title: Obstructive hypertrophic cardiomyopathy is associated with enhanced thrombin generation and platelet activation.
abstract: OBJECTIVE
  To investigate the association of left ventricular outflow tract (LVOT) obstruction with blood coagulation, platelet activity and inflammatory response in patients with hypertrophic cardiomyopathy (HCM) and sinus rhythm.
  
  
  METHODS
  In 42 patients with HCM with sinus rhythm, including 16 patients with resting LVOT obstruction (gradient > or = 30 mm Hg) and 29 age- and sex-matched controls, markers of thrombin generation (thrombin-antithrombin complex (TAT), prothrombin fragment 1+2 (F1+2)), platelet activation (soluble CD40 ligand (sCD40L), beta-thromboglobulin (beta-TG), P-selectin) and inflammation (C-reactive protein (CRP), interleukin (IL)6, tumour necrosis factor-alpha (TNFalpha)) were determined.
  
  
  RESULTS
  Thrombin, platelet and inflammatory markers were higher in the entire HCM group than in controls (p<0.005 for all compared parameters). Compared with non-obstructive HCM, obstructive HCM was associated with increased thrombin formation (TAT, F1+2), platelet activation (sCD40L, beta-TG, P-selectin) and both CRP and IL6 levels. Only the level of TNFalpha was similar in both forms of HCM. In contrast, a comparison of non-obstructive HCM with controls showed that all these variables (except for P-selectin) were similar; P-selectin was higher in non-obstructive HCM. The LVOT gradient correlated positively with all the raised blood markers (r from 0.39 to 0.73; p<0.05), except for TNFalpha. In multiple regression analysis models, the LVOT gradient was the only independent predictor of TAT (R(2) = 0.61; p<0.001), sCD40L (R(2) = 0.59; p<0.001), F1+2 (R(2) = 0.55; p = 0.002), P-selectin (R(2) = 0.49; p = 0.004) and beta-TG (R(2) = 0.38; p = 0.005) in patients with HCM.
  
  
  CONCLUSIONS
  LVOT obstruction is independently associated with enhanced thrombin generation and platelet activity in patients with HCM with sinus rhythm.
authors.affiliation: 2nd Department of Cardiology, Collegium Medicum Jagiellonian University, ul. Kopernika 17, 31-501 Krakow, Poland. dimitrow@mp.pl
authors.forename: P P
authors.initials: PP
authors.lastname: Dimitrow
authors.forename: A
authors.initials: A
authors.lastname: Undas
authors.forename: M
authors.initials: M
authors.lastname: Bober
authors.forename: W
authors.initials: W
authors.lastname: Tracz
authors.forename: J S
authors.initials: JS
authors.lastname: Dubiel
mesh_terms: D001281:Atrial Fibrillation / Q000378:metabolism / Q000503:physiopathology; D015415:Biomarkers / Q000378:metabolism; D002312:Cardiomyopathy, Hypertrophic / Q000378:metabolism / Q000503:physiopathology*; D016022:Case-Control Studies; D004452:Echocardiography / Q000379:methods; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D015539:Platelet Activation / Q000502:physiology*; D013917:Thrombin / Q000378:metabolism*; D016896:Treatment Outcome; D018487:Ventricular Dysfunction, Left / Q000378:metabolism / Q000503:physiopathology
chemical_list: D015415:Biomarkers; D013917:Thrombin