Infection-Induced Serum Metalloproteinase-2 Activity and Myocardial Interstitial Dissarray in Pulmonary Hypertention Dyspnea Patients.

SESSION TITLE: DVT/PE/Pulmonary HypertensionSESSION TYPE: Original Investigation SlidePRESENTED ON: Wednesday, October 29, 2014 at 07:30 AM - 08:30 AMPURPOSE: The study aims to investigate unknown pathophysiology of myocardial interstitial dissarray arising from Metalloproteinase-2 (MMP-2) activity in Pulmonary Hypertention (PH) dyspnea patients (Pts),all statistically correlated with serum Procalcitonine (PCT) levels and other Biomarkers.METHODS: 55 PH dyspnea Pts,34 males and 21 females (mean age 68±14 years) and 33,matched control,normal individuals,were submitted to 1)Serum evaluation of PCT, MMP-2,Troponin-I (Tr-I), Erythropoietin (EPOS) and NT-ProBNP. 2) Clinical,ECG,Chest X-ray and Computed Tomography(CT) examination, 3)Pulmonary Function Tests (PFTs), Arterial Blood Gasses (ABGs) and Blood tests, 4) EchocardiographyRESULTS: The results Showed: 1) Abnormal serum values of PCT= 0.39 ng/ml,MMP-2 = 376 ng/ml,Tr-I = 2 ng/ml,EPOS = 26 m/U/ml,NT-ProBNP = 4.242 pg/ml, 2) Restrictive impairment of pulmonary function tests and hypoxemia with extremely increased alveolo-arterial oxygen difference [P(A-a)02] = 49mmHg, 3) Normal ejection fraction (EF),left atrial and right ventricular enlargement (LAD,RVID), RVSP = 52 mmHg, 4) Primary significant correlation of MMP-2 with a) PCT (r = 0.630), b)Tr-I (r = 0.390), c) EPO (r = -0.340), d) PCO2 (r = 0.340),and e) NT-ProBNP (r = 0.310), 5) Statistical correlations of any significance were not confirmed with ABGs and PFTs ,excluding PCO2...CONCLUSIONS: We conclude that:1) Serum MMP-2 activity on the grounds of PH dyspnea Pts is obviously leading to myocardial interstitial disarray,arising mainly from the related serum PCT presence,expressing original contribution of an infective reaction pathophysiology. 2)The related serum Tr-I,EPOS and NT-ProBNP values indicate existance of myocardial cell apoptosis and congestive remodeling,due to pulmonary hypertention of cardiac origin, possibly co-induced from PCT infective reaction, 3)However,the infection related PCO2 levels looks contributing to myocardial interstitial fibrosis,further possibly connecting with inflammation and Thrombogenesis, 4)PFTs and the rest of ABGs do not seem correlated with infection induced pathophysiology of MMP-2 activity in pulmonary hypertention dyspnea pts.CLINICAL IMPLICATIONS: Furter studies should necessarily be contacted to discriminate the original role of infection induced MMP2 activity, leading to myocardial interstitial disarray and coincident cardiovascular pathology in Palmonary Hypertention dyspnea Pts.DISCLOSURE: The following authors have nothing to disclose: Ioannis Angomachalelis, George Kyriazis, Nestor AngomachalelisNo Product/Research Disclosure Information.