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Higher Life-Course Blood Pressure Associates With Reduced Myocardial Perfusion in Older Age: Insights From MyoFit46
Constantin-Cristian Topriceanu1,2,3,4, Matthew Webber1,2, Hunain Shiwani1,2,5
1Unit for Lifelong Health and Ageing at UCL (C.-C.T., M.W., H. Shiwani, F.C., E.M., D.F., M.A.S., J.B., H. Shah, S.D., A.W., R.H.D., N.C., A.D.H., G.C.), University College London, United Kingdom.
Insights
Higher blood pressure (BP) throughout life, especially steeper increases, is linked to reduced myocardial blood flow (MBF) later in life. This reduction in MBF is associated with increased risks of major adverse cardiovascular events and cardiac fibrosis.
Area of Science:
- Cardiovascular Medicine
- Cardiology
- Gerontology
Background:
- Elevated blood pressure (BP) is a significant risk factor for coronary artery disease.
- Understanding the long-term impact of BP trajectories on cardiac function is crucial for cardiovascular health.
- Life-course BP patterns may influence myocardial perfusion and reserve in later life.
Purpose of the Study:
- To investigate the association between life-course systolic and diastolic blood pressure patterns and myocardial perfusion in older adults.
- To determine how BP trajectories, including cumulative burden and rate of change, affect normalized stress myocardial blood flow (sMBFN) and perfusion reserve.
- To explore the relationship between these BP-related perfusion changes and major adverse cardiovascular events (MACE) and cardiac fibrosis.
Main Methods:
- The MyoFit46 study prospectively recruited participants from the 1946 birth cohort (≈77 years old).
- Cardiovascular magnetic resonance imaging was used to assess stress perfusion and late gadolinium enhancement.
- Life-course BP data (recorded at multiple ages) were analyzed to derive BP trajectories, including steepness and cumulative burden, using mixed-effects models.
Main Results:
- Higher systolic BP (SBP) between ages 36-69 was associated with lower sMBFN at age 77.
- Sustained higher SBP and steeper BP increases over time were linked to significantly reduced sMBFN.
- Each 1 mm Hg/year steeper SBP rise was associated with a 2-5% decrease in sMBFN, independent of baseline or final BP.
- Lower sMBFN was associated with increased odds of MACE and mediated the link between life-course SBP and late gadolinium enhancement.
Conclusions:
- Higher life-course BP, characterized by steeper increases and greater cumulative burden, is associated with reduced myocardial perfusion in older age.
- These perfusion deficits are linked to increased risks of major adverse cardiovascular events and cardiac fibrosis.
- The findings highlight the importance of monitoring BP trajectories for early detection and management of cardiovascular risk.
Background:
Elevated blood pressure (BP) is a major contributor to coronary artery disease. We explored the impact of life-course BP on later-life normalized stress myocardial blood flow (sMBFN) and myocardial perfusion reserve by cardiovascular magnetic resonance (CMR).
Methods:
MyoFit46 prospectively recruited ≈500 National Survey of Health and Development 1946 birth cohort participants, aged ≈77 years, to undergo stress perfusion and late gadolinium enhancement CMR. Systolic (SBPs) and diastolic BPs were recorded at 36, 43, 53, 63, 69, and 77 years. For each participant, the annual rates of BP change (steepness of BP increase) and area under the BP trajectory curve (cumulative life-course BP burden) were derived using mixed-effects models. The associations between BP measures and CMR metrics were tested using generalized linear and additive models, adjusted for antihypertensive use, demographics, lifestyle choices, and comorbidities. Cross-sectional associations between CMR metrics and major adverse cardiovascular events (myocardial infarction, stroke, and heart failure) were also tested. Mediation analyses explored the mechanistic pathways linking life-course BPs, myocardial perfusion, and myocardial fibrosis.
Results:
Among 459 included MyoFit46 participants, each 10 mm Hg higher SBP at 36 to 69 years was associated with 3% to 6% lower sMBFN by CMR at 77 years. At 43 to 63 years, as SBPs rose from 120 to 140 mm Hg, sMBFN was 18% to 24% lower. Having a sustained higher SBP by 10 mm Hg from 36 to 77 years was associated with 11% (95% CI, 8-14) lower sMBFN at 77 years. Each 1 mm Hg/y steeper SBP rise during age intervals 36 to 43, 43 to 53, 53 to 63, and 63 to 69 years was associated with 2% to 6% lower sMBFN at 77 years, associations not conditional on baseline or final BPs in each age interval. Associations may be clinically relevant as each 1% lower sMBFN was associated with 3% higher odds of major adverse cardiovascular events. sMBFN mediated ≈20% to ≈40% of the associations between life-course SBPs and late gadolinium enhancement at 77 years. Results were similar for diastolic BP, myocardial perfusion reserve, or sMBF (not normalized).
Conclusions:
Higher life-course BPs, steeper increases, and greater cumulative BP burden associate with lower myocardial perfusion by CMR at 77 years, which can be linked with higher odds of major adverse cardiovascular events and greater myocardial fibrosis burden. This underscores the importance of early life BP screening and guiding hyperetension treatment based on longitudinal BP trajectories (rather than relying solely on cross-sectional BPs).
Registration:
URL: https://www.clinicaltrials.gov; Unique identifier: NCT05455125.
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