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- 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. |
- Agewall, S, et al.
(författare)
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Levosimendan: perpetuum mobile?
- 2007
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Ingår i: European heart journal. - : Oxford University Press (OUP). - 0195-668X .- 1522-9645. ; 28:4, s. 515-515
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 6. |
- Almroth, Henrik, et al.
(författare)
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Atorvastatin and persistent atrial fibrillation following cardioversion : a randomized placebo-controlled multicentre study
- 2009
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Ingår i: European Heart Journal. - Philadelphia : Oxford University Press (OUP). - 0195-668X .- 1522-9645. ; 30:7, s. 827-833
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Tidskriftsartikel (refereegranskat)abstract
- AIMS: To evaluate the effect of atorvastatin in achieving stable sinus rhythm (SR) 30 days after electrical cardioversion (CV) in patients with persistent atrial fibrillation (AF). METHODS AND RESULTS: The study included 234 patients. The patients were randomized to treatment with atorvastatin 80 mg daily (n = 118) or placebo (n = 116) in a prospective, double-blinded fashion. Treatment was initiated 14 days before CV and was continued 30 days after CV. The two groups were well-balanced with respect to baseline characteristics. Mean age was 65 +/- 10 years, 76% of the patients were male and 4% had ischaemic heart disease. Study medication was well-tolerated in all patients but one. Before primary endpoint 12 patients were excluded. In the atorvastatin group 99 patients (89%) converted to SR at electrical CV compared with 95 (86%) in the placebo group (P = 0.42). An intention-to-treat analysis with the available data, by randomization group, showed that 57 (51%) in the atorvastatin group and 47 (42%) in the placebo group were in SR 30 days after CV (OR 1.44, 95%CI 0.85-2.44, P = 0.18). CONCLUSION: Atorvastatin was not statistically superior to placebo with regards to maintaining SR 30 days after CV in patients with persistent AF.
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| 7. |
- 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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