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Association of impaired left ventricular twisting‐untwisting with vascular dysfunction, neurohumoral activation and impaired exercise capacity in hypertensive heart disease
Author(s) -
Ikonomidis Ignatios,
Tzortzis Stavros,
Triantafyllidi Helen,
Parissis John,
Papadopoulos Costas,
Venetsanou Kyriaki,
Trivilou Paraskevi,
Paraskevaidis Ioannis,
Lekakis John
Publication year - 2015
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1002/ejhf.403
Subject(s) - medicine , cardiology , pulse wave velocity , arterial stiffness , speckle tracking echocardiography , natriuretic peptide , coronary artery disease , heart failure , heart rate , diastole , coronary flow reserve , blood pressure , ejection fraction
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 – Utw MVO ), at peak (% dpTw – Utw PEF ), and the end of early LV diastolic filling (% dpTw – Utw EDF ) 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 ( VO 2 ), measured by means of cardiopulmonary exercise test, was assessed in a subset of 80 patients. The PWV , CFR , longitudinal strain and strain rate, % dpTw‐Utw MVO , % dpTw‐Utw PEF , and % dpTw‐Utw EDF 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 – Utw EDF was related with increased NT‐proBNP and reduced VO 2 ( 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.