The Effect of Blood Cell Count on Coronary Flow in Patients With Coronary Slow Flow Phenomenon

Abstract

Background and Objective: The coronary slow flow phenomenon (CSFP) is a coronary artery disease with a benign course, but its pathological mechanisms are not yet fully understood.The purpose of this controlled study was to investigate the cellular content of blood in patients diagnosed with CSFP and the relationship of this with coronary flow rates. Methods: Selective coronary angiographies of 3368 patients were analyzed to assess Thrombolysis in Myocardial Infarction (TIMI) frame count (TFC) values. Seventy eight of them had CSFP, and their demographic and laboratory findings were compared with 61 patients with normal coronary flow. Results: Patients’ demographic characteristics were similar in both groups. Mean corrected TFC (cTFC) values were significantly elevated in CSFP patients (p<0.001). Furthermore, hematocrit and hemoglobin values, and eosinophil and basophil counts of the CSFP patients were significantly elevated compared to the values obtained in the control group (p=0.005, p=0.047, p=0.001 and p=0.002, respectively). The increase observed in hematocrit and eosinophil levels showed significant correlations with increased TFC values (r=0.288 and r=0.217, respectively). Conclusion: Significant changes have been observed in the cellular composition of blood in patients diagnosed with CSFP as compared to the patients with normal coronary blood flow. The increases in hematocrit levels and in the eosinophil and basophil counts may have direct or indirect effects on the rate of coronary blood flow.

Immune cell subset differentiation and tissue inflammation

“…Eosinophils may exert their pro-atherosclerotic actions through proteins stored in prominent cytoplasmic granules, which may modulate the acute phase response and innate inflammatory response [ 130 ]. Similarly, basophils also promote atherosclerosis via these actions [ 131 ]. Mast cells are potent immune cells known for their functions in host defense responses and they drive the development of diseases such as asthma and allergies.…”

High absolute basophil count is a powerful independent predictor of inferior overall survival in patients with primary myelofibrosis

“…Basophils are circulating effector cells that harbor a large number of pro-inflammatory mediators inside metachromatic granules such as biogenic amines, leukotrienes and cytokines such as interleukin (IL)-4, IL-13 and granulocyte-macrophage colony-stimulating factor (GM-CSF) [30][31][32]. An increased number of circulating basophils can thus contribute to high inflammatory atmosphere characteristic for disease, might promote atherosclerosis [33] and potentiate development of constitutional symptoms as seen in our study. Our most interesting observation is the prognostic potential of ABC.…”

miRNA-22 as a Candidate Diagnostic Biomarker for Coronary Slow Flow

“…Although the pathophysiological mechanism of CSF remains unclear, several potential mechanisms have been suggested. Inflammation [32], vasoconstrictors [33], and even elevated levels of certain blood cells [34] may have direct and indirect effects on the process of CSF. Arksan et al found that serum neutrophil gelatinase-associated lipocalin level was elevated in CSF patients, which indicated that inflammation, especially active inflammation, played a very important role in the CSF process, as neutrophil gelatinase-associated lipocalin would be released after active inflammation, such as that in acute organ injury [32].…”

“…Zengin et al showed that serum urotensin-II levels were found to be significantly higher in the CSF group, suggesting that UII may be one of the factors involved in the pathogenesis of CSF [33]. Soylu et al indicated that increases in hematocrit levels and eosinophil and basophil counts may have direct or indirect effects on the rate of coronary blood flow [34]. Based on these three previous studies, the pathophysiological mechanism of CSF is still unclear and it seems impossible to explain the CSF process by only one mechanism.…”