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- Al-Khalili, F, et al.
(författare)
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Prognostic value of exercise testing in women after acute coronary syndromes (The Stockholm Female Coronary Risk Study)
- 2000
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Ingår i: American Journal of Cardiology. - Karolinska Hosp, Dept Cardiol, S-17176 Stockholm, Sweden. Karolinska Hosp, Dept Publ Hlth Sci, Div Prevent Med, S-17176 Stockholm, Sweden. Karolinska Inst, Stockholm, Sweden. : EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC. - 0002-9149 .- 1879-1913. ; 86:2, s. 211-213
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Tidskriftsartikel (refereegranskat)
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| 4. |
- Engdahl, J, et al.
(författare)
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Can we define patients with no and those with some chance of survival when found in asystole out of hospital?
- 2000
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Ingår i: American Journal of Cardiology. - : Excerpta Medica, Inc.. - 0002-9149 .- 1879-1913. ; 86:6, s. 610-614
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Tidskriftsartikel (refereegranskat)abstract
- We describe the epidemiology, prognosis, and circumstances at resuscitation among a consecutive population of patients with out-of-hospital cardiac arrest (OHCA) with asystole as the arrhythmia first recorded by the Emergency Medical Service (EMS), and identify factors associated with survival. We included all patients in the municipality of Göteborg, regardless of age and etiology, who experienced an OHCA between 1981 and 1997. There were a total of 4,662 cardiac arrests attended by the EMS during the study period. Of these, 1,635 (35%) were judged as having asystole as the first-recorded arrhythmia: 156 of these patients (10%) were admitted alive to hospital, and 32 (2%) were discharged alive. Survivors were younger (median age 58 vs 68 years) and had a witnessed cardiac arrest more often than nonsurvivors (78% vs 50%). Survivors also had shorter intervals from collapse to arrival of ambulance (3.5 vs 6 minutes) and the mobile coronary care unit (MCCU) (5 vs 10 min), and they received atropine less often on scene. There were also a greater proportion of survivors with noncardiac etiologies of cardiac arrest (48% vs 27%). Survivors to discharge also displayed higher degrees of consciousness on arrival to the emergency department in comparison to nonsurvivors. Multivariate analysis among all patients with asystole indicated age (p = 0.01) and witnessed arrest (p = 0.03) as independent predictors of an increased chance of survival. Multivariate analysis among witnessed arrests indicated short time to arrival of the MCCU (p < 0.001) and no treatment with atropine (p = 0.05) as independent predictors of survival. Fifty-five percent of patients discharged alive had none or small neurologic deficits (cerebral performance categories 1 or 2). No patients > 70 years old with unwitnessed arrests (n = 211) survived to discharge.
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- Olsson, Anders, et al.
(författare)
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Effect of rosuvastatin on low-density lipoprotein cholesterol in patients with hypercholesterolemia
- 2001
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Ingår i: American Journal of Cardiology. - 0002-9149 .- 1879-1913. ; 88:5, s. 504-508
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Tidskriftsartikel (refereegranskat)abstract
- Rosuvastatin is a new, synthetic, orally active statin, with marked low-density lipoprotein (LDL) cholesterol-lowering activity. We conducted 2 dose-ranging studies. In the first study, after a 6-week dietary run-in, 142 moderately hypercholesterolemic patients were randomized equally to receive double-blind placebo or rosuvastatin 1, 2.5, 5, 10, 20, or 40 mg or open-label atorvastatin 10 or 80 mg once daily for 6 weeks, in the second study, conducted to extend the rosuvastatin dose range, 64 patients were randomized to double-blind, once-daily placebo or rosuvastatin 40 or 80 mg (1:1:2 ratio) for 6 weeks. Data from both studies were combined for analysis of lipid effects. No statistical comparison of atorvastatin arms with placebo or rosuvastatin was performed. Rosuvastatin was associated with highly significant dose-dependent reductions in LDL cholesterol compared with placebo (p <0.001), decreases ranged from 34% (1 mg) to 65% (80 mg). Linear regression analysis indicated an additional 4.5% LDL cholesterol reduction for each doubling of the rosuvastatin dose. Across the dose range, approximately 90% of LDL cholesterol reduction occurred within the first 2 weeks of treatment. Significant, dose-dependent reductions in total cholesterol and apolipoprotein B with rosuvastatin were also observed (p <0.001). High-density lipoprotein cholesterol increases and triglyceride reductions were consistently observed and statistically significant at some dose levels. All lipid ratios were significantly reduced at all rosuvastatin dose levels (p <0.001). Adverse events were similar across placebo and active treatments. No significant increases in alanine aminotransferase or creatine kinase were seen in any patient. Over 6 weeks, rosuvastatin produced large, rapid, dose-dependent LDL cholesterol reductions and was well tolerated in hypercholesterolemic patients. © 2001 by Excerpta Medica, Inc.
