Open heart · 2026
Association of Life's Simple 7 with metabolic-associated steatotic liver disease and non-invasive fibrosis markers.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Hofer Hannah, Wernly Sarah, Semmler Georg, Flamm Maria, Völkerer Andreas, Singhartinger Franz, Jung Christian, Erkens Ralf, Ausserwinkler Mathias, Aigner Elmar, Datz Christian, Wernly Bernhard
Аннотация
BACKGROUND: Metabolic-associated steatotic liver disease (MASLD) is a prevalent chronic liver disease affecting approximately a third of the global population. Early identification is critical for timely intervention, yet effective screening tools remain limited. The American Heart Association's Life's Simple 7 (LS7), originally developed to assess cardiovascular health, captures several metabolic domains that overlap with the diagnostic criteria of MASLD. Consequently, observed associations between LS7 and MASLD are expected to partly reflect shared metabolic components rather than independent risk prediction.
METHODS: We analysed data from 3204 participants undergoing screening colonoscopy in the Salzburg Colon Cancer Prevention Initiative (Sakkopi). LS7 was derived from seven modifiable lifestyle factors (smoking, body mass index, blood pressure, cholesterol, fasting glucose, physical activity and diet). MASLD was assessed using abdominal ultrasonography, while liver fibrosis was evaluated through non-invasive markers (Aspartate Aminotransferase to Platelet Ratio Index and transient elastography). Poisson regression with robust SEs was used to estimate risk ratios (RRs) for MASLD and liver fibrosis across LS7 categories (poor: 0-4, intermediate: 5-9, ideal: 10-14), adjusting for age, sex and socioeconomic status.
RESULTS: MASLD prevalence was highest in individuals with poor LS7 (82%) compared with those with intermediate (47%) and ideal (16%) scores. Higher LS7 was significantly associated with a lower risk of MASLD (RR 0.80; 95% CI 0.79 to 0.82; p<0.001) and liver fibrosis after adjustment for confounders.
CONCLUSION: LS7 showed a strong association with MASLD and hepatic steatosis, while associations with non-invasive fibrosis markers were weaker and marker-dependent, underscoring the close interplay between cardiometabolic health and liver disease. Future studies should evaluate whether changes in LS7 over time are associated with longitudinal changes in hepatic steatosis and fibrosis-related outcomes.
METHODS: We analysed data from 3204 participants undergoing screening colonoscopy in the Salzburg Colon Cancer Prevention Initiative (Sakkopi). LS7 was derived from seven modifiable lifestyle factors (smoking, body mass index, blood pressure, cholesterol, fasting glucose, physical activity and diet). MASLD was assessed using abdominal ultrasonography, while liver fibrosis was evaluated through non-invasive markers (Aspartate Aminotransferase to Platelet Ratio Index and transient elastography). Poisson regression with robust SEs was used to estimate risk ratios (RRs) for MASLD and liver fibrosis across LS7 categories (poor: 0-4, intermediate: 5-9, ideal: 10-14), adjusting for age, sex and socioeconomic status.
RESULTS: MASLD prevalence was highest in individuals with poor LS7 (82%) compared with those with intermediate (47%) and ideal (16%) scores. Higher LS7 was significantly associated with a lower risk of MASLD (RR 0.80; 95% CI 0.79 to 0.82; p<0.001) and liver fibrosis after adjustment for confounders.
CONCLUSION: LS7 showed a strong association with MASLD and hepatic steatosis, while associations with non-invasive fibrosis markers were weaker and marker-dependent, underscoring the close interplay between cardiometabolic health and liver disease. Future studies should evaluate whether changes in LS7 over time are associated with longitudinal changes in hepatic steatosis and fibrosis-related outcomes.