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- Herlitz, Johan, et al.
(författare)
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A short delay from out of hospital cardiac arrest to call for ambulance increases survival
- 2003
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Ingår i: European Heart Journal. - : Oxford University Press. - 1522-9645 .- 0195-668X. ; 24:19, s. 1750-1755
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Tidskriftsartikel (refereegranskat)abstract
- Aim To describe the relative impact on survival of the delay from estimated time of collapse to call for an ambulance among patients who suffer from a bystander witnessed out of hospital cardiac arrest of a cardiac aetiology. Methods A majority of all ambulance organizations in Sweden (covering 85% of Sweden inhabitants) participate in a National survey of out of hospital cardiac arrest. Results In all there were 9340 patients with a bystander witnessed cardiac arrest of a cardiac aetiology in whom cardiopulmonary resuscitation (CPR) was attempted participating in this survey. Survival at one month among patients with a delay between estimated time of collapse and call for ambulance of less than or equal to4 min (median) was 6.9% versus 2.8% among patients with a median of >4 min (P<0.0001). When adjusting for age, sex, initial rhythm, estimated interval between collapse and start of CPR, place of arrest and the interval between call for ambulance and arrival of the rescue team, the odds ratio for survival was 0.70 (0.95% Cl. 0.58-0.84) per unit increase of the natural logarithm of delay in minutes between collapse and call. Conclusion Among patients with a bystander witnessed out of hospital cardiac arrest of a cardiac aetiology increased delay from estimated time of collapse to call for an ambulance decreased the chance of survival. (C) 2003 Published by Elsevier Ltd on behalf of The European Society of Cardiology.
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| 2. |
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| 3. |
- Aburawi, Elhadi, et al.
(författare)
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Relation of aortic root dilatation and age in Marfan's syndrome
- 2007
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Ingår i: European Heart Journal. - : Oxford University Press (OUP). - 1522-9645 .- 0195-668X. ; 28:3, s. 376-379
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Tidskriftsartikel (refereegranskat)abstract
- Aims The main aim of this study was to describe the age at which pathological aortic root dilation occurs in patients with Marfan's syndrome (MFS). Methods and results A total of 160 patients with MFS attending a regional cardiac centre were reviewed retrospectively. Dilation of the ascending aorta was diagnosed by comparing the maximum aortic sinus measurement with control data from the literature. We employed a Kaplan-Meier survival curve to estimate the age at which dilatation occurs. The mean age of the total group at presentation was 15.5 years (range 1.5-40 years). Skeletal abnormalities were present in 95%. Eye involvement was found in 18%. In the 115/160 patients with an abnormal aortic root, 78/115 (68%) developed aortic root dilatation before 19 years of age. From the Kaplan-Meier curve, it can be estimated that about 35% of the patients have aortic root dilatation already at the age of 5 years and 70% before the age of 20 years, and at least 80% by 40 years. There were 31 patients with normal aortic root when first seen but 24/31 (77%) developed aortic root dilatation before the age of 19 years and 7/31 (22.6%) after 19 years of age. Of those (seven patients) who developed new pathological aortic root dilatation after age 19 years, the age range was between 21 and 40 years with a mean of 27 years. Overall, 13 patients (8%) had surgery for aortic root replacement. Conclusion Aortic root dilatation develops early in MFS and was present in 35% by the age of 5 years and 68% by 19 years. Even though new aortic root dilation is relatively rare, it is not possible to safely discharge patients with MFS as about one-third of the patients in our series who developed new pathological aortic root dilation did so after the age of 19 years.
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| 4. |
- Allahyari, Ali, et al.
(författare)
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Application of the 2019 ESC/EAS dyslipidaemia guidelines to nationwide data of patients with a recent myocardial infarction : a simulation study
- 2020
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Ingår i: European Heart Journal. - : Oxford University Press (OUP). - 0195-668X .- 1522-9645. ; 41:40, s. 3900-3909
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Tidskriftsartikel (refereegranskat)abstract
- AIMS: To estimate the proportion of patients with a recent myocardial infarction (MI) who would be eligible for additional lipid-lowering therapy according to the 2019 European Society of Cardiology (ESC)/European Atherosclerosis Society (EAS) guidelines for the management of dyslipidaemias, and to simulate the effects of expanded lipid-lowering therapy on attainment of the low-density lipoprotein cholesterol (LDL-C) target as recommended by the guidelines.METHODS AND RESULTS: Using the nationwide SWEDEHEART register, we included 25 466 patients who had attended a follow-up visit 6-10 weeks after an MI event, 2013-17. While most patients (86.6%) were receiving high-intensity statins, 82.9% of the patients would be eligible for expanded lipid-lowering therapy, as they had not attained the target of an LDL-C level of <1.4 mmol and a ≥50% LDL-C level reduction. When maximized use of high-intensity statins followed by add-on therapy with ezetimibe was simulated using a Monte Carlo model, the LDL-C target was reached in 19.9% using high-intensity statin monotherapy and in another 28.5% with high-intensity statins and ezetimibe, while 50.7% would still be eligible for proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors. When use of alirocumab or evolocumab was simulated in those who were eligible for PCSK9 inhibitors, around 90% of all patients attained the LDL-C target.CONCLUSION : Our study suggests that, even with maximized use of high-intensity statins and ezetimibe, around half of patients with MI would be eligible for treatment with PCSK9 inhibitors according to the 2019 ESC/EAS guidelines. Considering the current cost of PCSK9 inhibitors, the financial implications of the new guidelines may be substantial.
