2013;8(9):295. Cardiologia CROATICA Objectives: Pulmonary hypertension (PH) and vascular re- sistance in patients with pulmonary arterial hypertension (PAH) are caused by remodeling and thrombosis of small and medium sized pulmonary arteries and arterioles, as well as vasoconstriction. These patients have increased platelet aggregation and the activated platelets are major source of thromboxane A2 which is a strong vasopressor and pro- aggregation molecule. PGI2 and PGE1 have opposite ef- fects. Misbalance in eicosanoids synthesis was observed in patients with PH. The results from vasoreactivity test, in which we measure the hemodynamic response to vasodila- tor, particularly change in mean pulmonary pressure (mPAP), pulmonary vascular resistance (PVR) and trans- pulmonary gradient (TPG) in patients with PH due to the left heart disease, influence the decision on future course of treatment. The goal: to test whether the change of platelet aggregation during vasoreactivity testing is related to hemo- dynamic response measured as the change in mPAP, PVR and TPG. Patients and Methods: Our pilot study included 38 patients with secondary PH due to the left heart disease, 29 men (76%) and 9 women (24%). The right heart catheterization was performed in all patients and vasoreactivity testing with PGE1 in 19 patients (50%). Platelet aggregation induced by addition of AA (ASPI test), ADP (ADP test) and collagen (COL-test) was measured in blood samples from pulmonary artery with Multiplate and repeated after vasoreactivity te- sting. Results: Patients with the reduction of platelet aggre- gation in ASPI test had stronger, but insignificant reduction in mPAP (p=0.08) and PVR (p=0.15). Significant reduction was observed in the reduction of TPG (p=0.03). The reduc- tion of platelet aggregation in ADP test was not related to hemodynamic response to PGE1. Patients with the reduc- tion of aggregation in collagen test had stronger, though in- significant reduction in mPAP (p=0.08). However, they had significant reduction in PVR (p=0.01) and TPG (p=0.05) in comparison to those with increased aggregation. Conclusion: The data analysis in our pilot study shows in- sufficient size of the sample to reach a final conclusion. However, it suggest a significant potential difference in va- soreactivity among patients who respond with a decrease and those who respond with an increase in platelet aggrega- tion after testing with PGE1. We hypothesize that variations in platelet response to PGE1 modulate its hemodynamic effect on pulmonary circulation. KEYWORDS: pulmonary hypertension, platelet aggrega- tion, vasoreactivity. CITATION: Cardiol Croat. 2013;8(9):295. Proπireni saæetak / Extended abstract Variation in platelet response may affect the hemodynamic response to vasoreactivity testing in patients with secondary pulmonary hypertension due to left heart disease Boπko SkoriÊ*, Jure SamardæiÊ, Hrvoje Jurin, Jana Ljubas, Ivo Planinc, Miroslav Krpan, Marija Brestovac, Marijan PaπaliÊ, Davor MiliËiÊ University of Zagreb School of Medicine, University Hospital Centre Zagreb, Zagreb, Croatia Received: 15 th Aug 2013 *Address for correspondence: KliniËki bolniËki centar Zagreb, KiπpatiÊeva 12, HR- 10000 Zagreb, Croatia. Phone: +385-1-2367467 E-mail: bskoric3@yahoo.com Literature 1. Can MM, Tanboga IH, Demircan HC, et al. Enhanced hemostatic indices in patients with pulmonary arterial hypertension: an observational study. Thromb Res. 2010;126(4):280- 2. 2. Varol E, Uysal BA, Ozaydin M. Platelet indices in patients with pulmonary arterial hypertension. Clin Appl Thromb Hemos. 2011;17(6):E171-4.