Cardiovascular risk is traditionally assessed using chronological age, yet individuals of the same age exhibit strikingly different risks of cardiac death. This discrepancy suggests that biological age-the cumulative imprint of genetic, environmental, and lifestyle exposures on the cardiovascular system-may be a more meaningful determinant of risk than calendar years alone.
In this project, we will use UK Biobank data to (1) derive and compare multiple biological age metrics (e.g. composite indices based on clinical biomarkers, imaging-derived cardiac structure and function, and other organ-system measures), and (2) evaluate their incremental value for predicting incident cardiac death beyond chronological age and conventional risk factors.
Our primary research question is: Which biological-age markers, or combinations thereof, best predict future cardiac death independently of chronological age? We will develop and validate biological age “clocks” and quantify their association with incident cardiac death using time-to-event models.
A secondary objective is to examine whether modifiable exposures and clinical interventions-including changes in lifestyle factors, pharmacotherapy, and major cardiovascular procedures-are associated with deceleration or partial reversal of these biological age clocks over follow-up. By linking longitudinal exposure patterns and clinical events to trajectories of biological age, we aim to explore whether early, targeted interventions can “slow” cardiovascular ageing in high-risk individuals.
This work will clarify the relative importance of biological versus chronological age for cardiac death, identify specific biological ageing signatures that are most informative for early prediction, and provide preliminary evidence on how primary and secondary prevention strategies may beneficially influence cardiovascular biological ageing.