Association of impaired left ventricular twisting-untwisting with vascular dysfunction, neurohumoral activation and impaired exercise capacity in hypertensive heart disease

Επιστημονική δημοσίευση - Άρθρο Περιοδικού uoadl:3109791 21 Αναγνώσεις

Μονάδα:
Ερευνητικό υλικό ΕΚΠΑ
Τίτλος:
Association of impaired left ventricular twisting-untwisting with vascular dysfunction, neurohumoral activation and impaired exercise capacity in hypertensive heart disease
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Aims We investigated the association between left ventricular (LV) torsional deformation and vascular dysfunction, fibrosis, neurohumoral activation, and exercise capacity in patients with normal ejection fraction Methods and results In 320 newly-diagnosed untreated hypertensive patients and 160 controls, we measured: pulse wave velocity (PWV); coronary flow reserve (CFR) by Doppler echocardiography; global longitudinal strain and strain rate, peak twisting, the percentage changes between peak twisting, and untwisting at mitral valve opening (%dpTw - UtwMVO), at peak (%dpTw - UtwPEF), and the end of early LV diastolic filling (%dpTw - UtwEDF) by speckle tracking imaging; transforming growth factor (TGFb-1), metalloproteinase-9 (MMP-9), tissue inhibitor of matrix metalloptoteinase-1(TIMP-1), markers of collagen synthesis, and N-terminal pro-brain natriuretic peptide (NT-proBNP). Oxygen consumption (VO2), measured by means of cardiopulmonary exercise test, was assessed in a subset of 80 patients. The PWV, CFR, longitudinal strain and strain rate, %dpTw-UtwMVO, %dpTw-UtwPEF, and %dpTw-UtwEDF were impaired in hypertensive patients compared with controls. In multivariable analysis, CFR, PWV, LV mass, and systolic blood pressure were independent determinants of longitudinal strain, strain rate, and untwisting markers (P < 0.05). Increased TGFb-1 was related with increased collagen synthesis markers, TIMP-1 and MMP-9 and these biomarkers were associated with impaired longitudinal systolic strain rate, untwisting markers, CFR and PWV (P < 0.05). Delayed untwisting as assessed by reduced %dpTw - UtwEDF was related with increased NT-proBNP and reduced VO2 (P < 0.05). Conclusions Impaired LV untwisting is associated with increased arterial stiffness and coronary microcirculatory dysfunction, and is linked to reduced exercise capacity and neurohumoral activation in hypertensive heart disease. A fibrotic process may be the common link between vascular dysfunction and abnormal myocardial deformation. © 2015 The Authors European Journal of Heart Failure.
Έτος δημοσίευσης:
2015
Συγγραφείς:
Ikonomidis, I.
Tzortzis, S.
Triantafyllidi, H.
Parissis, J.
Papadopoulos, C.
Venetsanou, K.
Trivilou, P.
Paraskevaidis, I.
Lekakis, J.
Περιοδικό:
European Journal of Heart Failure
Εκδότης:
John Wiley and Sons Ltd
Τόμος:
17
Αριθμός / τεύχος:
12
Σελίδες:
1240-1251
Λέξεις-κλειδιά:
amino terminal pro brain natriuretic peptide; gelatinase B; tissue inhibitor of metalloproteinase 1; transforming growth factor beta1; biological marker; brain natriuretic peptide; gelatinase B; peptide fragment; pro-brain natriuretic peptide (1-76); tissue inhibitor of metalloproteinase 1; transforming growth factor beta, adult; aerobic exercise; arterial stiffness; Article; cardiopulmonary exercise test; cardiovascular parameters; collagen metabolism; collagen synthesis; controlled study; coronary flow reserve; disease association; Doppler echocardiography; female; heart left ventricle filling; heart left ventricle mass; heart muscle fibrosis; human; hypertension; left ventricular twisting untwisting; major clinical study; male; microcirculation; middle aged; oxygen consumption; physical capacity; priority journal; pulse wave; systolic blood pressure; vascular disease; blood; blood pressure; echocardiography; heart disease; heart ventricle; hypertension; mitral valve; pathophysiology, Biomarkers; Blood Pressure; Echocardiography; Female; Heart Diseases; Heart Ventricles; Humans; Hypertension; Male; Matrix Metalloproteinase 9; Middle Aged; Mitral Valve; Natriuretic Peptide, Brain; Peptide Fragments; Tissue Inhibitor of Metalloproteinase-1; Transforming Growth Factor beta
Επίσημο URL (Εκδότης):
DOI:
10.1002/ejhf.403
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