Development of Left Ventricular Diastolic Dysfunction With Preservation of Ejection Fraction During Progression of Infant Right Ventricular Hypertrophy

Kitahori, Kazuo; He, Hui; Kawata, Mitsuhiro; Cowan, Douglas B.; Friehs, Ingeborg; Nido, Pedro J. del; McGowan, Francis X.

doi:10.1161/circheartfailure.109.862664

Cited by 38 publications

(42 citation statements)

References 40 publications

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“…11,15,19) In this study, RVFAC in the PAB group decreased from 3 weeks postoperatively ( Figure 2D), as RVMPI increased during the same period after surgery ( Figure 2E). The RV free wall in diastole thickened from 4 weeks after operation ( Figure 2F).…”

Section: Morphologysupporting

confidence: 52%

“…11,22) Clinically, long-term RV hypertension causes various complications in some congenital diseases such as surgically repaired tetralogy of Fallot. 5,6) The increased stress on the RV limits long-term survival.…”

Section: Discussionmentioning

confidence: 99%

“…We calculated this as previously described. 11,15,16,18) Two periods were measured in pulsed Doppler mode: the ejection time (a) and the time interval (b) between the end of LV inflow and onset. MPI was then calculated using the formula (b-a)/a.…”

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confidence: 99%

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Mechanism of Pressure-Overload Right Ventricular Hypertrophy in Infant Rabbits

Minegishi¹,

Kitahori

Murakami

et al. 2011

Int. Heart J.

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SummaryAlthough pressure-overload right ventricular hypertrophy is a long-term risk in some congenital heart diseases such as tetralogy of Fallot, how it develops is unclear. The aim of this study was to investigate the mechanism of development of this right ventricular heart failure.Pulmonary artery banding in 10-day-old rabbits induced pressure-overload right ventricular hypertrophy as they grew. Comparisons were made with age-matched sham controls (n = 24 per group). In weekly serial echocardiography, the right ventricular contraction and diastolic function decreased from 3 weeks after surgery (P < 0.01), and the right ventricle became hypertrophic from 4 weeks after (P < 0.05). Pressure-overload increased cardiomyocyte apoptosis from 4 weeks postoperatively (TUNEL staining and Western blotting analysis, P < 0.05); and fibrosis occurred in the right ventricular cardiomyocytes at 8 weeks after operation (Masson's trichrome stain, P < 0.01).In our model, pressure-overload to the right ventricle caused the right ventricular disorder, hypertrophy, and fibrosis. Apoptosis of right ventricular cardiomyocytes was involved in progression. We have shown for the first time the mechanism whereby pressure-overload right ventricular hypertrophy develops in an infant rabbit model. (Int Heart J 2011; 52: 56-60)

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Section: Morphologysupporting

confidence: 52%

Section: Discussionmentioning

confidence: 99%

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Mechanism of Pressure-Overload Right Ventricular Hypertrophy in Infant Rabbits

Minegishi¹,

Kitahori

Murakami

et al. 2011

Int. Heart J.

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“…Subsequently, others described the "working heart" model, in which the myocardium performs both pressure and volume work. 2 Such preparations have been instrumental in elucidating mechanisms of myocardial action, 3 myocardial metabolism, [4][5][6] and effects of cardiotonic medications. [7][8][9] The use of medications that enhance myocardial contractility is common in critically ill patients.…”

Section: Introductionmentioning

confidence: 99%

Rodent Working Heart Model for the Study of Myocardial Performance and Oxygen Consumption

DeWitt

Black

Kheir

2016

JoVE

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Isolated working heart models have been used to understand the effects of loading conditions, heart rate and medications on myocardial performance in ways that cannot be accomplished in vivo. For example, inotropic medications commonly also affect preload and afterload, precluding load-independent assessments of their myocardial effects in vivo. Additionally, this model allows for sampling of coronary sinus effluent without contamination from systemic venous return, permitting assessment of myocardial oxygen consumption. Further, the advent of miniaturized pressure-volume catheters has allowed for the precise quantification of markers of both systolic and diastolic performance. We describe a model in which the left ventricle can be studied while performing both volume and pressure work under controlled conditions. In this technique, the heart and lungs of a Sprague-Dawley rat (weight 300-500 g) are removed en bloc under general anesthesia. The aorta is dissected free and cannulated for retrograde perfusion with oxygenated Krebs buffer. The pulmonary arteries and veins are ligated and the lungs removed from the preparation. The left atrium is then incised and cannulated using a separate venous cannula, attached to a preload block. Once this is determined to be leak-free, the left heart is loaded and retrograde perfusion stopped, creating the working heart model. The pulmonary artery is incised and cannulated for collection of coronary effluent and determination of myocardial oxygen consumption. A pressurevolume catheter is placed into the left ventricle either retrograde or through apical puncture. If desired, atrial pacing wires can be placed for more precise control of heart rate. This model allows for precise control of preload (using a left atrial pressure block), afterload (using an afterload block), heart rate (using pacing wires) and oxygen tension (using oxygen mixtures within the perfusate).

