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ACC 2025: Lifetime Benefit by Control of Modifiable Risk Factors
Published: 03 Apr 2025
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ACC 2025 - Individual-level data collected across 126 worldwide cohorts show controlling modifiable cardiovascular risk factors can potentially benefit life-years for freedom from CVD and death from any cause.
Prof Christina Magnussen (University Heart and Vascular Centre Hamburg, Hamberg, DE) joins us onsite at ACC to discuss modifiable cardiovascular risk factors collected by the Global Cardiovascular Risk Consortium, enrolling over 2 million participants from 133 cohorts across 39 countries and 8 geographic regions.
The study aims to estimate sex-specific lifetime risk for CVD and death, provide the estimated mean lifetime difference between those with and without classical risk factors, evaluate the lifetime difference related to risk factor modification and identify the most useful regional targets for effective primary prevention strategies. The five classical risk factors included arterial hypertension, hyperlipidemia, underweight or overweight/obesity, current smoking and diabetes.
Findings showed that even among those with none of the classical risk factors, the lifetime risk for CVD remained substantial, at 13% in women and 21% in men. The abscence of these risk factors at age 50 was associated with over a decade greater life expectancy than those who had all five risk factors in both sexes. Modification of arterial hypertension from present to absent during midlife was related to the most additional life-years for freedom from CVD.
Interview Questions:
1. What is the importance behind the data collection?
2. What were the key findings?
3. How should your research impact clinical practice?
4. What are the next steps for the Global Cardiovascular Risk Consortium in expanding this research?
Recorded on-site at ACC in Chicago, 2025.
Editors: Yazmin Sadik, Jordan Rance
Videographers: Tom Green, David Ben-Harosh
Support: This is an independent interview produced by Radcliffe CVRM.
I'm Christina Magnussen. I'm Professor of Cardiology in the Department of Cardiology at the University Medical Centre Hamburg.
What is the importance behind the data collection?
So we performed a real global study which summarises more than two million individual-level data from 133 cohorts out of 39 countries.
What were the key findings?
So the two key findings were in the absence of the classical risk factors—arterial hypertension, hyperlipidemia, abnormal weight, current smoking and diabetes—that was related to a lifetime difference, so to a more than one decade longer life expectancy compared to individuals having all these risk factors.
Additionally, the modification of arterial hypertension and smoking was related to the most additional life years, especially for CVD, but also for death from any cause.
How should your research impact clinical practice?
So our study calls for very effective primary prevention strategies because we could show that the lifetime risk for CVD was substantial at 13% in women and 21% in men, even if no risk factor was present.
And our study also calls for specific prevention strategies, especially modification of hypertension and smoking during midlife, as these risk factors or modification of these risk factors was associated with the most additional life years.
And we also wanted to get a paradigm shift from just recognising risk towards the potential of the association of risk factors with additional life years. So to improve the self empowerment of an individual.
What are the next steps for the Global Cardiovascular Risk Consortium in expanding this research?
In the first paper that was published in the New England Journal in 2023, we could show that the five risk factors account of 50% of cardiovascular disease. In this New England Journal paper, we could show that the absence of the five risk factors was related to a lifetime difference of more than a decade.
And our next question will be, what is the residual risk? So if the five risk factors explain about 50% of cardiovascular diseases, which are the factors that explain the residual risk? Are there any exposomal or genetic factors that could also be made responsible for a CVD risk?
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