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

2015 ◽  
Vol 17 (12) ◽  
pp. 1240-1251 ◽  
Author(s):  
Ignatios Ikonomidis ◽  
Stavros Tzortzis ◽  
Helen Triantafyllidi ◽  
John Parissis ◽  
Costas Papadopoulos ◽  
...  
Keyword(s):  
Heart Disease ◽  
Exercise Capacity ◽  
Vascular Dysfunction ◽  
Hypertensive Heart Disease ◽  
Left Ventricular ◽  
Neurohumoral Activation

Abstract 16018: Impaired Intrinsic Myocardial Shortening in Both Two Directions and Compensatory Mechanism to Maintain Left Ventricular Ejection Fraction in Patients With Hypertensive Heart Disease

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Satoshi Yamada ◽  
Kazunori Okada ◽  
Hisao Nishino ◽  
Hiroyuki Iwano ◽  
Daisuke Murai ◽  
...  
Keyword(s):  
Heart Disease ◽  
Ejection Fraction ◽  
Wall Thickness ◽  
Circumferential Strain ◽  
Hypertensive Heart Disease ◽  
Wall Stress ◽  
Left Ventricular ◽  
Relative Wall Thickness ◽  
Left Ventricular Ejection ◽  
Compensatory Mechanism

Background: Longitudinal myocardial shortening is known to be reduced even if left ventricular (LV) ejection fraction (EF) is preserved in patients with hypertensive heart disease (HHD). However, the compensatory mechanism remains to be elucidated. Thus layer-specific longitudinal and circumferential strain as well as stress-strain relationship was observed in HHD patients. Methods: In 46 HHD patients with preserved EF (>50%) and 29 age-matched control subjects, global longitudinal strain (LS) and layer-specific circumferential strain (CS) were measured from the apical 4-chamber view and mid-ventricular short-axis view, respectively, by using speckle tracking echocardiography. LS was measured at innermost LV wall layer, and CS at innermost, midwall, and outermost layers. Layer-specific end-systolic circumferential wall stress (CWS) according to Mirsky’s formula and endocardial meridional wall stress (MWS) were calculated. Results: Systolic blood pressure (147±20 mm Hg), interventricular septal thickness (13±2 mm), and LV dimension (48±4 mm) were greater in HHD than controls, whereas EF was comparable (66±8 vs 66±5%). LS was smaller in HHD than controls (-13±3 vs -17±3%, p<0.001) in spite of reduced MWS (520±141 vs 637±164 dyn·mm -2 , p<0.01), suggesting impaired longitudinal myocardial function in HHD. Similarly, CS was smaller in HHD than controls at outer layer (-6.8±2.2 vs -8.8±2.2%, p<0.01) and at midwall (-11.3±3.4 vs -13.9±3.2%, p<0.01) in spite of reduced CWS (outer: 238±82 vs 336±110 dyn·mm -2 , p<0.001; mid: 360±107 vs 473±131 dyn·mm -2 , p<0.001). In contrast, at the innermost layer, both CS (-26±5 vs -25±5%, p=0.41) and CWS (979±153 vs 992±139 dyn·mm -2 , p=0.72) were comparable between groups. Furthermore, the difference of CS between inner and outer layers significantly correlated with relative wall thickness (r=-0.33, p<0.01). Finally, CS at inner layer significantly correlated with EF (r=-0.43, p<0.001), whereas LS did not. Conclusions: In patients with HHD, intrinsic myocardial shortening was impaired both longitudinally and circumferentially. Some compensatory mechanism associated with increased relative wall thickness might work to maintain subendocardial CS, resulting in preserved EF.

Abstract P219: Differences in Phosphoproteins in Rodent versus Human Hearts: Implications for Translational Studies of Hypertensive Heart Disease

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Robert S Danziger ◽  
Kumar Kotlo ◽  
Allen Samarel ◽  
Hua Chen ◽  
Jared Aldstadt
Keyword(s):  
Heart Disease ◽  
Light Chain ◽  
Myosin Light Chain ◽  
Troponin T ◽  
Hypertensive Heart Disease ◽  
Left Ventricular ◽  
Current Evidence ◽  
Tissue Samples ◽  
Pixel Intensity ◽  
Translational Studies

Background: Rodent models are commonly used to study hypertensive heart disease. Several recent studies have probed the level of correlation between specific signaling pathways and proteins in human and rodents. Current evidence is overwhelming that protein phosphorylations play a key role in cardiac remodeling. Methods: Left ventricular tissue samples were obtained from human systolic failing (n=5) and control (n=5) hearts and 3 rat models of hypertensive heart failure (aortic banding, Dahl salt-sensitive, and spontaneously hypertensive rats (SHR)) and corresponding controls. Total proteins were extracted and and phosphoenrichment performed. Phosphoproteins were separated by 2D-DIGE with Cydye staining. Gel images were registered and rectified for composite analysis and statistical comparisons using pixel intensity. Phosphoproteins were identified by MALDI-TOF/TOF Mass Spectrometry. Results: The patterns of overall protein abundance from normal and failing hearts were not statistically different. However, when the composite of human hearts were compared with composite patterns of phosphoproteins in normal and failing rodent hearts, there were profound differences in the phosphoprotein patterns in 26% of pixels in registered images (P < 0.05). Targeted pair wise analyses showed differences (P < 0.05) between human and rodent hearts for troponin T, myosin light chain, peroxiredoxin, and haptoglobin phosphorylations. Conclusions: Together, the present results indicate significant differences in cardiac phosphoproteins in human versus rodent heart and the importance of confirming findings from rodent studies in humans for translational studies of kinases, phosphatases, and phosphoproteins. This may specifically relate to studies of phosphorylation of myosin light chain and troponin.

