Abstract 4365796: Cumulative Life-course Blood Pressure Burden and Steepness of Increase Are Associated with Reduced Myocardial Perfusion in Older Age: Insights from MyoFit46

C Constantin-Cristian Topriceanu (University College London, London, United Kingdom) M Matthew Webber (University College London, London, United Kingdom) H Hunain Shiwani (University College London, London, United Kingdom) F Fiona Chan (University College London, London, United Kingdom) E Emma Martin (Centre for Inflammation Research) D Debbie Falconer (University College London, London, United Kingdom) J Jonathan Bennett (University College London, London, United Kingdom) P Pablo Gonzalez Martin (University College London, London, United Kingdom) H Haytham Shah (University College London, London, United Kingdom) A Andrew Wong I Iain Pierce (Barts Heart Centre, London, United Kingdom) R Rhodri Davies (University College London, London, United Kingdom) P Pier Lambiase (Heart Hospital, UCL, London, United Kingdom) N Nishi Chaturvedi P Peter Kellman (NIH, BETHESDA, Maryland, United States) R Rebecca Hardy J James Moon (Barts Heart Centre, London, United Kingdom) A Alun Hughes (University College London, London, United Kingdom) G Gabriella Captur (University College London, London, United Kingdom)

Abstract

Background: High blood pressure (BP) leads to coronary artery disease. Aim: We explored the impact of life-course BP, especially the steepness of BP increase and cumulative BP burden, on later-life stress myocardial blood flow (sMBF) and perfusion reserve (MPR) by cardiovascular magnetic resonance (CMR). Methods: MyoFit46 prospectively undertook stress perfusion and late gadolinium enhancement (LGE) CMR at age 76 in age-matched participants of the National Survey of Health and Development 1946 birth cohort. Myocardial perfusion was quantified as global sMBF normalized (sMBF N ) to contemporaneous rate pressure product (heart rate x central aortic BP) and MPR. Systolic (SBPs) and diastolic BPs (DBPs) were recorded at 36, 43, 53, 62, 69, and 76 years. For each participant, annual rates of BP change (steepness) and the area under the BP trajectory curve (AUC BP ; cumulative burden) were calculated using mixed-effect models. Participants were clustered by BP trajectory using latent class mixed models. Associations between BP and CMR metrics were tested using generalized models, adjusted for antihypertensive use, demographics, lifestyle, and comorbidities. Mediation analyses explored mechanistic pathways. Results: Among 459 participants (53% male), each 10mmHg SBP increase at 36, 43, 53, 62, and 69 years associated with a 3-6% lower sMBF N at 76. For midlife BPs (43-62 years), associations were independent of SBP at 76 and the decrease in sMBF N was steepest as SBPs rose from 120 to 140mmHg ( Figure 1 ). Having a sustained higher SBP by 10mmHg from 36 to 76 years associated with an 11% (95% CI: 8-14) lower sMBF N . Exemplar CMR perfusion maps based on AUC SBP are shown in Figure 2 . Each 1 mmHg/year steeper SBP rise during age intervals 36–43, 43–53, 53–62, and 62–69 was associated with a 2–5% lower sMBF N at age 76, independent of baseline or final BPs in each interval. sMBF N mediated 20-40% of the life-course SBPs and myocardial fibrosis by LGE associations. Results were similar for DBP, MPR, or unnormalized sMBF. Participants with the steepest BP rises from 36 to 53 years had the lowest myocardial perfusion at 76 ( Figure 3 ). Conclusion: Higher life-course BPs (even from age 36), steeper increases (regardless of final BP), and more years spent at higher BP levels associate with lower myocardial perfusion in older age. This underscores the importance of early-life BP screening, guiding treatment based on BP trajectories and cumulative burden, and rigorous midlife BP control.

Article Details

Journal Circulation
Volume / Issue Vol. 152, Issue Suppl_3
Published November 04, 2025
ISSN 0009-7322
Publisher Lippincott Williams & Wilkins

Journal Info

Circulation

Lippincott Williams & Wilkins

ISSN: 0009-7322 Health Sciences

Authors (19)

C

Constantin-Cristian Topriceanu

University College London, London, United Kingdom

M

Matthew Webber

University College London, London, United Kingdom

H

Hunain Shiwani

University College London, London, United Kingdom

F

Fiona Chan

University College London, London, United Kingdom

E

Emma Martin

Centre for Inflammation Research

D

Debbie Falconer

University College London, London, United Kingdom

J

Jonathan Bennett

University College London, London, United Kingdom

P

Pablo Gonzalez Martin

University College London, London, United Kingdom

H

Haytham Shah

University College London, London, United Kingdom

A

Andrew Wong

I

Iain Pierce

Barts Heart Centre, London, United Kingdom

R

Rhodri Davies

University College London, London, United Kingdom

P

Pier Lambiase

Heart Hospital, UCL, London, United Kingdom

N

Nishi Chaturvedi

P

Peter Kellman

NIH, BETHESDA, Maryland, United States

R

Rebecca Hardy

J

James Moon

Barts Heart Centre, London, United Kingdom

A

Alun Hughes

University College London, London, United Kingdom

G

Gabriella Captur

University College London, London, United Kingdom