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

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 con...

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Published inEuropean journal of heart failure Vol. 17; no. 12; pp. 1240 - 1251
Main Authors Ikonomidis, Ignatios, Tzortzis, Stavros, Triantafyllidi, Helen, Parissis, John, Papadopoulos, Costas, Venetsanou, Kyriaki, Trivilou, Paraskevi, Paraskevaidis, Ioannis, Lekakis, John
Format Journal Article
LanguageEnglish
Published Oxford, UK John Wiley & Sons, Ltd 01.12.2015
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Summary: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.
Bibliography:Table S1. Clinical characteristics of patients undergoing CPET vs. the remaining hypertensive patients. Table S2. Univariate and multivariable association of relative wall thickness with LV twisting-untwisting parameters in hypertensive heart disease.
Hellenic Cardiology Society
ArticleID:EJHF403
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ObjectType-Article-1
SourceType-Scholarly Journals-1
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content type line 23
ISSN:1388-9842
1879-0844
DOI:10.1002/ejhf.403