David S. Winlaw, MBBS, MD, FRACS
Central Message
Although impressive clinical results have been reported with pulmonary artery banding in children with cardiomyopathy, supporting mechanisms at a cellular and molecular level remain elusive.
See Article page 2416.
Surgeons are reductionists; we know what works for patients, often on the basis of personal experience. We can sometimes suggest a plausible mechanism, citing basic mechanisms at work. Surgeons are also sceptics; we value clarity and simplicity and are quick to note when the “science” fails to demonstrate mechanisms supporting observations made in the clinical domain. There is a lot to be sceptical about, because so many procedures lack an evidence base or a defined mechanism of action.
So it is when Yerebakan and colleagues
1
in this issue of the Journal present a series of animal experiments that seek to demonstrate cellular and molecular mechanisms underlying the apparent beneficial effects of pulmonary artery banding in children with cardiomyopathy. The Giessen group and an international collaborative2
have reported benefits of this approach in clinical practice, and there is a registered clinical trial3
underway. Septal repositioning and initiation of a regenerative response are proposed as mechanisms, drawing on experience suggested by similar approaches in l-transposition,4
, - Ma K.
- Gao H.
- Hua Z.
- Yang K.
- Hu S.
- Zhang H.
- et al.
Palliative pulmonary artery banding versus anatomic correction for congenitally corrected transposition of the great arteries with regressed morphologic left ventricle: long-term results from a single center.
J Thorac Cardiovasc Surg. 2014; 148: 1566-1571
5
albeit a very different clinical presentation.Important experimental design and methodologic issues need to be considered. First, the mortality from both initial and sham banding was substantial, and medical therapy was not used on either group. Second, the criterion standard assessment of ventricular performance with conductance catheters largely failed to demonstrate a difference between treatment and control groups, which is surprising considering the gross morphologic changes. Finally, analysis of ventricular muscle was limited to simple histologic examination, without comprehensive analysis of cell type, proportion of c-kit-positive cells, angiogenic milieu, measures of apoptosis, or gene expression data that might support the regenerative hypothesis.
In a drug-toxicity model of ventricular failure, damage is caused primarily by oxidative stress,
6
and this may not adequately mimic the pathogenesis of dilated cardiomyopathy, where disruption of the dystrophin-associated complex is a more prominent feature.7
Nevertheless, there were improvements in left ventricular size and ejection fraction in the treatment group, and it is suggested that in this way the model recapitulates the therapeutic effect of central pulmonary artery banding in cardiomyopathy. It is an important step toward better understanding a phenomenon that may be useful in preventing or delaying the need for mechanical support and transplantation in children. Should molecular evidence be forthcoming in future studies, it will be broadly relevant to management of corrected transposition and perhaps even in the achievement of “growth” in hypoplastic ventricles.
For now, the big picture remains fuzzy. The reductionists amongst us still seek an understanding of the basic mechanisms. and the sceptics will prevail until molecular data support the intimation that there is regeneration and improved “cross talk” between ventricles. Could we simply be observing the superimposition of restrictive physiology on the pathology of dilated cardiomyopathy?
References
- Effects of pulmonary artery banding in doxorubicin-induced left ventricular cardiomyopathy.J Thorac Cardiovasc Surg. 2019; 157: 2416-2428.e4
- Pulmonary artery banding for functional regeneration of end-stage dilated cardiomyopathy in young children: world network report.Circulation. 2018; 137: 1410-1412
- Reversible pulmonary artery banding as simplified management of end-stage dilated left ventriculopathy in early life.(Available at:) (Accessed March 16, 2019)
- Palliative pulmonary artery banding versus anatomic correction for congenitally corrected transposition of the great arteries with regressed morphologic left ventricle: long-term results from a single center.J Thorac Cardiovasc Surg. 2014; 148: 1566-1571
- Intention-to-treat analysis of pulmonary artery banding in conditions with a morphological right ventricle in the systemic circulation with a view to anatomic biventricular repair.Circulation. 2005; 111: 405-411
- Molecular mechanism of doxorubicin-induced cardiomyopathy—an update.Eur J Pharmacol. 2018; 818: 241-253
- Dilated cardiomyopathy.Lancet. 2010; 375: 752-762
Article info
Publication history
Published online: February 26, 2019
Accepted:
February 11,
2019
Received:
February 10,
2019
Footnotes
Disclosures: Author has nothing to disclose with regard to commercial support.
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© 2019 by The American Association for Thoracic Surgery
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- Effects of pulmonary artery banding in doxorubicin-induced left ventricular cardiomyopathyThe Journal of Thoracic and Cardiovascular SurgeryVol. 157Issue 6Open Archive
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