcium stone formation. Approached from a different perspective, in patients with urolithiasis and dRTA, autoantibodies and various autoimmune diseases are not uncommon. In search for signs of autoimmune disease, we analysed antinuclear antibodies and total levels of serum IgG in 197 hypocitraturic stone formers (67 women and 130 men). Antinuclear antibodies were present in 1.5% of the men and in 18% of the women. An isolated increase in serum IgG was found in 9% of the men and in 3% of the women. Anti-SS-A antibodies were analysed in a subgroup of 46 women and were estimated to occur in 16% of all hypocitraturic stone forming women. Four of 4 examined women, but no men, fulfilled the criteria of definite or possible primary Sjögren's syndrome. We recommend the analysis of anti-SS-A antibodies in female hypocitraturic stone formers.

Adult

Progression of coronary atherosclerosis is associated with a common genetic variant of the human stromelysin-1 promoter which results in reduced gene expression.

There is a common polymorphism in the promoter sequence of the human stromelysin-1 gene, with one allele having a run of six adenosines (6A) and the other five adenosines (5A). We have previously reported, in a 3-year follow-up study of patients with coronary atherosclerosis, that those patients who are homozygous for the 6A allele show a more rapid progression of the disease. In this study, we have investigated whether the 5A/6A promoter polymorphism plays a role in the regulation of stromelysin-1 gene expression. In transient transfection experiments, a stromelysin-1 promoter construct with 6A at the polymorphic site was found to express less of the chloramphenicol acetyltransferase reporter gene than a construct containing 5A. Electrophoretic mobility shift assay and DNase I footprinting revealed the interaction of one or more nuclear protein(s) with the DNA sequence at the 5A/6A polymorphic site. The binding of one of the nucleoprotein factors was more readily detectable with an oligonucleotide probe corresponding to the 6A allele as compared with a probe corresponding to the 5A allele. Replacing the core binding sequence with a random DNA sequence abolished the interaction between the nuclear protein(s) and the probe and also increased reporter gene expression in transiently transfected cells. Thus, the common 5A/6A polymorphism of the human stromelysin-1 promoter appears to play an important role in regulating stromelysin-1 gene expression and may be involved in the progression of coronary heart disease.

Alleles

Risk factors of calcium stone formation in patients with primary Sjögren's syndrome.

Distal renal tubular acidosis (dRTA), which occurs in patients with primary Sjögren's syndrome (SS), is a risk factor for the development of urolithiasis. Twenty-seven patients with SS were evaluated with respect to biochemical risk factors of calcium stone formation. Sixteen had no history of urolithiasis (group 1) whereas 11 had such a history (group 2). The stone composition was known for seven of the patients, and calcium phosphate was the major stone constituent in all of them. dRTA was present in all patients in group 2, and in 7 of the 16 patients in group 1. Hypocitraturia was common in both groups, and the urinary excretion of citrate did not differ between the two groups. There was a higher urinary excretion of calcium and urate in group 2 and this group also had a higher urine volume. The risk of forming a urine supersaturated with calcium oxalate (CaOx) expressed in terms of AP(CaOx)index(s), which is an approximate estimate of the ion-activity product of CaOx calculated for a 24-h urine volume of 1500 ml, was higher in stone formers. A similarly derived estimate of the ion-activity product of calcium phosphate, AP(CaP)index(s), was calculated for a urine pH of 7. Although AP(CaP)index(s) was not significantly higher in group 2, there was a good correlation between AP(CaP)index(s) and AP(CaOx)index(s). We conclude that the urine composition in patients with SS, dRTA and urolithiasis is similar to that of other stone-forming patients with dRTA, and recurrence preventive therapy can be designed as for these patients.

Acidosis

Sleep-disordered breathing in women: occurrence and association with coronary artery disease.

