Abstract 4365796: Cumulative Life-course Blood Pressure Burden and Steepness of Increase Are Associated with Reduced Myocardial Perfusion in Older Age: Insights from MyoFit46
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
Authors (19)
Constantin-Cristian Topriceanu
University College London, London, United Kingdom
Matthew Webber
University College London, London, United Kingdom
Hunain Shiwani
University College London, London, United Kingdom
Fiona Chan
University College London, London, United Kingdom
Emma Martin
Centre for Inflammation Research
Debbie Falconer
University College London, London, United Kingdom
Jonathan Bennett
University College London, London, United Kingdom
Pablo Gonzalez Martin
University College London, London, United Kingdom
Haytham Shah
University College London, London, United Kingdom
Andrew Wong
Iain Pierce
Barts Heart Centre, London, United Kingdom
Rhodri Davies
University College London, London, United Kingdom
Pier Lambiase
Heart Hospital, UCL, London, United Kingdom
Nishi Chaturvedi
Peter Kellman
NIH, BETHESDA, Maryland, United States
Rebecca Hardy
James Moon
Barts Heart Centre, London, United Kingdom
Alun Hughes
University College London, London, United Kingdom
Gabriella Captur
University College London, London, United Kingdom