PAR-1 antagonist vorapaxar favorably improves global thrombotic status in patients with coronary disease.

To assess the effect of vorapaxar on global thrombotic and thrombolytic status. The propensity for thrombus formation is determined by the balance between prothrombotic factors and endogenous thrombolysis. Impaired thrombolytic status increases cardiovascular risk. Vorapaxar is a novel, oral, protease-activated receptor-1 antagonist that inhibits thrombin-induced platelet activation. In the TRACER and TRA 2°P-TIMI 50 studies, patients with acute coronary syndromes and established atherosclerosis were randomized to vorapaxar 2.5 mg daily or placebo, in addition to standard care. In 57 patients enrolled in a single center, blood was tested with the point-of-care global thrombosis test, on and off treatment. This automated test employs non-anticoagulated blood to assess thrombotic and thrombolytic status, measuring the time required to form a shear-induced thrombus under physiological conditions (occlusion time, OT), and subsequently, the time to achieve endogenous lysis of the thrombus (lysis time, LT). Patients on vorapaxar exhibited longer OT on vs. off treatment [median 561 s (interquartile range 422-654) vs. 372 s(338-454), P = 0.003] and shorter LT on treatment than off [1,158 s(746-1,492) vs. 1,733 s(1,388-2,230), P = 0.016]. Patients on placebo showed no difference in OT [419 s(343-514) vs. 411 s(346-535), P = 0.658] or LT [1,236 s(985-1,594) vs. 1,400 s(1,092-1,686), P = 0.524] on and off treatment. During treatment, OT was longer in patients taking vorapaxar [561 s(422-654) vs. 419 s(343-514), P = 0.009], but LT was similar in vorapaxar and placebo arms [1,158 s(746-1,492) vs. 1,236 s(985-1,594), P = 0.277]. Vorapaxar prolongs OT and shortens LT, with favorable effects on thrombotic and thrombolytic status. In addition to its antiplatelet effect, vorapaxar may enhance endogenous thrombolysis, which is frequently impaired in coronary disease.

Periodontal health improves systemic inflammatory and haemostatic status in subjects with coronary heart disease.

OBJECTIVES: A relationship between poor oral health and coronary heart disease (CHD) and systemic inflammatory and haemostatic factors has been recently documented in an Italian population. The present study was performed to assess whether intensive dental care may produce a periodontal improvement along with a change in systemic inflammatory and haemostatic factors. MATERIAL AND METHODS: The study population consisted of 18 males aged 40-65 years with proven CHD and elevated values of systemic inflammatory and haemostatic factors. A detailed description of their oral status was given by using two different dental indices (clinical periodontal sum score and clinical and radiographic sum score). Blood samples were taken for measurement of the following systemic markers of inflammation [(C-reactive protein (CRP), leucocytes, fibrinogen)] and haemostatic factors [(von Willebrand factor, fibrin D-dimer and oxidized-low density lipoprotein (Ox-LDL)]. All parameters were determined in each subject at baseline, after 4 months as a control and 3 months after an intensive protocol of scaling and root planing. anova for repeated measures was used for the statistical analysis. RESULTS: No statistical difference was found between values at baseline and at the 4-month-control. All oral indexes showed a significant decrease (p< .01) 3 months after periodontal treatment. All systemic inflammatory indexes decreased but only the decrease in CRP reached statistical significance (p< .05). A significant decrease (p< .01) was also found as regards Ox-LDL among haemostatic factors. CONCLUSIONS: Preliminary results from the present study suggest an association between poor oral status and CHD, and provide evidence that the improvement of periodontal status may influence the systemic inflammatory and haemostatic situation.

Poor oral health is associated with coronary heart disease and elevated systemic inflammatory and haemostatic factors.

OBJECTIVES: To assess the relationship between poor oral health and coronary heart disease (CHD) and systemic inflammatory and haemostatic factors in an Italian population. MATERIAL AND METHODS: The study population consisted of 63 males aged 40-65 years with proven CHD and 50 controls matched for age, geographic area, and socioeconomic status. A detailed description of their oral status was given using four different dental indices (total dental index (TDI), panoramic tomography score, clinical periodontal sum score (CPSS), and clinical and radiographic sum score (CRSS)). Blood samples were taken for measurement of the following CHD risk factors: serum total cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, and glucose; a series of systemic markers of inflammation (C-reactive protein, leucocytes, fibrinogen, homocysteine) and a series of haemostatic factors (von Willebrand factor, fibrin D-dimer, prothrombinic fragment F1.2, plasminogen activator inhibitor type I (PAI-1), and serum antibodies) against oxidized LDL (anti-Ox-LDL). RESULTS: Multiple logistic regression adjusted for all risk factors for CHD showed statistically significant relationships (p<0.01) between all dental indices and CHD. Significant relationships (p always <0.01) were found between CPSS and CRSS and leucocyte count. Significant relationships (p always <0.05) were also found between TDI and the von Willebrand factor, and between CPSS and the von Willebrand factor, anti-Ox-LDL, and PAI-1. CONCLUSIONS: The present study suggests an association between poor oral status and CHD, and provides evidence that inflammatory and haemostatic factors could play an important role in this association.