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Tytuł pozycji:

Inflammation, non-endothelial dependent coronary microvascular function and diastolic function-Are they linked?

Tytuł :
Inflammation, non-endothelial dependent coronary microvascular function and diastolic function-Are they linked?
Autorzy :
Suhrs HE; Department of Cardiology, Bispebjerg Hospital, University of Copenhagen, Copenhagen, Denmark.
Schroder J; Department of Cardiology, Bispebjerg Hospital, University of Copenhagen, Copenhagen, Denmark.
Bové KB; Department of Cardiology, Bispebjerg Hospital, University of Copenhagen, Copenhagen, Denmark.
Mygind ND; Department of Cardiology, Bispebjerg Hospital, University of Copenhagen, Copenhagen, Denmark.; Department of Cardiology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Frestad D; Department of Cardiology, Hvidovre Hospital, University of Copenhagen, Copenhagen, Denmark.
Michelsen MM; Department of Cardiology, Bispebjerg Hospital, University of Copenhagen, Copenhagen, Denmark.
Lange T; Department of Public Health, Section of Biostatistics, University of Copenhagen, Copenhagen, Denmark.; Center for Statistical Science, Peking University, Beijing, China.
Gustafsson I; Department of Cardiology, Bispebjerg Hospital, University of Copenhagen, Copenhagen, Denmark.
Kastrup J; Department of Cardiology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Prescott E; Department of Cardiology, Bispebjerg Hospital, University of Copenhagen, Copenhagen, Denmark.
Pokaż więcej
Źródło :
PloS one [PLoS One] 2020 Jul 16; Vol. 15 (7), pp. e0236035. Date of Electronic Publication: 2020 Jul 16 (Print Publication: 2020).
Typ publikacji :
Journal Article; Research Support, Non-U.S. Gov't
Język :
English
Imprint Name(s) :
Original Publication: San Francisco, CA : Public Library of Science
MeSH Terms :
Coronary Circulation*
Diastole*
Stroke Volume*
Angina Pectoris/*epidemiology
Coronary Vessels/*physiopathology
Inflammation/*physiopathology
Adult ; Aged ; Aged, 80 and over ; Angina Pectoris/etiology ; Angina Pectoris/metabolism ; Angina Pectoris/pathology ; Biomarkers/metabolism ; Case-Control Studies ; Cross-Sectional Studies ; Female ; Follow-Up Studies ; Humans ; Inflammation/metabolism ; Inflammation Mediators/metabolism ; Male ; Middle Aged ; Prognosis
References :
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Substance Nomenclature :
0 (Biomarkers)
0 (Inflammation Mediators)
Entry Date(s) :
Date Created: 20200717 Date Completed: 20200917 Latest Revision: 20200917
Update Code :
20201023
PubMed Central ID :
PMC7365405
DOI :
10.1371/journal.pone.0236035
PMID :
32673354
Czasopismo naukowe
Purpose: Systemic inflammation and coronary microvascular dysfunction (CMD) may be causal drivers of heart failure with preserved ejection fraction (HFpEF). We tested the hypothesis that subclinical inflammation is associated with non-endothelial dependent CMD and diastolic dysfunction.
Methods: In a cross-sectional study of 336 women with angina but no flow limiting coronary artery stenosis (180 with diabetes) and 95 asymptomatic controls, blood samples were analysed for 90 biomarkers of which 34 were part of inflammatory pathways. CMD was assessed as coronary flow velocity reserve (CFVR) by transthoracic Doppler echocardiography and defined as CFVR<2.5. We used E/e' as an indicator of diastolic function in age-adjusted linear regressions to assess correlations between biomarkers, CFVR and diastolic function.
Results: CMD was found in 59% of participants whereas only 4% fulfilled strict criteria for diastolic dysfunction. Thirty-five biomarkers, 17 of them inflammatory, were negatively correlated with CFVR and 25, 15 inflammatory, were positively correlated with E/e'. A total of 13 biomarkers, 9 inflammatory, were associated with both CFVR and E/e'. CFVR and E/e' were only correlated in the subgroup of patients with CMD and signs of increased filling pressure (E/e'>10) (p = 0.012).
Conclusion: This is the first study to link a large number of mainly inflammatory biomarkers to both CMD and E/e', thus confirming a role of inflammation in both conditions. However, despite a high prevalence of CMD, few patients had diastolic dysfunction and the data do not support a major pathophysiologic role of non-endothelial dependent CMD in diastolic dysfunction.
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