Left ventricular morphology influences mortality after the Norwood operation

Walsh, Mark A.; McCrindle, Brian W.; Dipchand, Anne I.; Manlhiot, Cedric; Hickey, Edward; Caldarone, Christopher A.; Arsdell, Glen S. Van; Schwartz, Steven M.

doi:10.1136/hrt.2008.156612

Cited by 42 publications

(25 citation statements)

References 28 publications

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“…Much attention has recently focussed on the subgroup of patients with HLHS that has a significant LV, implying disadvantageous properties of this "piggyback" ventricle on ventricular function and outcome [9][10][11].…”

Section: Introductionmentioning

confidence: 99%

Comprehensive evaluation of right ventricular function in children with different anatomical subtypes of hypoplastic left heart syndrome after Fontan surgery

Petko

Möller

Hoffmann

et al. 2011

International Journal of Cardiology

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Section: Introductionmentioning

confidence: 99%

Comprehensive evaluation of right ventricular function in children with different anatomical subtypes of hypoplastic left heart syndrome after Fontan surgery

Petko

Möller

Hoffmann

et al. 2011

International Journal of Cardiology

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“…105 Likewise, a larger interventricular septum may increase the risk for death or transplantation in this population. 106 This may be yet another manifestation of the effects of ventricular-ventricular interactions on RV function. Although further discussion of these phenomena in the functionally single ventricle is beyond the purview of this review, we believe that an improved understanding of regional and global responses of the myocardium in these patients will likely lead to novel therapeutic strategies such are those that are evolving from studies of the biventricular heart discussed here.…”

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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“…As pointed out by Atallah et al (10), the established independent risk factors for interstage mortality in postNorwood palliation include tricuspid valve regurgitation and right ventricular dysfunction. The focus of the study by Khoo et al (2) is on the systemic right ventricle function, but the variations of the left ventricle in HLHS may also have clinical influence, albeit less significant (11). The right ventricular function in patients with systemic right ventricle after Fontan operation has also been studied with echocardiographic parameters as in the study by Chow et al (12), and RV dysfunction in these patients remains a clinical concern at follow-up.…”

mentioning

confidence: 95%