Obstructive Lung Diseases |

Serum Troponin-I Levels Distinguishing Dyspnea of Original COPD History Patients From Possibly Coincident Dyspnea of Latent Cardiovascular Pathology FREE TO VIEW

Ioannis Angomachalelis, PhD; George Kyriazis, PhD; Nestor Angomachalelis, PhD; Demetrios Vassilakos, PhD
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Aristotle University of Thessaloniki School of Medicine, Thessaloniki, Greece

Chest. 2015;148(4_MeetingAbstracts):676A. doi:10.1378/chest.2266304
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SESSION TYPE: Original Investigation Slide

PRESENTED ON: Monday, October 26, 2015 at 01:30 PM - 02:30 PM

PURPOSE: The purpose of the present investigation is to discriminate dyspnea patients(pts) with original COPD history from other dyspnea of possibly coincident cardiovascular pathology.

METHODS: 42pts with original history of COPD dyspnea,32 males and 10 females(mean age 68 years) and 33, matched control,normal individuals,underwent: 1)Serum Troponin-I(Tr-I) and other biomarkers evaluation. 2)Clinical and ECG examination. 3)Pulmonary function tests(PFTs),arterial blood gasses(ABGs) and blood tests. 4)Echocardiographic estimation of right/left ventricular function and pulmonary circulation.

RESULTS: The results showed: 1) Serum Tr-I values = 0,45 ng/ml, NT-ProBNP = 3.378 pg/ml,upper marginal Homocysteine (Hcy) and Creatinine (Cr) levels. 2)Hypoxemia:PO2=56mmHg, alveolo-arterial oxygen difference P(A-a)O2=56mmHg and (originally COPD) PFTs change to borderline restriction. 3) RVSP = 46 mmHg, RVID = 2,9cm,Preserved EF=60%, LAD=4,3cm. 4) Significant statistical correlation of Tr-I with Hcy (p=0,01,r=0,690), Cr( p=0,001,r=0,470), Carnitine (p=0,001,r=0,690) and DLCO (p=0,01,r=0,660). 5)Furthermore, consequent correlations of a) Hcy (p=0,001,r=0,620) and b) Cr(p=0,01,r=0,420) with serum NT-ProBNP, 6) However, no correlations of any kind and significance were confirmed with PFTs and ABGs.

CONCLUSIONS: We conclude that: 1) COPD Pts dyspnea has been led from PFTs original obstructive indices to borderline restrictive abnormalities,possibly arising from either COPD or left ventricular origin pulmonary hypertention and pathophysiology, 2) Co-existance of abnormal serum Tr-I and significant correlations to Hcy and Cr levels seems establishing coincident silent myocardial ischemia, cell apoptosis and renal disfunction, resulted either from or to congestive cardiovascular remodelling, 3) Serum Tr-I statistical correlation with carnitine levels looks possibly consequent to bi-ventricular remodelling, 4) PFTs and ABGs should consequently be considered quite independent indices of pulmonary COPD dyspnea 5) Reported investigation data suggest proper combined etiologic therapy of COPD history Pts,depending on dyspnea multi-origin,arising from primary COPD,Pulmonary hypertention,latent ischemia,hypertrophy,congestive remodelling and renal dysfunction.

CLINICAL IMPLICATIONS: Further investigation should confirm reliability, classification and differentiation of COPD-history dyspnea from either silent or symptomatic cardiovascular pathophysiology,promoting proper pharmacotherapy.

DISCLOSURE: The following authors have nothing to disclose: Ioannis Angomachalelis, George Kyriazis, Nestor Angomachalelis, Demetrios Vassilakos

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