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| 7. |
- Pedersen, T.R., et al.
(författare)
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Follow-up study of patients randomized in The Scandinavian Simvastatin Survival Study (4S) of cholesterol lowering
- 2000
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Ingår i: American Journal of Cardiology. - 0002-9149 .- 1879-1913. ; 86:3, s. 257-262
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Tidskriftsartikel (refereegranskat)abstract
- The Scandinavian Simvastatin Survival Study (4S) and other randomized clinical trials have demonstrated that cholesterol-lowering treatment with statins improves prognosis in patients with coronary atherosclerosis compared with placebo. The effect of therapy with statins beyond the typical 5 to 6 years' duration of the trials, in particular regarding the risk of cancer, has not been investigated. This study examines the long-term effects of simvastatin for up to 8 years on cause-specific mortality in patients with coronary heart disease (CHD). We performed an observational, government registry-based study of mortality in the groups originally randomized to simvastatin or placebo in the 4S over an additional 2-year follow-up period, so that the median total follow-up period was 7.4 years (range 6.9 to 8.3 in surviving patients). Randomization took place at outpatient clinics at 94 clinical centers in Denmark, Finland, Iceland, Norway, and Sweden from 1988 to 1989. Of 4,444 patients with CHD, 2,223 and 2,221 were randomized to treatment with placebo or simvastatin therapy, respectively. Patients received treatment with simvastatin, starting at 20 mg/day, with titration to 40 mg/day at 12 or 24 weeks if total cholesterol was >5.2 mmol/L (200 mg/dl), or placebo. After the double-blind period, most patients in both treatment groups received simvastatin as open-label prescription. Of the 1,967 patients originally treated with placebo and surviving the double-blind period, 97 (4.9%) died during the following 2 years. In the group randomized to simvastatin the corresponding number was 74 of the 2,039 survivors (3.6%). Adding these deaths to those occurring during the original trial, the total was 353 (15.9%) and 256 (11.5%) deaths in the groups originally randomized to placebo and simvastatin, respectively. The relative risk was 0.70 (95% confidence interval 0.60 to 0.82, p = 0.00002). The total number of cancer deaths was 68 (3.1%) in the placebo group and 52 (2.3%) in the simvastatin group (relative risk 0.73, 95% confidence interval 0.51 to 0.05, p = 0.087), and the numbers of noncardiovascular and other deaths were similar in both groups. We therefore conclude that treatment with simvastatin for up to 8 years in patients with CHD is safe and yields continued survival benefit. Copyright (C) 2000 Excerpta Medica Inc.
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| 8. |
- Sutherland, George, et al.
(författare)
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Quantitation of left-ventricular asynergy by cardiac ultrasound
- 2000
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Ingår i: American Journal of Cardiology. - 0002-9149 .- 1879-1913. ; 86:4, s. 4-9
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Tidskriftsartikel (refereegranskat)abstract
- The clinical evaluation of regional delays in myocardial motion (myocardial asynchrony) has proved problematic, yet it remains an important functional parameter to evaluate. Prior attempts to quantify regional asynergy have met with limited success, often thwarted by the low temporal resolution of imaging-system data acquisition. If a delay in onset of motion of 30–40 msec is clinically important to measure, then data acquisition at frame rates of 50–100 per second is required. This is out of the current temporal resolution of angiographic, nuclear, or magnetic resonance studies. Only cardiac ultrasound can currently achieve the necessary frame rates. Furthermore, quantitative studies into the accuracy with which a trained observer can identify computed regional myocardial asynchrony in a left-ventricular 2-dimensional (2-D) image have shown that regional delays of <80 msec are not normally recognized in a moving image. This may be improved to 60 msec when either training is undertaken or comparative image review is used. However, this is still out of the temporal resolution required in clinical practice. Thus, visual interpretation of asynchrony is not sufficiently accurate. Two ultrasound data sets based on either integrated backscatter or Doppler myocardial imaging data may provide the solution. Doppler myocardial imaging is a new ultrasound technique which, in either its pulsed or color Doppler format, can achieve the required temporal resolution (with temporal resolutions of 8 msec and 16 msec, respectively). In contrast, color Doppler myocardial imaging, in its curved M-mode format, can display the timing of events during the cardiac cycle for all in-plane myocardial segments. This should allow the quantitation of regional delay for all systolic and diastolic events. Potentially, asynchrony due to regional ischemia, bundle branch block, ventricular premature beats, and ventricular preexcitation could all be identified and the degree of delay quantified. This overview will aim to establish the potential role of these new ultrasound methodologies in the recognition and quantitation of left-ventricular asynergy and how they might best be introduced into clinical practice.
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