PubMed · 3982629
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
P Lasjaunias, K TerBrugge, M Chiu. 1985. Dural AVM.. https://doi.org/10.1097/00006123-198503000-00029
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Statins lower low-density lipoprotein cholesterol and are widely used for the prevention of atherosclerotic cardiovascular disease. Whether statin-induced low-density lipoprotein reduction increases risk of intracerebral haemorrhage has been debated for almost two decades. Here, we explored whether genetically predicted on-statin low-density lipoprotein response is associated with intracerebral haemorrhage risk using Mendelian randomization. Using genomic data from randomized trials, we derived a polygenic score from 35 single nucleotide polymorphisms of on-statin low-density lipoprotein response and tested it in the population-based UK Biobank. We extracted statin drug and dose information from primary care data on a subset of 225 195 UK Biobank participants covering a period of 29 years. We validated the effects of the genetic score on longitudinal low-density lipoprotein measurements with generalized mixed models and explored associations with incident intracerebral haemorrhage using Cox regression analysis. Statins were prescribed at least once to 75 973 (31%) of the study participants (mean 57 years, 55% females). Among statin users, mean low-density lipoprotein decreased by 3.45 mg/dl per year [95% confidence interval (CI): (-3.47, -3.42)] over follow-up. A higher genetic score of statin response [1 standard deviation (SD) increment] was associated with significant additional reductions in low-density lipoprotein levels [-0.05 mg/dl per year, (-0.07, -0.02)], showed concordant lipidomic effects on other lipid traits as statin use and was associated with a lower risk for incident myocardial infarction [hazard ratio per SD increment 0.98 95% CI (0.96, 0.99)] and peripheral artery disease [hazard ratio per SD increment 0.93 95% CI (0.87, 0.99)]. Over a 11-year follow-up period, a higher genetically predicted statin response among statin users was associated with higher intracerebral haemorrhage risk in a model adjusting for statin dose [hazard ratio per SD increment 1.16, 95% CI (1.05, 1.28)]. On the contrary, there was no association with intracerebral haemorrhage risk among statin non-users (P = 0.89). These results provide further support for the hypothesis that statin-induced low-density lipoprotein reduction may be causally associated with intracerebral haemorrhage risk. While the net benefit of statins for preventing vascular disease is well-established, these results provide insights about the personalized response to statin intake and the role of pharmacological low-density lipoprotein lowering in the pathogenesis of intracerebral haemorrhage.
This review details the evidence that the risk of stroke is increased in the peripartum and postpartum period rather than the entire 9 months of pregnancy. In women with prior stroke, available evidence suggests that the excess risk of a stroke recurrence in pregnancy is approximately 1% to 2%. Although certain conditions have a particularly strong association with stroke in pregnancy, such as eclampsia, or with the postpartum period, such as cerebral venous thrombosis, the clinical and therapeutic approach to women with stroke during pregnancy should be similar to the approach to stroke in young adults. Strategies for stroke prevention should take into account the competing risks to mother and fetus.
OBJECTIVE: To compare the survival and short term morbidity of all New Zealand very low birthweight (VLBW) infants born in two epochs, 1986 and 1998-1999. SETTING: All level III and level II neonatal intensive care units (NICUs) in New Zealand. METHODS: In 1986, data were prospectively collected for a study of retinopathy of prematurity (ROP). In 1998-1999, prospective data were collected by the Australian and New Zealand Neonatal Network (ANZNN). Both cohorts included all VLBW infants born during the calendar year and admitted to a NICU. Data were collected from birth until discharge home or death. RESULTS: More VLBW infants were admitted for care in 1998-1999 (n = 1084, 0.96% of livebirths) than in 1986 (n = 413, 0.78% of livebirths; p < 0.001), including a higher proportion of VLBW infants of < 1000 g birth weight (38% v 32% respectively; p < 0.05). Survival to discharge home increased from 81.8% in 1986 to 90.3% in 1998-1999 (p < 0.001). The 1998-1999 cohort had a higher proportion of infants born in a hospital with a level III NICU (87% v 72% in 1986; p < 0.001) and receiving antenatal corticosteroids (80% v 58% in 1986; p < 0.001). In 1998-1999, the incidence of several morbidities had decreased compared with 1986, including oxygen dependency at 28 days (29% v 39% respectively; p = 0.001) and at 36 weeks postmenstrual age (16% v 23%; p = 0.002), grade 1 intraventricular haemorrhage (IVH) (8% v 24%; p < 0.001), grade 2/3 IVH (5% v 11%; p < 0.001), and stage 3/4 ROP for infants < 1000 g (6% v 13%; p < 0.001). CONCLUSIONS: The outlook for VLBW infants in New Zealand has improved since 1986.