@misc {maleckar2021b,
	title = {B-PO02-022 Combining simulation and machine learning to accurately predict arrhythmic risk in post-infarction patients},
	howpublished = {Heart Rhythm},
	volume = {18},
	number = {8},
	year = {2021},
	pages = {S104},
	publisher = {Elsevier},
	address = {Boston, MA},
	author = {Maleckar, Molly and Per Magne {Florvaag} and Str{\o}m, Vilde and Glinge, Charlotte and Jabbari, Reza and Vejlstrup, Niels and Engstrom, Thomas and Kiril A. {Ahtarovski} and Jespersen, Thomas and Tfelt-Hansen, Jacob and Arevalo, Hermenegild}
}
@article {maleckar2021combined,
	title = {Combined In-silico and Machine Learning Approaches Toward Predicting Arrhythmic Risk in Post-infarction Patients},
	journal = {Frontiers in physiology},
	volume = {12},
	year = {2021},
	pages = {745349},
	publisher = {Frontiers},
	author = {Maleckar, Molly and Myklebust, Lena and Julie Johanne {Uv} and Per Magne {Florvaag} and Str{\o}m, Vilde and Glinge, Charlotte and Jabbari, Reza and Vejlstrup, Niels and Engstr{\o}m, Thomas and Ahtarovski, Kiril and Jespersen, Thomas and Tfelt-Hansen, Jacob and Arevalo, Hermenegild}
}
@misc {27158,
	title = {A Combined In-Silico and Machine Learning Approach towards Predicting Arrhythmic Risk in Post-Infarction Patients},
	howpublished = {Computing in Cardiology, Singapore},
	year = {2019},
	author = {Per Magne {Florvaag} and Str{\o}m, Vilde and Glinge, Charlotte and Jabbari, Reza and Vejlstrup, Niels and Engstrom, Thomas and Kiril A. {Ahtarovski} and Jespersen, Thomas and Tfelt-Hansen, Jacob and Naumova, Valeriya and Arevalo, Hermenegild}
}
@inproceedings {25226,
	title = {A multiple kernel learning framework to investigate the relationship between ventricular fibrillation and first myocardial infarction},
	journal = {Functional Imaging and Modelling of the Heart},
	year = {2017},
	publisher = { Springer},
	isbn = {978-3-319-59448-4},
	doi = {10.1007/978-3-319-59448-4_16},
	author = {Marciniak, Maciej and Arevalo, Hermenegild and Tfelt-Hansen, Jacob and Kiril A. {Ahtarovski} and Jespersen, Thomas and Jabbari, Reza and Glinge, Charlotte and Vejlstrup, Niels and Engstrom, Thomas and Maleckar, Molly and Kristin Sarah {Mcleod}},
	editor = {Pop, Mihaela and Wright, Graham}
}
@inproceedings {24886,
	title = {From MR image to patient-specific simulation and population-based analysis:Tutorial for an openly available image-processing pipeline},
	journal = {MICCAI Workshop on Statistical Atlases and Cardiac Models of the Heart},
	year = {2016},
	publisher = {Springer},
	address = {Berlin},
	author = {Marciniak, Maciej and Arevalo, Hermenegild and Tfelt-Hansen, Jacob and Jespersen, Thomas and Jabbari, Reza and Glinge, Charlotte and Kiril A. {Ahtarovski} and Vejlstrup, Niels and Maleckar, Molly and Kristin Sarah {Mcleod}},
	editor = {Engstrom, Thomas}
}
@article {Simula.simula.2204,
	title = {Investigations of the NaV\beta1b Sodium Channel Subunit in Human Ventricle; Functional Characterization of the H162P Brugada Syndrome Mutant},
	journal = {Heart and Circulatory Physiology},
	volume = {306},
	number = {8},
	year = {2014},
	month = {February},
	pages = {H1204-H1212},
	abstract = {Brugada Syndrome (BrS) is a rare inherited disease which can give rise to ventricular arrhythmia and ultimately sudden cardiac death. Numerous loss-of-function mutations in the cardiac sodium channel NaV1.5 have been associated with BrS. However, few mutations in the auxiliary NaV\beta1-4 subunits have been linked to this disease. Here we investigate differences in expression and function between NaV\beta1 and NaV\beta1b, and whether the H162P/NaV\beta1b mutation found in a BrS patient is likely to be the underlying cause of disease. The impact of NaV\beta1-subunits were investigated by patch-clamp electrophysiology and the obtained in vitro values were used for subsequent in silico modeling. We find that NaV\beta1b transcripts are expressed at higher levels than NaV\beta1 transcripts in the human heart. NaV\beta1 and NaV\beta1b co-expressed with NaV1.5 show similar kinetics, but the current level of NaV\beta1b was higher. When co-expressed with NaV1.5, the NaV\beta1b/H162P mutated subunit peak current density was reduced by 47\% (-626.5\pm89 vs. - 333.5\pm71 pA/pF), V{\textonehalf} steady-state inactivation shifted by -8.7 mV (-70.2\pm1.9 vs. -77.0\pm2.3 mV), and time-dependent recovery from inactivation slowed by more than 50\% as compared to co-expression with NaV\beta1b WT. Computer simulations revealed that these electrophysiological changes result in a reduction in both action potential amplitude and maximum upstroke velocity. The experimental data thereby indicate that NaV\beta1b/H162P results in reduced sodium channel activity functionally effecting the ventricular action potential. This result is an important replication to support the notion that BrS can be linked to the function of NaV\beta1b and is associated with loss-of-function of the cardiac sodium channel.},
	author = {Yuan, Lei and Koivum{\"a}ki, Jussi and Liang, Bo and Lasse G. {Lorentzen} and Jesper H. {Svendsen} and Tfelt-Hansen, Jacob and Maleckar, Molly and Schmitt, Nicole and Morten S. {Olesen} and Jespersen, Thomas}
}