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| 5. |
- Amisten, Stefan, et al.
(författare)
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Increased risk of acute myocardial infarction and elevated levels of C-reactive protein in carriersof the Thr-87 variant of the ATP receptor P2Y11.
- 2007
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Ingår i: European Heart Journal. - : Oxford University Press (OUP). - 1522-9645 .- 0195-668X. ; 28:1, s. 13-18
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Tidskriftsartikel (refereegranskat)abstract
- Aims Extracellular ATP acting on the P2Y(11) receptor regulates inflammatory cells. We hypothesized that polymorphisms in the receptor could influence the risk of acute myocardial infarction (AMI). Methods and results In the Malmo diet and cancer AMI case-control study (n = 3732) the P2Y(11) gene Thr-87 polymorphism was present in 19.8% of the controls and 22.9% in AMI patients (OR 1.21; P = 0.03). Stronger associations were found in patients with family history (FH) of AMI, 1.32; early-onset (EO) AMI, 1.43; or EO AMI combined with FH, 1.50; supporting a genetic mechanism. The Thr-87 homozygotes had an even greater risk of AMI, 1.94 (P = 0.04); and 2.48 in the EO AMI subgroup, suggesting a genetic dosage effect. In the cardiovascular risk factor group (n = 6055), 21.3% carried the Thr-87 allele. C-reactive protein was elevated in Thr-87 carriers: 1.6 mg/L vs. 1.3 mg/L (P = 0.001). No difference was seen for blood pressure, lipids, body mass index, smoking, or diabetes mellitus. Conclusion The common Ala-87-Thr polymorphism of the P2Y(11) receptor is associated with AMI and increased levels of C-reactive protein. We hypothesize that an inflammatory mechanism might be involved. The P2Y(11) receptor is a promising new drug target in the prevention of AMI.
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| 7. |
- Andersson, Tommy, 1970-, et al.
(författare)
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All-cause mortality in 272 186 patients hospitalized with incident atrial fibrillation 1995-2008 : a Swedish nationwide long-term case-control study
- 2013
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Ingår i: European Heart Journal. - : Oxford University Press (OUP). - 0195-668X .- 1522-9645. ; 34:14, s. 1061-1067
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Tidskriftsartikel (refereegranskat)abstract
- Aims To evaluate long-term all-cause risk of mortality in women and men hospitalized for the first time with atrial fibrillation (AF) compared with matched controls. Methods and results A total of 272 186 patients (44% women) <= 85 years at the time of hospitalization with incidental AF 1995-2008 and 544 344 matched controls free of in-hospital diagnosis of AF were identified. Patients were followed via record linkage of the Swedish National Patient Registry and the Cause of Death Registry. Using Cox regression models, the long-term relative all-cause mortality risk, adjusted for concomitant diseases, in women vs. controls was 2.15, 1.72, and 1.44 (P < 0.001) in the age categories <= 65, 65-74, and 75-85 years, respectively. The corresponding figures for men were 1.76, 1.36, and 1.24 (P < 0.001). Among concomitant diseases, neoplasm, chronic renal failure, and chronic obstructive pulmonary disease contributed most to the increased all-cause mortality vs. controls. In patients with AF as the primary diagnosis, the relative risk of mortality was 1.63, 1.46, and 1.28 (P < 0.001) in women and 1.45, 1.17, and 1.10 (P < 0.001) in men. Conclusion Atrial fibrillation was an independent risk factor of all-cause mortality in patients with incident AF. The concomitant diseases that contributed most were found outside the thromboembolic risk scores. The highest relative risk of mortality was seen in women and in the youngest patients compared with controls, and the differences between genders in each age category were statistically significant.
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| 9. |
- Ashar, Foram N., et al.
(författare)
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A comprehensive evaluation of the genetic architecture of sudden cardiac arrest
- 2018
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Ingår i: European Heart Journal. - : Oxford University Press. - 0195-668X .- 1522-9645. ; 39:44, s. 3961-
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Tidskriftsartikel (refereegranskat)abstract
- Aims: Sudden cardiac arrest (SCA) accounts for 10% of adult mortality in Western populations. We aim to identify potential loci associated with SCA and to identify risk factors causally associated with SCA.Methods and results: We carried out a large genome-wide association study (GWAS) for SCA (n = 3939 cases, 25 989 non-cases) to examine common variation genome-wide and in candidate arrhythmia genes. We also exploited Mendelian randomization (MR) methods using cross-trait multi-variant genetic risk score associations (GRSA) to assess causal relationships of 18 risk factors with SCA. No variants were associated with SCA at genome-wide significance, nor were common variants in candidate arrhythmia genes associated with SCA at nominal significance. Using cross-trait GRSA, we established genetic correlation between SCA and (i) coronary artery disease (CAD) and traditional CAD risk factors (blood pressure, lipids, and diabetes), (ii) height and BMI, and (iii) electrical instability traits (QT and atrial fibrillation), suggesting aetiologic roles for these traits in SCA risk.Conclusions: Our findings show that a comprehensive approach to the genetic architecture of SCA can shed light on the determinants of a complex life-threatening condition with multiple influencing factors in the general population. The results of this genetic analysis, both positive and negative findings, have implications for evaluating the genetic architecture of patients with a family history of SCA, and for efforts to prevent SCA in high-risk populations and the general community.
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