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Focus Issue on Devices

Volume 36, Issue 37, 1 October 2015









  • Jonas Ghouse, Christian Theil Have, Peter Weeke, Jonas Bille Nielsen, Gustav Ahlberg, Marie Balslev-Harder, Emil Vincent Appel, Tea Skaaby, Søren-Peter Olesen, Niels Grarup, Allan Linneberg, Oluf Pedersen, Stig Haunsø, Jesper Hastrup Svendsen, Torben Hansen, Jørgen Kim Kanters, Morten Salling Olesen Eur Heart J (2015) 36 (37): 2523-2529 DOI: http://dx.doi.org/10.1093/eurheartj/ehv297 First published online: 9 July 2015 (7 pages)

    The present study indicates that the clinicians should be cautious when interpreting a positive genetic result. In cases where a clear co-segregation of phenotype (prolonged QT interval) and genotype exist, the diagnosis of congenital long QT syndrome (cLQTS) is straightforward. In cases where only the proband in the family has a clear phenotype, even in cases where a positive genotype is identified in the LQTS genes, the clinician should be aware of the possibility that the given genetic variant might not necessarily be related to cLQTS in the proband. This should not affect the treatment, but caution is advised in the decision-making of geno-positive relatives without any relevant clinical symptoms.

  • Jian Guo, Anton Mihic, Jun Wu, Yuemei Zhang, Kaustabh Singh, Sanjiv Dhingra, Richard D. Weisel, Ren-Ke Li Eur Heart J (2015) 36 (37): 2530-2540 DOI: http://dx.doi.org/10.1093/eurheartj/ehv294 First published online: 9 July 2015 (11 pages)

    During ischaemic injury, cardiac tissue undergoes compensatory hypertrophy to preserve function, but this hypertrophy can progress to adverse ventricular dilatation and eventually to heart failure. Increased angiogenesis, requiring secreted angiogenic growth factors, may be critical to maintaining beneficial compensatory hypertrophy and preventing adverse cardiac remodelling. We generated mice that overexpress the newly discovered angiogenic factor CNPY2 in heart tissue and showed that they had reduced ventricular dilatation and adverse remodelling after ischaemic injury, with better preserved systolic and diastolic heart function and cardiac vasculature than normal controls. Moreover, we showed that transgenic mice that overexpress CNPY2 had decreased p53 activation in hearts after injury and better maintained expression of the p53 target Hif-1α, thereby potentially retaining a beneficial pro-angiogenic programme. These results suggest that CNPY2 may be a useful component of angiogenic therapy delivered to injured hearts and may help to better preserve their cardiac function and prevent the switch from beneficial compensatory hypertrophy to ventricular dilatation and eventual heart failure.