PURPOSE: To examine the occurrence of sleep apnea and nocturnal hypoxemia in women with and without coronary artery disease (CAD) and to investigate the relationship between sleep-disordered breathing and coronary artery disease. PATIENTS AND METHODS: In a case-control study, 102 cases were randomly selected among women with angina pectoris and angiographically verified coronary disease. Fifty age-matched controls without known heart disease were selected from the population registry. Pulse oximetry, oronasal thermistors, body position indicator, and recording of body and respiratory movements were used to quantify oxygen desaturations (the number of desaturations > or = 4% per hour of sleep, oxygen desaturation index [ODI]) and apneas (the number of apneas or hypopneas per hour of sleep, apnea-hypopnea index [AHI]). RESULTS: Women with CAD had a high occurrence of disordered breathing measured as AHI > or = 5, 54% (n = 54), AHI > or = 10, 30% (n = 30) or ODI > or = 5, 34% (n = 35) while the same proportions in controls were 20% (n = 10, P < 0.0001), 10% (n = 5, P < 0.01) and 18% (n = 9, P < 0.05), respectively. In a multiple logistic regression model, sleep apnea (AHI > or = 5), hypertension, and smoking habits were independent predictors of CAD with odds ratios of 4.1 (95% confidence interval [CI] 1.7 to 9.7, P < 0.01), 3.4 (CI 1.3 to 8.9, P < 0.05) and 2.4 (CI 1.0 to 5.7, P < 0.05), respectively. CONCLUSION: Sleep apnea is common in women with CAD and remains as a significant predictor of coronary disease after adjustment for age, body mass index, hypertension, smoking habits, and diabetes.

Adult

Urolithiasis and distal renal tubular acidosis preceding primary Sjögren's syndrome: a retrospective study 5-53 years after the presentation of urolithiasis.

OBJECTIVES: Distal renal tubular acidosis (dRTA) can be associated with autoimmune diseases such as primary Sjögren's syndrome (SS). Our objective was to study SS-associated symptoms, autoantibodies and renal histopathology in patients with urolithiasis and dRTA. SETTING: The patients were from the Departments of Nephrology and Rheumatology. University Hospital of Linköping, which is a tertiary referral hospital, as well as a secondary referral centre for the immediate area around the city of Linköping. SUBJECTS: Ten female patients with dRTA, who presented with urolithiasis and not with subjective sicca symptoms, were from the Department of Nephrology, University Hospital, Linköping. Autoantibodies were detected in eight of these patients, and they were studied with respect to clinical and laboratory evidence of SS (urolithiasis group). Fifteen women with SS, who presented with sicca symptoms and not with urolithiasis or dRTA, served as the reference group. RESULTS: In the urolithiasis group, all of the eight patients had anti-SS-A antibodies, and SS (or possible SS) developed in seven of the eight patients 1-48 (mean 15) years after the onset of urolithiasis. Histological features of tubulointerstitial nephritis were found in four of five biopsied patients in the urolithiasis group, and in two of four patients (with dRTA) in the reference group. CONCLUSIONS: Urolithiasis and dRTA can precede subjective sicca symptoms, and patients with dRTA may have SS in the absence of subjective sicca symptoms. Anti-SS-A antibodies are common in patients with urolithiasis and dRTA. Therefore, we hypothesize the possibility of a Sjögren-related renal disease in these patients.

Acidosis, Renal Tubular

Ischaemia detected by continuous on-line vectorcardiographic monitoring predicts unfavourable outcome in patients admitted with probable unstable coronary disease.

BACKGROUND: Several methods have been suggested for risk stratification of patients with unstable coronary syndromes. However, most of these are applied several days after hospital admission. METHODS: In this study we investigated the prognostic value of continuous ST-segment and QRS vector monitoring with computerized vectorcardiography (VCG), serial measurements of creatine kinase isoenzyme MB (CK-MB), predischarge stress testing and baseline data in patients with unstable angina pectoris or non-Q-wave infarction. RESULTS: During the 24 h VCG monitoring, 56 (29%) of the 195 patients had ST-vector magnitude (ST-VM) episodes of ischaemia. Seventy-four (38%) patients had a peak CK-MB value of 6 micrograms/l or higher during the 48 h sampling period. Several discrete variables were associated with death or non-fatal infarction at 1 year of follow-up in an univariate analysis. Among these were age > or = 65 years, female sex, St depression on the admission ECG or VCG monitoring, and elevated CK-MB levels, but neither the occurrence, duration nor intensity of chest pain. With Cox's proportional hazards regression analysis, ST-VM episodes on VCG monitoring were identified as independent markers of the risk of death (P = 0.013), death or non-fatal infarction (P = 0.035) and death, non-fatal infarction, unstable angina during the first year, or revascularization before hospital discharge (P = 0.005). CONCLUSIONS: VCG monitoring of ischaemia provides independent prognostic information in unstable angina. High-risk patients can easily be identified within 24 h of hospital admission. Whether early intervention based on these criteria will result in improved prognosis remains to be shown in future studies.

Adult

Long term follow up of patients with anterior myocardial infarction complicated by left ventricular thrombus in the thrombolytic era.

