Clin Res Cardiol 107, Suppl 1, April 2018 |
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Maturating B lymphocytes in the setting of acute myocardial infarction |
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R. Feldtmann1, A. Kümmel1, E. Abdiu1, B. Chamling1, S. B. Felix1, R. Busch1, A. Strohbach1 | ||
1Klinik und Poliklinik für Innere Medizin B, Universitätsmedizin Greifswald, Greifswald; | ||
Objective: Acute myocardial infarction (MI) is
typically caused by an abrupt blockage of a coronary artery, leading to
necrosis of the affected heart tissue. Immediately, distinct leukocyte cell
populations infiltrate the injured heart. B cells have come to the forefront as
viable targets in various autoimmune diseases, which are associated with
increased cardiovascular risk. Here, we address the role of different
maturating B cells which orchestrate a variety of adaptive immune responses
relevant to human diseases, but that has relatively been neglected in the
setting of ischemic injury.
Methods: We quantified the number of different maturating B cell subpopulations in arterial blood of 31 patients (23% women) with acute MI who were 66±15 years old. The study population included 14 patients with ST-segment elevation MI (STEMI) who were 64±14 years old and 17 patients with non-ST-segment elevation MI (NSTEMI) who were 68±15 years old. Myocardial ischemia was determined by coronary angiography. The left ventricular ejection fraction averaged 53% (range of 40-60%) in STEMI and 57% (range of 38-63%) in NSTEMI patients. Absolute cell counts were assessed in whole blood, drawn from the arterial port prior to coronary intervention, by multi-color FACS analysis. Mature CD19+ B cells were further subdivided in CD19+/IgD+/CD27- naïve B cells, CD19+/IgD+/CD27-/CD38++/CD24++ transitional B cells, CD19+/IgD-/CD27++ plasma cells, and CD19+/IgD+/CD27+ memory B cells. Absolute quantification was achieved by means of blood analysis. Results were correlated with plasma markers of severity of myocardial damage. Additionally, 10 healthy individuals (30% women) were included who were 57±7 years old. The study was approved by the local institutional review board, and participants provided witnessed, written informed consent. Results: Overall, the number of CD19+ B cells was significantly increased in STEMI patients compared to healthy controls (31.9±6.2 x104 versus 13.6±3.3 x104 cells/mL; p=0.026) and NSTEMI group (31.9±6.2 x104 versus 15.9±2.1 cells/mL; p=0.016). Linear regression analysis was performed to correlate total B cell counts with troponin I and creatine kinase plasma levels in MI patients. The multivariate regression model comprised sex, age, current smoking, symptom duration, leukocyte count, and CRP-levels and revealed a strong correlation of the CD19+ B cell counts with the markers of the severity of infarction (ß-coefficients are given in table 1). Further investigation of B cell subpopulations revealed a continuously increased number of cells in STEMI patients compared to healthy individuals and to NSTEMI group (table 1). Noteworthy, only naïve B cells and memory cells show a correlation to troponin I (Pearson r=0.770; p=0.0005 and r=0.717; p=0.0058, respectively) and creatine kinase (Pearson r=0.827; p=0.0005 and r=0.717; p=0.0058, respectively), indicating a prevalent role for these subsets in myocardial damage after MI. Finally, the number of memory cells correlates to the 6 months probability of death from admission, which was calculated from the GRACE Score (Pearson r=0.609; p=0.0466). Conlusion: Our data indicate a potential relation of elevated B cell counts with adverse outcomes in patients with acute MI. How B cells contribute to the injured heart itself is an area of future investigations.Table 1 |
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http://www.abstractserver.de/dgk2018/jt/abstracts//V824.htm |