Article Text

37 Dynamic Changes in T-Lymphocyte Counts Following Primary Percutaneous Coronary Intervention Predict Infarct Size and Microvascular Obstruction
  1. Stephen Boag1,
  2. Evgeniya Schmeleva1,
  3. Rajiv Das2,
  4. Mohaned Egred2,
  5. Azfar Zaman2,
  6. Alan Bagnall2,
  7. W Andrew Owens1,
  8. Bernard Keavney1,
  9. Javed Ahmed2,
  10. Ioakim Spyridopoulos1
  1. 1Newcastle University
  2. 2Freeman Hospital


Introduction Although primary percutaneous coronary intervention (PPCI) has revolutionised treatment of myocardial infarction, ischaemia-reperfusion (I/R) injury remains an important complication. Microvascular obstruction (MVO) is one component of I/R injury, and is of prognostic significance independent of infarct size. We have previously demonstrated changes in T-lymphocyte counts in the blood following PPCI for STEMI. The goal of this study was to investigate a potential role for T-cells in myocardial I/R injury.

Methods We analysed blood from 38 STEMI patients undergoing PPCI. Samples were taken at the start of the procedure and at 15, 30, 90 min, and 24 h post reperfusion. In 6 patients with anterior infarcts, coronary sinus (CS) blood was also obtained at 30–60 min, along with simultaneous aortic blood. Differential leucocyte counts, including detailed lymphocyte subsets, were obtained using 8 colour flow cytometry. Cardiac MRI was performed at 1–7 days, and infarct size, MVO (on late gadolinium enhancement images), area at risk (on T2-weighted STIR images) and salvage index quantified.

Results Different leucocyte populations displayed characteristic dynamic changes in their cell counts following reperfusion. T-lymphocytes dropped between 0 and 90 min by a mean of 33% (0min mean 1520 cells/μl, 90min mean 918/μl), followed by recovery until 24 h (mean 1630/μl). Changes in CD8 T-cells were greater than CD4 T-cells (mean 0–90min drop and 90min-24hr increase: 45% and 128% respectively for CD8s, 24% and 75% for CD4s). In both CD4 and CD8 T-cells, the more highly differentiated CCR7- subpopulations (effector memory and TEMRA cells) displayed greater changes than CCR7+ cells (naive and central memory) e.g. 0–90min drop for CD8 naive: 19%, CD8 TEMRA: 53%.

The increase in total T-cell and CD4 T-cell count between 90 min and 24hrs correlated in infarct size (total T-cells: r = 0.482, p < 0.01, CD4 T-cells: r = 0.521, p < 0.01) and negatively with salvage index (total T-cells: r = -0.481, p = 0.03, CD4 T-cells: r = -0.495, p = 0.02). MVO, however, showed a very strong relationship with the drop between 15 and 30 min post reperfusion (total T cells: r = -0.711, p < 0.001, CD4: r = -0.711, p < 0.001, CD8: r = -0.664, p < 0.001).

Simultaneous CS and aortic sampling in a subset of anterior STEMIs (n = 6) demonstrated a significant drop in total T-cells (mean drop 3.5%) and CD4 T-cells (3.3%) across the coronary circulation.

Conclusions Acute dynamics in T-cell counts following PPCI for STEMI predict infarct size, salvage index and MVO. In particular, the strong correlation between MVO and early changes following reperfusion suggest a possible mechanistic link. The presence of a trans-coronary gradient in total T-cell and CD4 T-cell counts suggests that some of these cells may be sequestered into the reperfused myocardium, where they contribute to I/R injury. This provides the first evidence in humans of a role for T-cells in myocardial I/R injury.

  • Myocardial infarction
  • Lymphocytes
  • Ischaemia-reperfusion injury

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