Left ventricular global systolic dysfunction has a significant role in the development of diastolic heart failure in patients with systemic hypertension

Kono, M; Kisanuki, Akira; Ueya, Nami; Kubota, Kayoko; Kuwahara, Eiji; Takasaki, Kunitsugu; Yuasa, Toshinori; Mizukami, Naoko; Miyata, Masaaki

doi:10.1038/hr.2010.142

Cited by 8 publications

(6 citation statements)

References 26 publications

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“…Hypertension induces remodeling, leading to functional consequences associated with heart failure 3, 4) , which involves excess parallel signal transduction events 35,36) . Innate immunity is activated in the injured heart in different ways and is evident in the form of cytokine release from the heart and the activation of TLRs that play a role in recognizing danger as well as NF-κB, which regulates gene programs involved in inflammation 8, 11,37) .…”

Section: Discussionmentioning

confidence: 99%

“…Specifically, the direct cardiac effects of angiotensin II (AngII) contribute to the pathogenesis and progression of cardiac hypertrophy and fibrosis via the production of oxidative stress and inflammation 1,2) , both systolic and diastolic dysfunction 3,4) characterized by the signs and symptoms of heart failure and a preserved ejection fraction and abnormal left ventricular (LV) diastolic function caused by decreased LV compliance and relaxation 5) . Cardiac hypertrophy may be reversed by the administration of angiotensin II type 1 (AT1) receptor antagonists 6) .…”

Section: Introductionmentioning

confidence: 99%

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Angiotensin Ⅱ Activates MCP-1 and Induces Cardiac Hypertrophy and Dysfunction via Toll-like Receptor 4

Matsuda

Umemoto

Yoshimura

et al. 2015

J Atheroscler Thromb

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Aim Angiotensin II (AngII) produces reactive oxygen species (ROS), thus contributing to the development of cardiac hypertrophy and subsequent heart failure, and stimulates the expression of monocyte chemoattractant protein-1 (MCP-1). In addition, Toll-like receptor 4 (TLR4) is involved in the upregulation of MCP-1. In order to clarify whether TLR4 is involved in the onset of cardiac dysfunction caused by AngII stimulation, we investigated the effects of TLR4 on oxidative stress, the MCP-1 expression and cardiac dysfunction in mice with AngII-induced hypertension. Methods TLR4-deficient (Tlr4lPS-d) and wild-type (WT) mice were randomized into groups treated with AngII, norepinephrine (NE) or a subdepressor dose of the AngII receptor blocker irbesartan (IRB) and Angll for two weeks. Results AngII and NE similarly increased systolic blood pressure in all drug-treated groups compared to that observed in the control group among both WT and T1r4lps-d mice (p< 0.05). In the WT mice, AngII induced cardiac hypertrophy as well as vascular remodeling and perivascular fibrosis of the intramyocardial arteries and monocyte/macrophage infiltration in the heart (P<0.05). Furthermore, AngII treatment decreased the left ventricular diastolic function and resulted in a greater left ventricular end-systolic dimension (P<0.05) in addition to producing a five-fold increase in the NADPH oxidase activity, ROS content and MCP-1 expression (P<0.05). In contrast, the Tlr4lps-d mice showed little effects of AngII on these indices. In the WT mice, IRB treatment reversed these changes compared to that seen in the mice treated with AngII alone. NE produced little effect on any of the indices in either the WT or T1r4lps-d mice. Conclusions TLR4 may be involved in the processes underlying the increased oxidative stress, selectively activated MCP-1 expression and cardiac hypertrophy and dysfunction seen in cases of AngII-induced hypertension.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Angiotensin Ⅱ Activates MCP-1 and Induces Cardiac Hypertrophy and Dysfunction via Toll-like Receptor 4

Matsuda

Umemoto

Yoshimura

et al. 2015

J Atheroscler Thromb

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“…LV systolic dysfunction, expressed by ICT, has been reported to play an important role in the development of diastolic heart failure in patients with hypertension. 21 …”

Section: Ict and Irt In Hypertensionmentioning

confidence: 99%

Left Ventricular Dysfunction Assessed by Cardiac Time Interval Analysis Among Different Geometric Patterns in Untreated Hypertension

