Activation of the endogenous coagulation system in patients with atrial flutter: relationship to echocardiographic markers of thromboembolic risk.
BACKGROUND
Atrial thrombus formation in patients with atrial flutter raises concerns of stroke risk. We investigated patients with isthmus-dependent atrial flutter for coagulation abnormalities before and after cardioversion to sinus rhythm by catheter ablation, and evaluated the relationship of the abnormalities to the echocardiographic risk markers of stroke.


RESULTS
Plasma samples were drawn prior to insertion of catheters, immediately after the procedure, and 24 hours afterwards. At baseline, coagulation abnormalities were found in 22 out of 25 patients (88%). von Willebrand factor antigen (vWF-Ag) and factor VIII:C were elevated in 17 patients (68%) and 15 patients (60%), respectively. At baseline, mean plasma levels of vWF-Ag (250.1 +/- 144.4%) and factor VIII:C (215.0 +/- 77.1%) were increased. Key markers of thrombin generation, thrombin-antithrombin III complex (TAT; 47.8 +/- 30.9 microg/L vs 14.5 +/- 13.8 microg/L; p < 0.05) and prothrombin fragments 1.2 (F1.2; 2.5 +/- 0.5 nmoL/L vs 1.2 +/- 1.0 nmoL/L) were significantly elevated in the presence of spontaneous echo contrast. Further, both markers of thrombin generation inversely correlated with left atrial appendage emptying velocity (r = -0.42 and -0.63, p < 0.05). Levels of TAT and F1.2 increased after conversion and ablation.


CONCLUSIONS
Endothelial-dependent coagulation factors were enhanced in most patients with atrial flutter. Spontaneous echo contrast and decreased atrial contractility were associated with increased thrombin generation. After conversion and ablation, an increase in thrombin generation and fibrinolysis suggest a transient pro-thrombotic state.
Kamath
Ganesh S
GS
Division of Cardiology, St. Luke's and Roosevelt Hospitals, 1111 Amsterdam Avenue, New York, NY 10025, USA.
Herweg
Bengt
B
Cotiga
Delia
D
Pierce
Walter
W
Cohen
Alice J
AJ
Chaudhry
Farooq A
FA
Drejka
Michele L
ML
Steinberg
Jonathan S
JS
D000368:Aged; D000990:Antithrombin III; D001281:Atrial Fibrillation / Q000097:blood / Q000150:complications* / Q000000981:diagnostic imaging / Q000601:surgery; D015415:Biomarkers / Q000097:blood; D001777:Blood Coagulation; D017115:Catheter Ablation / Q000009:adverse effects; D018619:Echocardiography, Doppler, Pulsed; D017548:Echocardiography, Transesophageal; D005169:Factor VIII / Q000378:metabolism; D005260:Female; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000097:blood; D010447:Peptide Hydrolases / Q000097:blood; D011516:Prothrombin; D018570:Risk Assessment; D012307:Risk Factors; D020521:Stroke / Q000097:blood / Q000209:etiology*; D013917:Thrombin / Q000378:metabolism; D013923:Thromboembolism / Q000097:blood / Q000209:etiology*; D016896:Treatment Outcome; D014481:United States; D014841:von Willebrand Factor / Q000378:metabolism
D015415:Biomarkers; D010446:Peptide Fragments; C046193:antithrombin III-protease complex; C045879:prothrombin fragment 1.2; D014841:von Willebrand Factor; D000990:Antithrombin III; D011516:Prothrombin; D005169:Factor VIII; D010447:Peptide Hydrolases; D013917:Thrombin