Acute aortic dissection (AAD) causes transient inflammation with occasional pleural fluid (PF) accumulation. Although pentraxin 3 (PTX3) is a vascular inflammation-related biomarker, little is known about PTX3 levels in patients with AAD. We explored the serial changes in plasma PTX3 levels and the association of peak levels with the amount of PF accumulation. Consecutive patients (n = 41) with Stanford type B AAD were enrolled, and blood samples for the measurements of serum albumin, plasma PTX3 and high-sensitivity C-reactive protein (CRP) were collected daily until 7 days after symptom onset. PF accumulation on computed tomography imaging on the third hospital day was divided into 3 grades (I: none or slight, II: mild in the uni- or bilateral pleural cavity, III: moderate or more). PTX3 and CRP levels were analyzed after logarithmic transformation because of their skewed distributions. Peak PTX3 and CRP levels were observed at 4.3 ± 2.1 and 4.7 ± 2.0 days after symptom onset, and their values were 12.2 [interquartile range (IQR), 8.2-20.9] ng/mL and 12.0 (IQR, 8.6-15.2) mg/dL, respectively. On univariate analysis, the peak level of PTX3 had a negative correlation with the minimum level of serum albumin, and a positive correlation with PF grade and duration of intensive care unit stay. On multivariate analysis, the peak level of PTX3 was correlated with PF grade (P = 0.037). In conclusion, the peak level of PTX3 in patients with AAD was associated with the amount of transient PF accumulation, which may be associated with inflammatory vascular permeability.
Fractional flow reserve (FFR) is considered as the gold standard for physiological assessment of coronary artery stenosis. However, it may be difficult to interpret FFR for the stenosis of the donor artery of chronic total occlusion (CTO), because revascularization of CTO may improve FFR of the donor artery. We present a case of 32-year-old male who had a CTO in right coronary artery (RCA), 90% stenoses in left circumflex artery (LCx) and a mild stenosis in the middle segment of left anterior descending artery (LAD). FFR for the mild stenosis in LAD showed significant value (0.72). However LAD was the donor artery to CTO of RCA, revascularization to RCA was expected to improve FFR for LAD. As the patient had chronic granulocytic leukemia and the difficulty in continuing dual antiplatelet therapy, we selected coronary artery bypass grafting (CABG) to RCA and LCx, and we decided not to perform anastomosis to LAD. Although each graft was patent and collateral flow from LAD to RCA disappeared after CABG, FFR for LAD was still 0.72. Careful consideration should be given when interpreting FFR for the donor artery to a CTO lesion. When CABG is selected, it may be a practical approach to revascularize not only CTO but also FFR positive mild stenosis simultaneously, even though it appears angiographically mild stenosis.
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