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.
Original language | English (US) |
---|---|
Pages (from-to) | 255-260 |
Number of pages | 6 |
Journal | International Journal of Cardiology |
Volume | 276 |
DOIs | |
State | Published - Feb 1 2019 |
Externally published | Yes |
Keywords
- Blood pressure
- Coronary artery disease
- High-sensitivity troponin
- J-curve
- Soluble urokinase plasminogen activator receptor
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
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Topel, M. L., Sandesara, P. B., Stahl, E. P., Hayek, S. S., Tahhan, A. S., O'Neal, W. T., Ko, Y. A., Alkhoder, A., Gafeer, M. M., Kim, J. H., Wilson, P. W. F., Shaw, L. J., Epstein, S. E., Vaccarino, V., Sperling, L. S., & Quyyumi, A. A. (2019). Mechanisms underlying the J-curve for diastolic blood pressure: Subclinical myocardial injury and immune activation. International Journal of Cardiology, 276, 255-260. https://doi.org/10.1016/j.ijcard.2018.09.028
Mechanisms underlying the J-curve for diastolic blood pressure: Subclinical myocardial injury and immune activation. / Topel, Matthew L.; Sandesara, Pratik B.; Stahl, Eric P. et al.
In: International Journal of Cardiology, Vol. 276, 01.02.2019, p. 255-260.
Research output: Contribution to journal › Article › peer-review
Topel, ML, Sandesara, PB, Stahl, EP, Hayek, SS, Tahhan, AS, O'Neal, WT, Ko, YA, Alkhoder, A, Gafeer, MM, Kim, JH, Wilson, PWF, Shaw, LJ, Epstein, SE, Vaccarino, V, Sperling, LS & Quyyumi, AA 2019, 'Mechanisms underlying the J-curve for diastolic blood pressure: Subclinical myocardial injury and immune activation', International Journal of Cardiology, vol. 276, pp. 255-260. https://doi.org/10.1016/j.ijcard.2018.09.028
Topel ML, Sandesara PB, Stahl EP, Hayek SS, Tahhan AS, O'Neal WT et al. Mechanisms underlying the J-curve for diastolic blood pressure: Subclinical myocardial injury and immune activation. International Journal of Cardiology. 2019 Feb 1;276:255-260. doi: 10.1016/j.ijcard.2018.09.028
Topel, Matthew L. ; Sandesara, Pratik B. ; Stahl, Eric P. et al. / Mechanisms underlying the J-curve for diastolic blood pressure : Subclinical myocardial injury and immune activation. In: International Journal of Cardiology. 2019 ; Vol. 276. pp. 255-260.
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title = "Mechanisms underlying the J-curve for diastolic blood pressure: Subclinical myocardial injury and immune activation",
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.",
keywords = "Blood pressure, Coronary artery disease, High-sensitivity troponin, J-curve, Soluble urokinase plasminogen activator receptor",
author = "Topel, {Matthew L.} and Sandesara, {Pratik B.} and Stahl, {Eric P.} and Hayek, {Salim S.} and Tahhan, {Ayman Samman} and O'Neal, {Wesley T.} and Ko, {Yi An} and Ayman Alkhoder and Gafeer, {Mohamad Mazen} and Kim, {Jonathan H.} and Wilson, {Peter W.F.} and Shaw, {Leslee J.} and Epstein, {Stephen E.} and Viola Vaccarino and Sperling, {Laurence S.} and Quyyumi, {Arshed A.}",
note = "Publisher Copyright: {\textcopyright} 2018 Elsevier B.V.",
year = "2019",
month = feb,
day = "1",
doi = "10.1016/j.ijcard.2018.09.028",
language = "English (US)",
volume = "276",
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TY - JOUR
T1 - Mechanisms underlying the J-curve for diastolic blood pressure
T2 - Subclinical myocardial injury and immune activation
AU - Topel, Matthew L.
AU - Sandesara, Pratik B.
AU - Stahl, Eric P.
AU - Hayek, Salim S.
AU - Tahhan, Ayman Samman
AU - O'Neal, Wesley T.
AU - Ko, Yi An
AU - Alkhoder, Ayman
AU - Gafeer, Mohamad Mazen
AU - Kim, Jonathan H.
AU - Wilson, Peter W.F.
AU - Shaw, Leslee J.
AU - Epstein, Stephen E.
AU - Vaccarino, Viola
AU - Sperling, Laurence S.
AU - Quyyumi, Arshed A.
N1 - Publisher Copyright:© 2018 Elsevier B.V.
PY - 2019/2/1
Y1 - 2019/2/1
N2 - 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.
AB - 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.
KW - Blood pressure
KW - Coronary artery disease
KW - High-sensitivity troponin
KW - J-curve
KW - Soluble urokinase plasminogen activator receptor
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