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Circulating PCSK9 and Risk of Myocardial Infarction: The HUNT Study in Norway.

ABSTRACT: The usefulness of circulating proprotein convertase subtilisin-kexin type 9 (PCSK9) as a risk marker of coronary heart disease in the general population remains unclear. In a nested case-control study in Norway, 1,488 incident myocardial infarctions were registered during 11.3 years of follow-up and compared with 3,819 controls. Compared with participants in the lowest quartile of PCSK9, myocardial infarction risk was 47% higher in the highest quartile after adjustment for age and sex. After additional adjustment for low-density lipoprotein cholesterol, the association was strongly attenuated. Thus, circulating PCSK9 does not contribute useful information in the assessment of myocardial infarction risk in the general population beyond the information provided by lipid measurements.

SUBMITTER: Laugsand LE

PROVIDER: S-EPMC6113535 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature

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Circulating PCSK9 and Risk of Myocardial Infarction: The HUNT Study in Norway.

Laugsand Lars E LE Åsvold Bjørn O BO Vatten Lars J LJ Janszky Imre I Platou Carl G CG Michelsen Annika E AE Damås Jan K JK Aukrust Pål P Ueland Thor T

JACC. Basic to translational science 20161130 7

The usefulness of circulating proprotein convertase subtilisin-kexin type 9 (PCSK9) as a risk marker of coronary heart disease in the general population remains unclear. In a nested case-control study in Norway, 1,488 incident myocardial infarctions were registered during 11.3 years of follow-up and compared with 3,819 controls. Compared with participants in the lowest quartile of PCSK9, myocardial infarction risk was 47% higher in the highest quartile after adjustment for age and sex. After add ...[more]

PMID: 30167541

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| S-EPMC6512140 | biostudies-literature

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Genetic risk score associations for myocardial infarction are comparable in persons with and without rheumatoid arthritis: the population-based HUNT study.

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| S-EPMC3778278 | biostudies-literature

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Educational inequalities in acute myocardial infarction incidence in Norway: a nationwide cohort study.

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Project description:AimTo evaluate whether history of pregnancy complications [pre-eclampsia, gestational hypertension, preterm delivery, or small for gestational age (SGA)] improves risk prediction for cardiovascular disease (CVD).Methods and resultsThis population-based, prospective cohort study linked data from the HUNT Study, Medical Birth Registry of Norway, validated hospital records, and Norwegian Cause of Death Registry. Using an established CVD risk prediction model (NORRISK 2), we predicted 10-year risk of CVD (non-fatal myocardial infarction, fatal coronary heart disease, and non-fatal or fatal stroke) based on established risk factors (age, systolic blood pressure, total and HDL-cholesterol, smoking, anti-hypertensives, and family history of myocardial infarction). We evaluated whether adding pregnancy complication history improved model fit, calibration, discrimination, and reclassification. Among 18 231 women who were parous, ≥40 years of age, and CVD-free at start of follow-up, 39% had any pregnancy complication history and 5% experienced a CVD event during a median follow-up of 8.2 years. While pre-eclampsia and SGA were associated with CVD in unadjusted models (HR 1.96, 95% CI 1.44-2.65 for pre-eclampsia and HR 1.46, 95% CI 1.18-1.81 for SGA), only pre-eclampsia remained associated with CVD after adjusting for established risk factors (HR 1.60, 95% CI 1.16-2.17). Adding pregnancy complication history to the established prediction model led to small improvements in discrimination (C-index difference 0.004, 95% CI 0.002-0.006) and reclassification (net reclassification improvement 0.02, 95% CI 0.002-0.05).ConclusionPre-eclampsia independently predicted CVD after controlling for established risk factors; however, adding pre-eclampsia, gestational hypertension, preterm delivery, and SGA made only small improvements to CVD prediction among this representative sample of parous Norwegian women.

| S-EPMC6451770 | biostudies-literature

Low grade albuminuria as a risk factor for subtypes of stroke - the HUNT Study in Norway.

Project description:BACKGROUND AND PURPOSE:Albuminuria is a marker for endothelial dysfunction and knowledge on its association with stroke and stroke subtypes are limited. METHODS:Corresponding data from 7261 participants of the population-based HUNT2 study (1995-1997) was linked with hospital records, identified all patients registered and diagnosed with a first-time stroke. Each diagnosis was validated by reviewal of the medical record appertaining to the individual. We then applied Cox proportional hazard models to estimate the hazard ratios (HRs) for the association between albuminuria (measured as albumin-to-creatinine-ratio, ACR) and diagnosis of stroke and stroke subtypes. RESULTS:703 (9.7%) participants developed a first ischemic stroke during a median follow-up of 15 years. Higher albuminuria was associated with a higher rate for ischemic stroke and the risk rose steadily with increasing ACR (15% increment per unit increase in ACR concentration in mg/mmol). In the fully adjusted model, the HR for all ischemic strokes was 1.56 (95% CI 1.24-1.95) for those with an ACR ≥3 mg/mmol compared to participants with an ACR < 1 mg/mmol. Overall, increasing ACR was associated with a higher risk of all ischemic stroke subtypes. This was seen to be strongest for lacunar stroke (HR 1.75, CI 1.12-2.72, p = 0.019), and also for stroke of undetermined etiology (HR 1.53, CI 1.11-2.11, p = 0.009) and those caused by atherosclerosis in the large arteries (HR 1.51, CI 0.78-2.94, p = 0.186) than for cardio-embolic stroke (HR 1.22, CI 0.64-2.3, p = 0.518). CONCLUSIONS:Albuminuria is an important risk factor, potentially already at low grade, for ischemic stroke especially for lacunar subtype. Measuring albuminuria is both cheap and readily available. This offers the opportunity to evaluate the risk for endothelial dysfunction and thus the subsequent risk for stroke and cerebral small vessel disease.

| S-EPMC7196218 | biostudies-literature

Mannose-binding lectin deficiency is associated with myocardial infarction: the HUNT2 study in Norway.

Project description:OBJECTIVES: Mannose-binding lectin (MBL) and ficolins activate the complement cascade, which is involved in atherogenesis. Based on a pilot study, we hypothesized that functional polymorphisms in the MBL gene (MBL2) leading to dysfunctional protein are related to development of myocardial infarction (MI). The aim of the present study was to study polymorphisms in MBL2 and ficolin genes in relation to the risk of MI. METHODS AND RESULTS: Using the population-based HUNT Study in Norway, 57,133 persons were followed up for a first-time MI from 1995-1997 until the end of 2008. The 370 youngest MI patients were matched by age (range 29-62 years) and gender to 370 controls. A younger population was selected because disease in this group might be less dependent on non-genetic risk factors. The study size was based on power calculation. Polymorphisms in MBL2 and in the genes of ficolin-1, ficolin-2 and ficolin-3 were genotyped by pyrosequencing and related to the risk of MI, estimated as odds ratios (OR). Functional haplotypes were analyzed and stringent alpha levels of significance were set by permutation testing. Variant MBL2 haplotypes causing MBL deficiency were associated with a two-fold higher risk of MI (OR 2.04, 95%CI 1.29-3.24). Adjustments for conventional cardiovascular risk factors did not substantially influence the association. The ficolins were not associated with MI risk. CONCLUSION: In a young to middle aged and relatively healthy Caucasian population, MBL2 variants related to functional MBL deficiency were associated with a doubling of the risk for MI, independent of conventional risk factors. This supports that MBL deficiency may lead to increased atherosclerosis or development of vulnerable plaques.

| S-EPMC3407165 | biostudies-literature

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