Myoarchitecture and connective tissue in hearts with tricuspid atresia

Sánchez‐Quintana, Damian; Climent, Vicente; Ho, Siew Yen; Anderson, Robert H.

doi:10.1136/hrt.81.2.182

Cited by 70 publications

(54 citation statements)

References 22 publications

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“…As demonstrated elegantly in pathological specimens and by diffusion tensor magnetic resonance imaging studies, these myofiber tracts originate predominantly in the superficial layer of the LV and cross to the RV ( Figure 5). 60,94 As for the LV, the aggregated RV myocytes form helical angles and intrude in the oblique orientation from the epicardial to endocardial layers. 21,60 In response to afterload, the hypertrophied RV maintains this basic structure and does not form an extensive layer of circular myocytes, which may explain the previously discussed shift from a longitudinal to circumferential strain pattern.…”

Section: March 4 2014mentioning

confidence: 99%

Right Versus Left Ventricular Failure

2014

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1033V entricular failure manifests in many forms, its underlying physiology ranging from overt left ventricular (LV) systolic dysfunction to isolated right ventricular (RV) diastolic dysfunction, and the wide portfolio of resulting symptoms vary from chronic fluid retention to acute multiorgan dysfunction and death. In this review, we discuss the morphological, functional, and molecular similarities and differences in RV and LV responses to adverse loading and failure. We further discuss whether LV and RV function and failure can truly be discussed as separate entities and thereby examine interactions between the ventricles that on one hand contribute to ventricular dysfunction but on the other may be harnessed for therapeutic benefit. Embryological and Physiological Differences Between the RV and LVThe RV and LV have different embryological origins.1 The LV originates from the primary heart field; the RV, from the secondary heart field. Consequently, several genes specifically control RV formation, including, among others, Hand2 and Tbx20.2 During gestation, the RV functions as the systemic ventricle ( Figure 1A). During fetal life, in addition to supplying the modest amount of pulmonary blood flow, the RV pumps blood to the lower body and placenta and contributes more than half of the combined cardiac output.3 With the transition from fetal to postnatal physiology and with the reduction in pulmonary vascular resistance, the subpulmonary RV transforms its morphology and geometry, becoming a thin-walled chamber to adopt its postnatal physiological characteristics. 4 Because it faces a low impedance pulmonary circulation, the normal postnatal RV maintains a cardiac output equal to that of the LV at approximately a fifth of the energy cost. The trapezoidal RV pressure-volume loop reflects this difference, with few if any isovolumic periods. Consequently, RV output starts early during pressure generation and is later maintained by a "hangout period" when antegrade flow continues into the pulmonary artery despite the onset of RV relaxation.5 In contrast, the rectangular LV pressure-volume loops reflect the LV square-wave pump function with distinct and well-developed isovolumic contraction and relaxation periods.6 Likewise, RV myocytes display faster twitch velocities than LV myocytes. 7The physiological differences are reflected in morphological differences between the ventricles (Table 1). The low-pressure RV is triangular in the sagittal plane and crescent-shaped in cross section as a result of the concave RV free wall and convex interventricular septum wrapping around the high-pressured, thick-walled, bullet-shaped LV. Consequently, although the normal RV has a lower ratio of volume to surface area and a thinner wall than the LV, 8 the low cavity pressure determines a lower wall stress and lower oxygen demands.Anatomic differences are also apparent in myocardial architecture. LV subepicardial and subendocardial fibers are oblique and helical with fiber angles ranging from 30° to 80° with a mean of ≈60°, whereas ...

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Section: March 4 2014mentioning

confidence: 99%

Right Versus Left Ventricular Failure

2014

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“…Not only are they enclosed by a common pericardium and share an intraventricular septum, but also the superficial layers of the myocardium are common to both ventricles. 9 Consequently, events that occur on the right side of the heart have important implications for left heart function, and vice versa. This is no better demonstrated than in the normal heart.…”

Section: Right-left Heart Interactionsmentioning

confidence: 99%

Low Cardiac Output Due to Acute Right Ventricular dysfunction and Cardiopulmonary Interactions in Congenital Heart Disease (2013 Grover Conference Series)

Redington

2014

Pulm. circ.

