Time course of changes in the mechanical properties of the canine right and left ventricles during hypertrophy caused by pressure overload.

Mirsky, Israel; Laks, Michael M.

doi:10.1161/01.res.46.4.530

Cited by 38 publications

(9 citation statements)

References 42 publications

(26 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Prior reports have already recommended that neither ventricular mass nor wall thickness should be used as a substitute for estimating myocardial stiffness, thus corroborating our findings [1, 43, 44]. …”

Section: Discussionsupporting

confidence: 91%

Quantification of myocardial stiffness using magnetic resonance elastography in right ventricular hypertrophy: initial feasibility in dogs

Silveira

Scansen

Wassenaar

et al. 2016

Magnetic Resonance Imaging

View full text Add to dashboard Cite

Introduction Myocardial stiffness is an important determinant of cardiac function and is currently invasively and indirectly assessed by catheter angiography. This study aims to demonstrate the feasibility of quantifying right ventricular (RV) stiffness noninvasively using cardiac magnetic resonance elastography (CMRE) in dogs with severe congenital pulmonary valve stenosis (PVS) causing RV hypertrophy, and compare it to remote myocardium in the left ventricle (LV). Additionally, correlations between stiffness and selected pathophysiologic indicators from transthoracic echocardiography (TTE) and cardiac magnetic resonance imaging were explored. Methods In-vivo CMRE was performed on nine dogs presenting severe congenital PVS using a 1.5T MRI scanner. T1-MOLLI, T2-prepared-bSSFP, gated-cine GRE-MRE and LGE (PSIR) sequences were used to acquire a basal short-axis slice. RV and LV-free-wall (FW) stiffness measurements were compared against each other and also correlated to ventricular mass, RV and LV FW thickness, T1 and T2 relaxation times, and extracellular volume fraction (ECV). Peak transpulmonary pressure gradient and myocardial strain were also acquired on eight dogs by TTE and correlated to RV-FW systolic stiffness. Potential correlations were evaluated by Spearman’s rho (rs). Results RV-FW stiffness was found to be significantly higher than the LV-FW stiffness both during end-systole (ES) (p=0.002) and end-diastole (ED) (p=0.029). Significant correlations were observed between RV-FW ES and LV-FW ED stiffness versus ECV (rs=0.75; p-value=0.05). Non-significant moderate correlations were found between LV-FW ES (rs=0.54) and RV-FW ED (rs=0.61) versus ECV. Furthermore, non-significant correlations were found between RV or LV-FW stiffness and the remaining variables (rs<0.54; p-value>0.05). Conclusion This study demonstrates the feasibility of determining RV stiffness. The positive correlations between stiffness and ECV might indicate some interdependence between stiffness and myocardial extracellular matrix alterations. However, further studies are warranted to validate our initial observations.

show abstract

Section: Discussionsupporting

confidence: 91%

Quantification of myocardial stiffness using magnetic resonance elastography in right ventricular hypertrophy: initial feasibility in dogs

Silveira

Scansen

Wassenaar

et al. 2016

Magnetic Resonance Imaging

View full text Add to dashboard Cite

show abstract

“…[17][18][19] The relation between average midwall circumferential wall stress and midwall circumferential strain was used to describe the intrinsic compliance of a circumferential myocardial hoop at the equator of the LV. To estimate midwall circumferential stress at the equator of the LV, an effective external LV pressure (ELVP) was calculated with the assumption that two thirds of the surface area of the LV is surrounded by the pleural cavity (since the pericardial incision was loosely approximated) and one third is surrounded by the RV'7 (i.e., ELVP=[2Pp +RV pressure]/3).…”

Section: Discussionmentioning

confidence: 99%

Altered left ventricular chamber stiffness and isovolumic relaxation in dogs with chronic pulmonary hypertension caused by emphysema.

