Changes in coagulation condition, cytokine, adhesion molecule after repair of type A aortic dissection.
OBJECTIVE
Because residual dissection often exists even after the repair of a type A dissection, we evaluated coagulation conditions, cytokine levels, and adhesion molecule levels in mid-term follow up after repair of type A dissections.


METHODS
Thrombin-antithrombin III complex (TAT), D-dimer, soluble interleukin-2 receptor (sIL-2R), soluble intercellular adhesion molecule (sICAM)-1, and type III procollagen peptide (PIIIP) were measured in 12 patients (mean age=63 years) following the repair of a type A aortic dissection at 6-82 months after repair (median=33 months).


RESULTS
In the chronic phase, TAT and D-dimer were significantly higher in patients following the repair of a type A dissection compared to healthy controls (TAT; 12+/-8 vs. 2.5+/-1.2 ng/ml, P = 0.0001, D-dimer; 779+/-1384 vs. 104+/-46 U/ml, P = 0.0001). Cytokine was significantly higher in the affected patients (sIL-2R; 556+/-205 vs. 398+/-132 U/ml, P = 0.003, sICAM-1; 255+/-131 vs. 211+/-48 ng/ml, P = 0.136). Collagen turnover (PIIIP) showed a significantly higher value in the affected patients (0.80+/-0.32, vs. 0.58+/-0.13 U/ml, P = 0.002). sIL-2R, sICAM-1 and PIIIP showed a negative correlation with the follow-up period (sIL-2R; r = -0.733, P = 0.0067, sICAM-1; r = -0.61, P = 0.035, PIIIP; r = -0.692, P = 0.0126). We found a positive correlation between aortic size and TAT (r = 0.644, P = 0.0238, n = 12) as well as with D-dimer (r = -0.7831, P = 0.0106, n = 12) and TAT showed significantly higher values in the residual dissection group compared to those without residual dissection (16.6+/-7.9 vs. 7.45+/-4.75 ng/ml, P = 0.035).


CONCLUSIONS
Hypercoagulation conditions continued even after repair. Both TAT and D-dimer would be good indices for following up patients having repaired aortic dissections. Furthermore, cytokine, adhesion molecules, and collagen turnover would return to a stable state unless impairment and expansion of the vessel wall occurred.
Nomura
F
F
Cardiovascular Surgery, National Hospital Kure Medical Center, Hiroshima, Japan. nomura@hayamaheart.gr.jp
Tamura
K
K
Yoshitatsu
M
M
Katayama
A
A
Katayama
K
K
Ihara
K
K
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000784:Aortic Dissection / Q000097:blood / Q000601:surgery*; D000933:Antifibrinolytic Agents / Q000097:blood; D000990:Antithrombin III; D001014:Aortic Aneurysm / Q000097:blood / Q000601:surgery*; D001777:Blood Coagulation / Q000502:physiology*; D024061:Collagen Type III / Q000097:blood; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood*; D008875:Middle Aged; D010447:Peptide Hydrolases / Q000097:blood; D011347:Procollagen; D015375:Receptors, Interleukin-2 / Q000097:blood*; D012995:Solubility
D000933:Antifibrinolytic Agents; D024061:Collagen Type III; D005338:Fibrin Fibrinogen Degradation Products; D011347:Procollagen; D015375:Receptors, Interleukin-2; C046193:antithrombin III-protease complex; C036309:fibrin fragment D; D018799:Intercellular Adhesion Molecule-1; D000990:Antithrombin III; D010447:Peptide Hydrolases