OBJECTIVES: To examine the appearance and resolution of left ventricular thrombi and to study the relation between thrombus and mortality during long term follow up after anterior myocardial infarction. DESIGN: Ninety nine consecutive patients were prospectively studied until the last included patient had been followed for one year. Streptokinase and aspirin were used routinely, anticoagulants only after a decision by the attending physician. Echocardiography was performed within 3 d of admission, before discharge, and after one, three, and 12 months. SETTING: Umeå University Hospital, a teaching hospital in Northern Sweden. MAIN OUTCOME MEASURES: Left ventricular thrombus, segmental myocardial function, and mortality during follow up. RESULTS: Thirty patients (30%) had a thrombus on discharge. One month, three months, and 12 months after hospital discharge, the thrombus had resolved in 81%, 84%, and 90% of the patients, respectively. The proportion of resolved thrombi at one month was high irrespective of whether anticoagulants were given (10/11, 91%) or not (12/16, 75%), P = 0.4. New thrombi appeared in 12 patients after discharge and resolution and reapperance of thrombi continued during the follow up period. Patients who developed a thrombus during the hospital stay (n = 44, 44%) had more extensive myocardial dysfunction on discharge (P < 0.001) and significantly higher mortality during the follow up period than those without a thrombus (23% v 7%, P < 0.01). CONCLUSIONS: With routine thrombolytic and aspirin treatment of anterior myocardial infarction, left ventricular thrombi usually resolve during the first month after hospital discharge. Appearance and resolution of thrombi continue, however, in a significant proportion of the patients during long term follow up. A left ventricular thrombus during the initial hospital stay is associated with high long term mortality.

Adult

Sleep-disordered breathing in men with coronary artery disease.

OBJECTIVE: To examine the occurrence of sleep apnea and nocturnal hypoxemia in men with symptomatic coronary artery disease (CAD) and to evaluate the relationship between disordered breathing and coronary artery disease. DESIGN: Case-control study. Cases were randomly selected from men undergoing coronary angiography because of angina pectoris. Controls were age matched and selected from the population registry. Pulse oximetry, oronasal thermistors, body position indicator, and recording of body and respiratory movements were used to quantify desaturations and apneas. SETTING: Norrland University Hospital, a referral center for northern Sweden. SUBJECTS: One hundred forty-two men with angina pectoris and angiographically verified CAD and 50 controls without known heart disease. MAIN OUTCOME MEASURES: The number of arterial oxygen desaturations of 4% or more per hour of sleep, oxygen desaturation index (ODI), and the number of apneas or hypopneas per hour of sleep, apnea-hypopnea index (AHI). RESULTS: Men with CAD had a high occurrence of sleep-disordered breathing measured as ODI of 5 or more, 39% (n=55), or AHI of 10 or more, 37% (n=50), while, the same proportions in controls were 22% (n=11, p<0.05) and 20% (n=10, p<0.05). Mean values of ODI in cases and controls were 6.4 and 2.7, respectively (p<0.001). Multiple logistic regression analysis identified ODI, AHI, body mass index, and hypertension as significant predictors of CAD (p<0.05). CONCLUSION: Sleep- disordered breathing is common in men with CAD. A significant association between sleep apnea with nocturnal hypoxemia and CAD remains after adjustment for age, hypertension, body mass index, diabetes, and smoking.

Adult

Glomerular filtration rate in primary Sjögren's syndrome with renal disease.

Renal disease in Primary Sjögren's syndrome (SS) is often overlooked, because of a paucity of symptoms. Distal renal tubular acidosis (dRTA) and tubulointerstitial nephritis (TIN) might be present. Only a few cases of SS with decreased glomerular filtration rate (GFR) have been reported. We have studied GFR in 27 female SS-patients, mean age 62 years (37-78). GFR was measured as the single injection 51Cr-EDTA plasma clearance. Eighteen women had normal GFR (group 1), and nine (33%) had values below the lower normal limit (group 2). In group 2, dRTA was present in 8/9 urolithiasis in 6/9, previous upper urinary tract infection (UTI) in 2/9 and TIN in 5/6 patients who were kidney biopsied. Among patients with dRTA 8/18 (44%) had decreased GFR. We conclude that decreased GFR is not unusual in SS-patients with dRTA, and decreased GFR is mostly associated with TIN. Urolithiasis and UTI may contribute to decreased GFR in some individuals.

Acidosis, Renal Tubular

Sleep-disordered breathing: a novel predictor of atrial fibrillation after coronary artery bypass surgery.

