Longitudinal assessment of inflammation in recipients of continuous-flow left ventricular assist devices.
BACKGROUND
The long-term effects of continuous-flow left ventricular assist device (CF-LVAD) support on trends of inflammatory markers over time are unknown. We examined the hypothesis that the levels of inflammatory markers in CF-LVAD recipients are higher than in healthy controls and that these levels increase over time with long-term CF-LVAD support.


METHODS
We examined the levels of inflammatory markers longitudinally at baseline before CF-LVAD implantation and at 3, 6, and 9 months after implantation. We then compared the levels of inflammatory markers to those in a healthy control group.


RESULTS
Compared with baseline values before CF-LVAD implantation, left ventricular end-diastolic diameter (LVEDd) and left ventricular end-systolic diameter (LVESd) decreased significantly at 3, 6, and 9 months after CF-LVAD implantation. Brain natriuretic peptide (BNP) levels dropped significantly after CF-LVAD implantation but did not normalize. Improvements in ejection fraction at 3, 6, and 9 months after CF-LVAD implantation did not reach significance. Monocyte chemoattractant protein-1, interferon γ-induced protein, and C-reactive protein levels were higher in the CF-LVAD recipients at each of the time points (baseline before CF-LVAD implantation and 3, 6, and 9 months after implantation) compared with levels in healthy controls. In CF-LVAD recipients, serum interleukin-8, tumour necrosis factor-α, and macrophage inflammatory protein-β increased significantly at 9 months, and macrophage-derived chemokine increased at 6 months after CF-LVAD implantation compared with baseline.


CONCLUSIONS
Despite improvements in LV dimensions and BNP levels, markers of inflammation remained higher in CF-LVAD recipients. High levels of inflammation in CF-LVAD recipients may result from heart failure preconditioning or the long-term device support, or both. Because inflammation may be detrimental to CF-LVAD recipients, future studies should determine whether inflammatory pathways are reversible.
Division of Cardiovascular Surgery, Peter Munk Cardiac Centre, University Health Network, University of Toronto, Toronto, Ontario, Canada; Faculty of Kinesiology and Physical Education, University of Toronto, Toronto, Ontario, Canada.
Liza
L
Grosman-Rimon
Faculty of Kinesiology and Physical Education, University of Toronto, Toronto, Ontario, Canada.
Ira
I
Jacobs
Division of Cardiovascular Surgery, Peter Munk Cardiac Centre, University Health Network, University of Toronto, Toronto, Ontario, Canada.
Laura C
LC
Tumiati
Division of Cardiovascular Surgery, Peter Munk Cardiac Centre, University Health Network, University of Toronto, Toronto, Ontario, Canada.
Michael A
MA
McDonald
Faculty of Kinesiology and Physical Education, University of Toronto, Toronto, Ontario, Canada.
Stacey Pollock
SP
Bar-Ziv
Division of Cardiovascular Surgery, Peter Munk Cardiac Centre, University Health Network, University of Toronto, Toronto, Ontario, Canada.
Avi
A
Fuks
Division of Cardiovascular Surgery, Peter Munk Cardiac Centre, University Health Network, University of Toronto, Toronto, Ontario, Canada.
Hiroyuki
H
Kawajiri
Division of Cardiovascular Surgery, Peter Munk Cardiac Centre, University Health Network, University of Toronto, Toronto, Ontario, Canada.
Julieta
J
Lazarte
Division of Cardiovascular Surgery, Peter Munk Cardiac Centre, University Health Network, University of Toronto, Toronto, Ontario, Canada.
Arash
A
Ghashghai
Division of Cardiovascular Surgery, Peter Munk Cardiac Centre, University Health Network, University of Toronto, Toronto, Ontario, Canada.
Daniel J
DJ
Shogilev
Division of Nephrology, University Health Network, University of Toronto, Toronto, Ontario, Canada.
David Z
DZ
Cherney
Division of Cardiovascular Surgery, Peter Munk Cardiac Centre, University Health Network, University of Toronto, Toronto, Ontario, Canada. Electronic address: vivek.rao@uhn.ca.
Vivek
V
Rao
D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood*; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D018932:Chemokine CCL2 / Q000097:blood; D005260:Female; D006333:Heart Failure / Q000097:blood* / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy*; D006353:Heart-Assist Devices; D006801:Humans; D007249:Inflammation / Q000097:blood*; D020382:Interleukin-18 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D045283:Natriuretic Agents / Q000097:blood; D020097:Natriuretic Peptide, Brain / Q000097:blood; D011237:Predictive Value of Tests; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D016277:Ventricular Function, Left
D015415:Biomarkers; D018932:Chemokine CCL2; D020382:Interleukin-18; D016209:Interleukin-8; D045283:Natriuretic Agents; D014409:Tumor Necrosis Factor-alpha; D020097:Natriuretic Peptide, Brain; D002097:C-Reactive Protein