1993

View full text Add to dashboard Cite

Background. In chronic obstructive lung disease, a right to left ventricular septal shift that occurs as a consequence of right ventricular pressure overload is the usual mechanism given to explain a decrease in left ventricular (LV) diastolic performance. The purpose of the present study was to examine the extent to which this mechanism could account for a decrease in LV diastolic function in a canine model in which pulmonary artery pressure was elevated to a level found in human disease.Methods and Results. Severe emphysema was produced in dogs by repeated instillations of the enzyme papain into the lung. To assess LV diastolic function, we used sonomicrometry, in which three pairs of subendocardial crystal transducers were implanted along the three orthogonal axes of the LV. LV end-diastolic dimensions and pressure-strain relations along the three axes, as well as the time constant of LV isovolumic relaxation (T), were measured before (baseline) and after 1 year of emphysema (post-l-year study). The results showed that after 1 year of pulmonary hypertension, LV pressure-strain relations were decreased along the septal-lateral and anterior-posterior axes, but a right to left ventricular septal shift was not detected. The relation of average midwall circumferential stress to midwall circumferential strain was used to describe the intrinsic compliance of the LV. The results showed that myocardial stiffness increased in emphysema but that chamber volume was not reduced. At the post-i-year study, T was abnormally increased in the emphysema group in response to augmented preload and afterload compared with preemphysema measurements.Conclusions. We conclude that mechanisms other than ventricular interdependence may be operative in leading to altered LV diastolic filling in chronic emphysema. (Circulation 1993;87:247-260)

show abstract

“…It has been suggested that collagen fibres could serve as a transducer regulating myocyte growth and protein synthesis Jalil et al 1989). Moreover, several reports have shown that structural and molecular changes in non-contractile proteins may cause such serious functional alterations of the heart as myocardial stiffness (Mirsky & Laks 1980;Mortz & Struer 1989).…”

Section: Methodsmentioning

confidence: 99%

Different Biventricular Remodelling of Myosin and Collagen in Pulmonary Hypertension

Ishikawa

Honda

Yamada

et al. 1992

Clin Exp Pharma Physio

View full text Add to dashboard Cite

1. To clarify the metabolism of contractile and non-contractile proteins of the ventricles during the development of right ventricular hypertrophy (RVH) and accompanying congestive heart failure (CHF) in response to a pressure overload, monocrotaline was injected subcutaneously into Sprague-Dawley (SD) rats. Myosin isoenzymes (MIE) were analysed by pyrophosphate gel electrophoresis under non-dissociating conditions. Acid-soluble collagens were analysed by an improved, noninterrupted sodium dodecylsulfate polyacrylamide gel electrophoresis (SDS-PAGE). Tissue collagen content was also measured after the estimation of hydroxyproline concentration in tissues. 2. Monocrotaline induced RVH, but not left ventricular hypertrophy, at 2 weeks after the injection of monocrotaline, with severe RVH with CHF present at 4 weeks. In the right ventricles (RV) treated with monocrotaline, MIE shifted significantly from V1 to V3 at 2 weeks. The shift of MIE was more pronounced at 4 weeks. The proportion of type III collagen increased significantly compared with controls at 2 weeks. At 4 weeks, the proportion of types III and V collagens increased significantly compared with controls. 3. In left ventricles (LV) treated with monocrotaline, a similar but less remarkable shift of MIE was observed without remodelling of collagen types at 2 and 4 weeks. The concentration of collagen in either the RV or LV treated with monocrotaline showed no significant changes at 2 and 4 weeks compared with controls. 4. These results demonstrate a remodelling of the contractile and non-contractile proteins during the development of RVH and accompanying CHF, and provide evidence for changes in protein metabolism of the counterpart of RV (i.e. the LV). These results may provide important insights into the pathophysiology of adaptive or non-adaptive cardiac hypertrophy in response to a pressure overload.

show abstract

Time course of changes in the mechanical properties of the canine right and left ventricles during hypertrophy caused by pressure overload.

Cited by 38 publications

References 42 publications

Quantification of myocardial stiffness using magnetic resonance elastography in right ventricular hypertrophy: initial feasibility in dogs

Quantification of myocardial stiffness using magnetic resonance elastography in right ventricular hypertrophy: initial feasibility in dogs

Altered left ventricular chamber stiffness and isovolumic relaxation in dogs with chronic pulmonary hypertension caused by emphysema.

Different Biventricular Remodelling of Myosin and Collagen in Pulmonary Hypertension

Contact Info

Product

Resources

About