BACKGROUND: Sleep-disordered breathing is a common condition associated with nocturnal hypoxaemia, sympathetic activation and haemodynamic stress that can trigger arrhythmias. We examined whether preoperatively diagnosed disordered breathing was associated with an increased incidence of atrial fibrillation after coronary artery bypass surgery. METHODS: A sleep study was performed in 121 consecutive patients, who were monitored prospectively until discharge from hospital after surgery. Disordered breathing was defined as an apnoea-hypopnoea index (AHI) > or = 5 or an oxygen desaturation index (ODI) > or = 5. All episodes of atrial fibrillation requiring pharmacological intervention or cardioversion were included in the analysis. RESULTS: Atrial fibrillation was diagnosed in 32% of patient with AHI > or = 5 (25 of 78) and in 18% patients with AHI < 5 (7 of 39, P = 0.11). Similarly, atrial fibrillation was diagnosed in 39% of patients with ODI > or = 5 (19 of 49) and in 18% of patients with ODI < 5 (13 of 72, P = 0.02). In a multiple-logistic regression model including age, left ventricular function, aortic cross clamp time, maximum postoperative level of lactate dehydrogenase and disordered breathing (ODI > or = 5), greater age and disordered breathing were independent predictors of postoperative atrial fibrillation. The relative risk of atrial fibrillation was 2.0 (95% confidence interval 1.1-3.8) for a 10-year increase in age and 2.8 (95% confidence interval 1.2-6.8) for disordered breathing (ODI > or = 5). CONCLUSIONS: Pre-operatively diagnosed sleep-disordered breathing with nocturnal hypoxaemia is an independent predictor of atrial fibrillation after coronary bypass surgery.

Aged

Neurotoxicity of cysteine: interaction with glutamate.

L-Cysteine produces excitotoxic brain damage but its chemical structure differs from that of other excitotoxins. Although it is an NMDAmimetic, its mode of action is complex and may encompass antiexcitotoxic components. The purpose of the present study was to investigate whether cysteine kills neurons by potentiating the effects of glutamate and/or by releasing glutamate. In primary cultures of cortical neurons, 24 h of exposure to glutamate caused a concentration-dependent, dizocilpine-sensitive cell death as measured by release of lactate dehydrogenase. Cysteine was also toxic but higher concentrations were required. In addition, N-acetylcysteine produced mild toxicity at 1 mM. There was no general potentiation between either glutamate and cysteine or glutamate and N-acetylcysteine although some combinations acted synergistically. In no case did the thiols inhibit glutamate toxicity. The interaction between glutamate and cysteine toxicity was also assessed in the immature rat arcuate nucleus in vivo. When given at a dose (0.5 mg/g) that did not cause any toxicity per se, cysteine enhanced the toxicity of glutamate (0.3-0.8 mg/g). Cortical microdialysis was carried out in anesthetized rats (8-10 days old) administered a toxic dose of cysteine (1 mg/g). The levels of taurine were elevated 15-fold, phosphoethanolamine 3-fold and alanine 2-fold. Despite the observation that glutamine decreased markedly and rapidly, there was only a delayed doubling of glutamate concentrations. It is therefore unlikely that cysteine induces neurotoxicity by releasing glutamate. Taken together, the results suggest that there is a synergistic effect between cysteine and glutamate. Speculatively, this potentiation may be produced by reduction by cysteine of the redox site of the glutamate-activated NMDA receptor-ionophore complex.

Animals

Bioallethrin causes permanent changes in behavioural and muscarinic acetylcholine receptor variables in adult mice exposed neonatally to DDT.

We recently reported changes in the density of muscarinic acetylcholine receptors in cerebral cortex of mice treated neonatally with DDT (1,1,1-trichloro-2,2-bis(p-chlorophenyl)-ethane) and receiving bioallethrin as adults. We also found behavioural aberrations in adult mice treated with bioallethrin, whether neonatally treated with DDT or the vehicle. To ascertain whether these changes were permanent, 10-day-old mice received an oral dose of DDT (0.5 mg/kg body weight) and at the age of 5 months they received bioallethrin orally (0.7 mg/kg body weight/day; 7 days). The animals were investigated at the age of 7 months. Here we report muscarinic acetylcholine receptor changes, additional behavioural disturbances and learning disabilities in mice receiving DDT as neonates and bioallethrin as adults, whereas the behavioural disturbances in mice receiving vehicle as neonates and bioallethrin as adults had diminished and changes in proportions of high- and low-affinity binding sites had developed. No changes in the density of nicotinic acetylcholine receptors were noted for any of the treated groups. In conclusion, exposure of neonates to DDT leads to increased susceptibility in adults to a short-acting pesticide with similar neurotoxic action. An adult exposure to this short-acting pesticide to mice neonatally exposed to DDT leads to irreversible muscarinic acetylcholine receptor changes and behavioural disturbances with additional changes 2 months after the exposure.

Allethrins