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. 2016 Apr 27;30(8):2792–2801. doi: 10.1096/fj.201500155R

TABLE 2.

Human plasma LMs from patients with CAD

LM Q1 Q3 CAD CAD + Lovaza
DHA bioactive metabolome
 RvD1 375 215
 RvD2 375 215
 RvD3 375 181
 RvD5 359 199
 RvD6 359 159 11.0 ± 3.4 22.5 ± 4.6
 AT-RvD1 375 141 14.6 ± 2.7 12.9 ± 2.6
 AT-RvD3 375 181 7.1 ± 3.7
 PD1 359 153
 AT-PD1 359 153 3.0 ± 0.5 6.0 ± 1.9
 MaR1 359 250
EPA bioactive metabolome
 RvE1 349 161
 RvE2 333 115 8.2 ± 8.2 44.8 ± 38.6
 RvE3 333 201 69.0 ± 11.6 61.7 ± 2.8
Arachidonic acid bioactive metabolome
 LXA4 351 115
 LXB4 351 115 453.9 ± 88.4 369.3 ± 105.2
 5S,15S-diHETE 335 235 45.0 ± 4.1 48.2 ± 10.5
 AT-LXA4 351 115
 AT-LXB4 351 221 20.5 ± 4.3
 LTB4 335 195
 PGD2 351 189 1.7 ± 0.2 0.9 ± 0.5
 PGE2 351 189 3.1 ± 0.3 1.7 ± 0.9
 PGF 353 193 3.1 ± 0.7 1.0 ± 0.5
 TxB2 369 169 3.2 ± 1.6 2.1 ± 1.4

Results are expressed as picograms per milliliter; means ± sem; n = 3. Limit of detection, ∼0.1 pg. Human plasma from patients with CAD who received aspirin or aspirin and Lovaza (3360 mg EPA and DHA daily for 1 yr) were extracted, and LM levels were investigated by LM metabololipidomics (see Materials and Methods for details). 5S,15S-diHETE, 5S,15S‐dihydroxy‐eicosatetraenoic acid; LTB4, leukotriene B4; TxB2, thromboxane B2; Q1, M-H (parent ion); Q3, diagnostic ion in the MS-MS (daughter ion). LMs with no CAD value are below the limit of detection. Those SPMs absent in patients with CAD who did not receive Lovaza were present in healthy volunteers from a prior study that used analysis conditions identical to those of the current report, with the exception of PD1, MaR1, LXA4, and AT-LXA4, which were absent in both healthy volunteers and patients with CAD (21).