Steepness of blood pressure increase from 36 years and cumulative life-course blood pressure burden predict reduced myocardial perfusion at 76 years
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Authors
Topriceanu C.
Webber M.
Shiwani H.
Chan F.
Martin E.
Falconer D.
Bennett J.
Davies R.H.
Lambiase P.D.
Chaturvedi N.
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Issue Date
2026
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Conference Proceedings
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Background: High blood pressure (BP) leads to coronary artery disease, yet the impact of life-course BP on later-life myocardial blood flow (MBF) or perfusion reserve (MPR) remains elusive. Method(s): MyoFit46 prospectively undertook stress perfusion and late gadolinium enhancement (LGE) cardiovascular magnetic resonance (CMR) imaging in participants aged 76 years of the National Survey of Health and Development 1946 birth cohort. Global myocardial perfusion was quantified as stress MBF normalized (sMBFn) to contemporaneous rate pressure product (=heart rate x central aortic SBP SBP]) and MPR. BPs were recorded at 36, 43, 53, 62, 69, and 76 years. For each participant, we calculated using linear mixed-models the annual rates of BP change between any two ages (ie, steepness of BP increase) and the area under the BP trajectory curve (BP AUC) (ie, cumulative lifecourse BP burden). Participants were clustered based on their BP trajectories using latent class mixed models. Associations between these BP measures and CMR metrics were tested using generalized linear and additive models, adjusted for antihypertensive use, age, sex, body mass index, socio-economic position, smoking, exercise, and diabetes, recorded at the time of BP measurements. Mediation analyses explored mechanistic pathways. Result(s): 459 participants aged 76 (53% male) were included. After adjusting for confounders, each 10mmHg SBP increase at 36, 43, 53, 62, and 69 years associated with a 3-6% lower sMBFn at 76, independent of SBP at 76. For analyses at 43 to 62, the decrease in sMBFn was nonlinear and steeper as SBPs increased from 120 to 140mmHg, compared with 140 to 180mmHg (Figure 1). A sustained SBP increase by 10mmHg from 36 to 76 years associated with a 11% (95% CI 8, 14]) lower sMBFn at 76. Figure 2 shows exemplar CMR perfusion maps illustrating the effect of SBP AUC. Each 1 mmHg/year steeper SBP rise from 36 to 43, 43 to 53, 53 to 62, and 62 to 69 years, associated with 2-5% lower sMBFn at 76. No interactions between these rates of BP change and start or end BPs were found, meaning that steepess is an independent predictor of initial or final BPs. sMBFn mediated 20-40% of the SBPs and myocardial fibrosis by LGE associations. Results were similar when using MPR, sMBF (not normalized), after excluding those on antihypertensives, or after further adjusting for myocardial infarction (MI). Effect sizes were larger for diastolic BP. Looking at participant clusters based on BP trajectories, those with steepest BP increases from 36 to 53 years had the lowest myocardial perfusion and the highest risk of MI at 76 years. Conclusion(s): Higher life-course BP, steeper increases (regardless of final BP), and spending more years with a higher BP associate with lower myocardial perfusion in older-age, with midlife emerging as a particularly sensitive period. Individuals who experienced the steepest BP increase between 36 and 53 years had the lowest myocardial perfusion at 76. (Figure present).
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European Heart Journal Cardiovascular Imaging
Volume
27