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Reduced progression in carotid intima-media thickness was observed after dietary counselling, whereas omega-3 PUFA supplementation imposed a favourable effect on arterial elasticity.

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Background The evidence of the long-term effects of multiple lifestyle intervention on cardiovascular risk is uncertain. We aimed to summarize the evidence from randomized clinical trials examining the efficacy of lifestyle intervention on major cardiovascular risk factors in subjects at high cardiovascular risk. Methods Eligible trials investigated the impact of lifestyle intervention versus usual care with minimum 24 months follow-up, reporting more than one major cardiovascular risk factor. A literature search updated April 15, 2020 identified 12 eligible studies. The results from individual trials were combined, using fixed and random effect models, using the standardized mean difference (SMD) to estimate effect sizes. Small-study effect was evaluated, and heterogeneity between studies examined, by subgroup and meta-regression analyses, considering patient- and study-level variables. Results Small-study effect was not identified. Lifestyle intervention reduced systolic blood pressure modestly with an estimated SMD of − 0.13, 95% confidence interval (CI): − 0.21 to − 0.04, with moderate heterogeneity (I2 = 59%), corresponding to a mean difference of approximately 2 mmHg (MD = − 1.86, 95% CI − 3.14 to − 0.57, p = 0.0046). This effect disappeared in the subgroup of trials judged at low risk of bias (SMD = 0.02, 95% CI − 0.08 to 0.11). For the outcome total cholesterol SMD was − 0.06, 95% CI − 0.13 to 0.00, with no heterogeneity (I2 = 0%), indicating no effect of the intervention. Conclusion Lifestyle intervention resulted in only a modest effect on systolic blood pressure and no effect on total cholesterol after 24 months. Further lifestyle trials should consider the challenge of maintaining larger long-term benefits to ensure impact on cardiovascular outcomes.

Objectives. To evaluate the predictive ability of the previously published NORRISK 2 cardiovascular risk model in Norwegian-born and immigrants born in South Asia living in Norway, and to add information about diabetes and ethnicity in an updated model for South Asians and diabetics (NORRISK 2-SADia). Design. We included participants (30-74 years) born in Norway (n ¼ 13,885) or South Asia (n ¼ 1942) from health surveys conducted in Oslo 2000-2003. Cardiovascular disease (CVD) risk factor information including self-reported diabetes was linked with information on subsequent acute myocardial infarction (AMI) and acute cerebral stroke in hospital and mortality registry data throughout 2014 from the nationwide CVDNOR project. We developed an updated model using Cox regression with diabetes and South Asian ethnicity as additional predictors. We assessed model performance by Harrell's C and calibration plots. Results. The NORRISK 2 model underestimated the risk in South Asians in all quintiles of predicted risk. The mean predicted 13-year risk by the NORRISK 2 model was 3.9% (95% CI 3.7-4.2) versus observed 7.3% (95% CI 5.9-9.1) in South Asian men and 1.1% (95% CI 1.0-1.2) versus 2.7% (95% CI 1.7-4.2) observed risk in South Asian women. The mean predictions from the NORRISK 2-SADia model were 7.2% (95% CI 6.7-7.6) in South Asian men and 2.7% (95% CI 2.4-3.0) in South Asian women. Conclusions. The NORRISK 2-SADia model improved predictions of CVD substantially in South Asians, whose risks were underestimated by the NORRISK 2 model. The NORRISK 2-SADia model may facilitate more intense preventive measures in this high-risk population.