Methods for detection of left ventricular hypertrophy: Application to hypertensive heart disease

1993 ◽  
Vol 14 (suppl D) ◽  
pp. 8-15 ◽  
Author(s):  
R. B. Devereux ◽  
M. J. Koren ◽  
G. de Simone ◽  
P. M. Okin ◽  
P. Kligfield
Keyword(s):  
Heart Disease ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Hypertensive Heart Disease ◽  
Left Ventricular

Abstract 1874: Circumferential and Radial Left Ventricular Mechanics in Elderly Canines with Hypertensive Heart Disease

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Josef Korinek ◽  
Brian P Shapiro ◽  
Carolyn S Lam ◽  
Donna M Meyer ◽  
Margaret M Redfield
Keyword(s):  
Heart Disease ◽  
Ejection Fraction ◽  
Myocardial Dysfunction ◽  
Radial Strain ◽  
Hypertensive Heart Disease ◽  
Wall Stress ◽  
Strain Imaging ◽  
Left Ventricular ◽  
Doppler Imaging ◽  
Ventricular Mechanics

Introduction: Cross-sectional studies in patient with hypertensive heart disease (HHD) and heart failure with normal ejection fraction (HFnlEF) suggested impairment of longitudinal myocardial mechanics as assessed by tissue Doppler imaging. It has been suggested that enhanced circumferential, and/or radial LV mechanics or LV remodeling compensates for depression in longitudinal function and thus, preserves EF in HHD or HFnlEF. Hypothesis : We hypothesized that if longitudinal performance is depressed, whether due to increased afterload or to intrinsic myocardial dysfunction, circumferential and radial LV mechanics would also be effected. To test this hypothesis, we used an aged canine model of hypertension. Methods: Elderly dogs (n=22) underwent bilateral renal wrapping to induce hypertension. 2D echocardiography (mid-short axis views) was performed before and 8 weeks after renal wrapping; peak radial (PR) and peak circumferential (PC) regional strains were measured by speckle tracking averaging data from 6 segments. Ejection fraction (EF), LV mass index (LVMI), systolic blood pressure (SBP), and circumferential wall stress (CWS) were assessed as well. Results : See table . PR correlated with PC (r=0.65), EF (r=0.67), LWMI (r=0.71) and CWS (r=0.58) (p<0.005 for all). PC correlated also with EF (r=0.60), LWMI (r=0.49) and CWS (r=0.48) (p<0.01 for all). The relationship between EF and CWS (r 2 =0.64, p<0.001) was modified by the addition of either PC (r 2 =0.74, p for PC =0.005) or PR strain(r 2 =0.69, p for PR =0.04). Conclusions : These data show that development of hypertension with LV hypertrophy does not enhance but impairs circumferential and radial LV mechanics as assessed with strain imaging, and that like EF, circumferential and radial strain are related to afterload (wall stress). However, both confer additional information regarding contractility. Conclusions regarding myocardial function based on strain imaging must account for its load dependence.

Multiple Autoantibodies against Cardiovascular Receptors as Biomarkers in Hypertensive Heart Disease

Cardiology ◽  
2019 ◽  
Vol 142 (1) ◽  
pp. 47-55 ◽  
Author(s):  
Xin Wang ◽  
Yuan Zhang ◽  
Juan Zhang ◽  
Yu-Xing Wang ◽  
Xiao-Rong Xu ◽  
...  
Keyword(s):  
Heart Disease ◽  
Angiotensin Ii ◽  
Muscarinic Receptors ◽  
Hypertensive Heart Disease ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Enzyme Linked Immunosorbent Assay ◽  
Ventricular Ejection Fraction ◽  
M2 Muscarinic Receptors ◽  
Normal Controls

Objectives: The pathogenesis of hypertensive heart disease (HHD) remains unclear, which might include autoimmunity. The aim of the present study was to determine whether a relationship exists between the presence of autoantibodies against β1, β2, α1 adrenoreceptors, M2-muscarinic receptors, angiotensin II type1 receptors and HHD. Methods: In the present study, 44 patients diagnosed with HHD, 36 patients with hypertension, and 40 controls were also enrolled. The measurement of these 5 autoantibodies was performed by enzyme-linked immunosorbent assay. Results: The frequencies of autoantibodies against β1, β2, α1 adrenoreceptors, autoantibodies against M2-muscarinic receptors and autoantibodies against angiotensin II type1 receptors were significantly higher in patients with HHD, when compared to patients with hypertension and normal controls (all p < 0.001). In addition, the titers of these 5 autoantibodies significantly increased in patients with HHD. Patients who were positive for all 5 autoantibodies had larger left ventricular end-diastolic diameter (60.5 ± 4.9 vs. 57.8 ± 5.0 vs. 52.5 ± 5.3 mm) and worse left ventricular ejection fraction (45.0 ± 11.0 vs. 56.6 ± 10.4 vs. 57.8 ± 5.3%), when compared to patients not positive for all the 5 autoantibodies and patients negative for all the 5 autoantibodies (χ2 = 9.524, p = 0.009 and χ2 = 7.689, p = 0.021). Furthermore, a significant positive correlation was observed between each 2 autoantibodies of these 5 autoantibodies (all p < 0.001). Conclusion: Multiple autoantibodies of cardiovascular receptors may be involved in the pathogenesis and may be predictive factors of HHD.

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