Herein, we describe the catalytic hydrogenation of CO2 to formate with (PNP)­Mn–H (PNP = 2,6-bis­(di-tert-butylphosphinomethyl)­pyridine; Mn = Mn­(CO)2). Contrary to the established mechanism for CO2 hydrogenation, mechanistic studies indicate that CO2 does not insert into the Mn–H bond of (PNP)­Mn–H to give the formate species, (PNP)­Mn–OCHO. The lack of reactivity is confirmed by thermochemical studies that show that (PNP)­Mn–H is not sufficiently hydridic to reduce CO2. Deprotonation of the hydride to give [(*PNP)­Mn–H] – (* indicates the deprotonated ligand) enhances the hydricity by ∼17 kcal·mol–1 and hence should be sufficiently hydridic to hydrogenate CO2. This reactivity is not observed, and CO2 instead binds to the backbone to generate another anionic hydride species [(CO 2 -PNP)­Mn–H]. The formate is lost only from this species, through hydride transfer to an external CO2. These findings are unexpected because substrate binding to the backbone of catalysts that can undergo metal–ligand cooperativity (MLC) is thought to be detrimental to catalysis; this work suggests that alternative mechanisms should be considered. The enhanced hydricity observed upon deprotonation may be broadly applicable to systems capable of undergoing MLC. Moreover, this work shows an example of how thermochemical analysis can be used to advance mechanistic understanding in (de)­hydrogenation catalysis.

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Background: Ventriculo-ventricular interactions are known to exist, though not well quantified. We hypothesised that the ventricular–vascular coupling ratio assessed by cardiovascular MRI would provide insight into this relationship. We also sought to compare MRI-derived ventricular–vascular coupling ratio to echocardiography and patient outcomes. Methods: Children with cardiac disease and biventricular physiology were included. Sanz’s and Bullet methods were used to calculate ventricular–vascular coupling ratio by MRI and echocardiography, respectively. Subgroup analysis was performed for right and left heart diseases. Univariate and multivariate regressions were performed to determine associations with outcomes. Results: A total of 55 patients (age 14.3 ± 2.5 years) were included. Biventricular ventricular–vascular coupling ratio by MRI correlated with each other (r = 0.41; p = 0.003), with respect to ventricle’s ejection fraction (r = −0.76 to −0.88; p < 0.001) and other ventricle’s ejection fraction (r = −0.42 to −0.47; p < 0.01). However, biventricular ejection fraction had only weak correlation with each other (r = 0.31; p = 0.02). Echo underestimated ventricular–vascular coupling ratio for the left ventricle (p < 0.001) with modest correlation to MRI-derived ventricular–vascular coupling ratio (r = 0.43; p = 0.002). There seems to be a weak correlation between uncoupled right ventricular–vascular coupling ratio with the need for intervention and performance on exercise testing (r = 0.33; p = 0.02). Conclusion: MRI-derived biventricular ventricular–vascular coupling ratio provides a better estimate of ventriculo-ventricular interaction in children and adolescents with CHD. These associations are stronger than traditional parameters and applicable to right and left heart conditions.

We report a rare case of aortic valve atresia and type C interrupted aortic arch with retrograde filling of the ascending aorta via the right common carotid artery through intracranial collateralisation and a presumed intact circle of Willis, who successfully underwent a complete biventricular repair in the neonatal period.

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