Takasaki

Miyata

Imamura

et al. 2012

Circ J

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Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp ssential hypertension is a major risk factor for cardiovascular disease. In hypertensive patients, pressure and/or volume overload leads to left ventricular (LV) hypertrophy, which is a powerful independent predictor of morbidity and mortality. 1 Hypertensive LV hypertrophy causes heart failure, especially diastolic heart failure, which is heart failure with a normal LV ejection fraction (LVEF) because of LV diastolic dysfunction. However, several studies have reported that patients with diastolic heart failure have not only diastolic dysfunction but also systolic dysfunction, when parameters other than LVEF were used to evaluate systolic function. 2-5 Therefore, global cardiac function including systolic and diastolic LV function should be evaluated by non-conventional functional parameters such as the Tei index. The Tei index, combining systolic and diastolic functional parameters, may be a better and simpler parameter to estimate LV global function than conventional indices of purely systolic or diastolic function in hypertensive patients.Based on LV mass and relative wall thickness, patients with essential hypertension can be classified into 4 different LV geometric patterns: normal, concentric remodeling, concentric hypertrophy and eccentric hypertrophy. 6-8 Previous studies have reported that abnormal LV geometric patterns are associated with a greater risk of hypertensive complications, and patients with concentric LV hypertrophy have the highest mortality and cardiovascular event rate. 7,9 The relation between these 4 different LV geometric patterns and LV function has not been elucidated. Therefore, we aimed to investigate the correlation Background: Left ventricular (LV) hypertrophy is a powerful independent predictor of morbidity and mortality in hypertensive patients. Abnormal LV geometric patterns are also associated with hypertensive complications, and concentric hypertrophy is associated with the highest mortality in hypertensive patients. However, the relationship between geometric patterns and cardiac dysfunction is not fully established. We hypothesized that the Tei index, which is a measure of global cardiac function, is a feasible parameter for estimating cardiac dysfunction among the different LV geometric patterns in hypertensive patients. E

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“…Similar changes in E’ and (E/E’)/EDV were observed also in HFpEF patients [ 32 , 39 , 45 ]. In DOCA pigs, increased (E/E’)/EDV may further be related to the prolonged IVRT at rest [ 46 , 47 ] and/or subtle stress-induced myocardial ischemia [ 48 ], as indicated by the lower global myocardial perfusion reserve during dobutamine in the hypertrophied LV myocardium in DOCA pigs.…”

Section: Discussionmentioning

confidence: 99%

Early-stage heart failure with preserved ejection fraction in the pig: a cardiovascular magnetic resonance study

Reiter

Manninger

et al. 2016

Journal of Cardiovascular Magnetic Resonance

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BackgroundThe hypertensive deoxy-corticosterone acetate (DOCA)-salt-treated pig (hereafter, DOCA pig) was recently introduced as large animal model for early-stage heart failure with preserved ejection fraction (HFpEF). The aim of the present study was to evaluate cardiovascular magnetic resonance (CMR) of DOCA pigs and weight-matched control pigs to characterize ventricular, atrial and myocardial structure and function of this phenotype model.MethodsFive anesthetized DOCA and seven control pigs underwent 3 T CMR at rest and during dobutamine stress. Left ventricular/atrial (LV/LA) function and myocardial mass (LVMM), strains and torsion were evaluated from (tagged) cine imaging. 4D phase-contrast measurements were used to assess blood flow and peak velocities, including transmitral early-diastolic (E) and myocardial tissue (E’) velocities and coronary sinus blood flow. Myocardial perfusion reserve was estimated from stress-to-rest time-averaged coronary sinus flow. Global native myocardial T1 times were derived from prototype modified Look-Locker inversion-recovery (MOLLI) short-axis T1 maps. After in-vivo measurements, transmural biopsies were collected for stereological evaluation including the volume fractions of interstitium (VV(int/LV)) and collagen (VV(coll/LV)). Rest, stress, and stress-to-rest differences of cardiac and myocardial parameters in DOCA and control animals were compared by t-test.ResultsIn DOCA pigs LVMM (p < 0.001) and LV wall-thickness (end-systole/end-diastole, p = 0.003/p = 0.007) were elevated. During stress, increase of LV ejection-fraction and decrease of end-systolic volume accounted for normal contractility reserves in DOCA and control pigs. Rest-to-stress differences of cardiac index (p = 0.040) and end-diastolic volume (p = 0.042) were documented. Maximal (p = 0.042) and minimal (p = 0.012) LA volumes in DOCA pigs were elevated at rest; total LA ejection-fraction decreased during stress (p = 0.006). E’ was lower in DOCA pigs, corresponding to higher E/E’ at rest (p = 0.013) and stress (p = 0.026). Myocardial perfusion reserve was reduced in DOCA pigs (p = 0.031). T1-times and VV(int/LV) did not differ between groups, whereas VV(coll/LV) levels were higher in DOCA pigs (p = 0.044).ConclusionsLA enlargement, E’ and E/E’ were the markers that showed the most pronounced differences between DOCA and control pigs at rest. Inadequate increase of myocardial perfusion reserve during stress might represent a metrics for early-stage HFpEF. Myocardial T1 mapping could not detect elevated levels of myocardial collagen in this model.Trial registrationThe study was approved by the local Bioethics Committee of Vienna, Austria (BMWF-66.010/0091-II/3b/2013).

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Left ventricular global systolic dysfunction has a significant role in the development of diastolic heart failure in patients with systemic hypertension

Cited by 8 publications

References 26 publications

Angiotensin Ⅱ Activates MCP-1 and Induces Cardiac Hypertrophy and Dysfunction via Toll-like Receptor 4

Angiotensin Ⅱ Activates MCP-1 and Induces Cardiac Hypertrophy and Dysfunction via Toll-like Receptor 4

Left Ventricular Dysfunction Assessed by Cardiac Time Interval Analysis Among Different Geometric Patterns in Untreated Hypertension

Early-stage heart failure with preserved ejection fraction in the pig: a cardiovascular magnetic resonance study

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