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The importance of right ventricular dysfunction, as a driver of symptoms and outcomes in the normal biventricular circulation, is increasingly recognized. However, the pathophysiologic mechanisms underlying the role of the right ventricle in acute and chronic hemodynamic deterioration are less well understood. This review aims to clarify the impact of acute right ventricular dysfunction on biventricular interactions and, in turn, to discuss the role of cardiopulmonary interactions in the normal circulation and when modified by the presence of associated structural malformations. Such interactions may be adverse or beneficial, and a more complete understanding of their importance may result in novel therapeutic strategies and improved outcomes.

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“…In addition, ventricular compliance is likely to be altered because congenital abnormalities as well as prolonged cyanosis and volume load may have an impact on the fibrous matrix of the myocardium. 7,11 In this study, we performed a differential analysis of PVR and aortopulmonary collateral blood flow in conjunction with global ventricular pump function, ventricular contractility, and diastolic compliance. Measurements were obtained at rest and during dobutamine stress using an MRI catheterization technique.…”

Section: Clinical Perspective On P 631mentioning

confidence: 99%

“…6,41 Finally, histopathologic studies in tricuspid atresia showed abnormal formation and arrangement of the fibrous matrix and the aggregation of myocyte chains. 11 Thus, the potential causes for the development of heart and pulmonary vascular dysfunction are multifactorial, as are the resulting forms of dysfunction, implying that it is essential to investigate these patients with methods that give a differential insight into the predominant form of failure that, in turn, will allow optimizing treatment concepts.…”

Section: Global Ventricular Myocontractile and Diastolic Functionmentioning

confidence: 99%

Pulmonary Vascular Resistance, Collateral Flow, and Ventricular Function in Patients With a Fontan Circulation at Rest and During Dobutamine Stress

Schmitt

Steendijk

Ovroutski

et al. 2010

Circ: Cardiovascular Imaging

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Background-The role, interplay, and relative importance of the multifactorial hemodynamic and myocardial mechanisms causing dysfunction of the Fontan circulation remain incompletely understood. Methods and Results-Using an MRI catheterization technique, we performed a differential analysis of pulmonary vascular resistance and aortopulmonary collateral blood flow in conjunction with global ventricular pump function, myocontractility (end-systolic pressure-volume relation), and diastolic compliance (end-diastolic pressure-volume relation) in 10 patients with a Fontan circulation at rest and during dobutamine stress. Pulmonary and ventricular pressures were measured invasively and synchronized with velocity-encoded MRI-derived pulmonary and aortic blood flows and cine MRI-derived ventricular volumes. Pulmonary vascular resistance and end-systolic and end-diastolic pressure-volume relations were then determined. Aortopulmonary collateral flow was calculated as the difference between aortic and pulmonary flow. Compared to rest, dobutamine caused a small increase in mean pulmonary pressures (PϽ0.05). Collateral flow was significantly augmented (PϽ0.001) and contributed importantly to an increase in pulmonary flow (PϽ0.01). Pulmonary vascular resistance decreased significantly (PϽ0.01). Dobutamine did not increase stroke volumes significantly despite slightly enhanced contractility (end-systolic pressure-volume relation). Active early relaxation () was inconspicuous, but the end-diastolic pressure-volume relation shifted upward, indicating reduced compliance. Conclusions-In patients with a Fontan circulation, aortopulmonary collateral flow contributes substantially to enhanced pulmonary flow during stress. Our data indicate that pulmonary vascular response to augmented cardiac output was adequate, but decreased diastolic compliance was identified as an important component of ventricular dysfunction. (Circ Cardiovasc Imaging. 2010;3:623-631.)

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Myoarchitecture and connective tissue in hearts with tricuspid atresia

Cited by 70 publications

References 22 publications

Right Versus Left Ventricular Failure

Right Versus Left Ventricular Failure

Low Cardiac Output Due to Acute Right Ventricular dysfunction and Cardiopulmonary Interactions in Congenital Heart Disease (2013 Grover Conference Series)

Pulmonary Vascular Resistance, Collateral Flow, and Ventricular Function in Patients With a Fontan Circulation at Rest and During Dobutamine Stress

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