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“…We have demonstrated that changes in cardiomyocyte viability, lack of adaptive capillary growth, fibrosis, and response to metabolic stress are differentially regulated in LV-AOB and RV-PAB (11,13,16,20). However, the mechanisms involved in the compensated phase of LV-AOB and RV-PAB have yet to be clearly elucidated.…”

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confidence: 97%

Pressure-overload hypertrophy of the developing heart reveals activation of divergent gene and protein pathways in the left and right ventricular myocardium

Friehs

Cowan

Choi

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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and left ventricular (LV) myocardium differ in their pathophysiological response to pressure-overload hypertrophy. In this report we use microarray and proteomic analyses to identify pathways modulated by LV-aortic banding (AOB) and RV-pulmonary artery banding (PAB) in the immature heart. Newborn New Zealand White rabbits underwent banding of the descending thoracic aorta [LV-AOB; n ϭ 6]. RV-PAB was achieved by banding the pulmonary artery (n ϭ 6). Controls (n ϭ 6 each) were sham-manipulated. After 4 (LV-AOB) and 6 (RV-PAB) wk recovery, the hearts were removed and matched RNA and proteins samples were isolated for microarray and proteomic analysis. Microarray and proteomic data demonstrate that in LV-AOB there is increased transcript expression levels for oxidative phosphorylation, mitochondria energy pathways, actin, ILK, hypoxia, calcium, and protein kinase-A signaling and increased protein expression levels of proteins for cellular macromolecular complex assembly and oxidative phosphorylation. In RV-PAB there is also an increased transcript expression levels for cardiac oxidative phosphorylation but increased protein expression levels for structural constituents of muscle, cardiac muscle tissue development, and calcium handling. These results identify divergent transcript and protein expression profiles in LV-AOB and RV-PAB and provide new insight into the biological basis of ventricular specific hypertrophy. The identification of these pathways should allow for the development of specific therapeutic interventions for targeted treatment and amelioration of LV-AOB and RV-PAB to ameliorate morbidity and mortality.heart; hypertrophy; microarray; proteomics VENTRICULAR OUTFLOW TRACT obstruction in congenital heart defects such as interrupted aortic arch, coarctation of the aorta on the left side, and pulmonary artery stenosis on the right side, causes progressive cardiac hypertrophy and, if unrelieved, leads to ventricular dilatation with contractile dysfunction and ultimately irreversible heart failure. Initially, the myocardium compensates to elevated pressure-loading by increasing wall thickness to normalize wall stress. These changes allow for maintenance of contractile function in left ventricular pressureoverload hypertrophy [LV-aortic banding (AOB)], whereas in right ventricular pressure-overload hypertrophy [RV-pulmonary artery banding (PAB)] these changes are less effective and progression to failure occurs more rapidly (2, 4, 15).Our previous studies using the rabbit model of LV-AOB and RV-PAB have demonstrated that disease progression involves both cellular and extracellular components of the myocardium. We have demonstrated that changes in cardiomyocyte viability, lack of adaptive capillary growth, fibrosis, and response to metabolic stress are differentially regulated in LV-AOB and RV-PAB (11,13,16,20). However, the mechanisms involved in the compensated phase of LV-AOB and RV-PAB have yet to be clearly elucidated. In this report we present microarray and proteomic analyses of the LV and RV during t...

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Development of Left Ventricular Diastolic Dysfunction With Preservation of Ejection Fraction During Progression of Infant Right Ventricular Hypertrophy

Cited by 38 publications

References 40 publications

Mechanism of Pressure-Overload Right Ventricular Hypertrophy in Infant Rabbits

Mechanism of Pressure-Overload Right Ventricular Hypertrophy in Infant Rabbits

Rodent Working Heart Model for the Study of Myocardial Performance and Oxygen Consumption

Pressure-overload hypertrophy of the developing heart reveals activation of divergent gene and protein pathways in the left and right ventricular myocardium

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