Publication

Mechanisms underlying the J-curve for diastolic blood pressure: Subclinical myocardial injury and immune activation

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Last modified
  • 05/14/2025
Type of Material
Authors
    Matthew Topel, Emory UniversityPratik B. Sandesara, Emory UniversityEric Stahl, Emory UniversitySalim S. Hayek, Emory UniversityAyman Samman Tahhan, Emory UniversityWesley T. O'Neal, Emory UniversityYi-An Ko, Emory UniversityAyman Alkhoder, Emory UniversityMohamad Mazen Gafeer, Emory UniversityJonathan Kim, Emory UniversityPeter Wilson, Emory UniversityLeslee Shaw, Emory UniversityStephen E. Epstein, MedStar Washington Hospital CenterViola Vaccarino, Emory UniversityLaurence Sperling, Emory UniversityArshed Quyyumi, Emory University
Language
  • English
Date
  • 2019-02-01
Publisher
  • ELSEVIER IRELAND LTD
Publication Version
Copyright Statement
  • © 2018 Elsevier B.V.
License
Final Published Version (URL)
Title of Journal or Parent Work
Volume
  • 276
Start Page
  • 255
End Page
  • 260
Grant/Funding Information
  • MLT is supported by the National Institutes of Health (NIH) T32 THL130025A and the Abraham J. & Phyllis Katz Foundation grant (Atlanta, GA). AAQ is supported by grants 5P01HL101398–02, 1P20HL113451–01, 1R56HL126558–01, 1RF1AG051633–01, R01 NS064162–01, R01 HL89650–01, HL095479–01, 1U10HL110302–01, 1DP3DK094346–01, 2P01HL086773–06A1.
Supplemental Material (URL)
Abstract
  • Background: Low diastolic blood pressure (DBP) is associated with increased risk of cardiovascular events. In patients with coronary artery disease (CAD), limitations in coronary blood flow and immune activity are implicated mechanisms, but evidence is lacking. We investigated the association between DBP, biomarkers of myocardial injury, inflammation, immune activation and incident events in patients with CAD. Methods: We studied 2448 adults (mean age 65 ± 12 years, 68% male, median follow-up 4.5 years) with CAD. DBP was categorized into 10 mm Hg increments. Biomarkers of myocardial injury (high sensitivity cardiac troponin-I [hs-cTnI]) and immune activity/inflammation (soluble urokinase plasminogen activator receptor [suPAR]) were dichotomized at their median values. DBP 70–79 mm Hg was used as the referent group, and individuals were followed prospectively for adverse outcomes. Results: After adjusting for demographic and clinical covariates, individuals with DBP < 60 mm Hg had increased odds of elevated levels of hs-cTnI (OR = 1.68; 95% CI = 1.07, 2.65) and suPAR (OR = 1.71; 95% CI = 1.10, 2.65) compared to the referent group. Additionally, DBP < 60 mm Hg was associated with increased adjusted risk of cardiovascular death or MI (HR = 2.04; 95% CI = 1.32, 3.16) and all-cause mortality (HR = 2.41; 95% CI = 1.69, 3.45). Conclusion: In patients with CAD, DBP < 60 mm Hg is associated with subclinical myocardial injury, immune/inflammatory dysregulation and incident events. Aggressive BP control may be harmful in these patients, and further investigation is warranted to determine appropriate BP targets in patients with CAD.
Author Notes
  • Matthew Topel, MD, MSc, Division of Cardiology, Department of Medicine, Emory University School of Medicine, 1462 Clifton Rd. NE, Suite 513, Atlanta, GA 30322, Tel: (404) 712-0120, Fax: (404) 712-8785, mtopel@emory.edu
Keywords
Research Categories
  • Health Sciences, Medicine and Surgery
  • Biology, Anatomy
  • Biology, Biostatistics
  • Health Sciences, Public Health

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