The DOI matches its Crossref record.
Alterations of K+ currents in isolated human ventricular myocytes from patients with terminal heart failure.
Abstract
Prolongation of the action potential has been postulated to be a major reason for the altered diastolic relaxation of the heart in patients with severe heart failure. To investigate the electrophysiological basis for this action potential prolongation in terminal heart failure, K+ currents were recorded in single ventricular myocytes isolated from 16 explanted hearts of patients undergoing transplantation. Results from diseased hearts were compared with ventricular cells isolated from six undiseased donor hearts. Action potential duration was significantly prolonged in cells from patients with heart failure. A delayed rectifier K+ current was hardly detectable in most cells, and if it could be recorded, it was very small in both diseased and undiseased cells. When currents were normalized for cell surface area, the average current density of the inward rectifier K+ current was significantly reduced in diseased cells when compared with normal control cells (hyperpolarization at -100 mV, -15.9 +/- 2.2 vs -9.0 +/- 1.2 microA/cm2; P < .01). In addition, a large transient outward K+ current could be recorded in human myocytes. The average current density of the time-dependent component of this transient outward K+ current was significantly reduced in heart failure (depolarization at +40 mV, 9.1 +/- 1.0 vs 5.8 +/- 0.64 microA/cm2; P < .01). Action potential prolongation in severe heart failure may partially be explained by a reduction in current densities of the inward rectifier K+ current and of the transient outward K+ current. These alterations may thereby have a significant effect on cardiac relaxation.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cited by
Basic Mechanisms of Cardiac Impulse Propagation and Associated Arrhythmias
KLÉBER, A. G., & RUDY, Y. (2004) · Physiological Reviews · doi:10.1152/physrev.00025.2003 · Cited by 1,083
Marbán, E. (2002) · Nature · doi:10.1038/415213a · Cited by 328
Mechanism-based facilitated maturation of human pluripotent stem cell-derived cardiomyocytes
Lieu, D. K., Fu, J.-D., Chiamvimonvat, N., Tung, K. C., McNerney, G. P., Huser, T., Keller, G., Kong, C.-W., & Li, R. A. (2013) · Circulation: Arrhythmia and Electrophysiology · doi:10.1161/circep.111.973420 · Cited by 179
Nicotine effect on cardiovascular system and ion channels
Hanna, S. T. (2006) · Journal of Cardiovascular Pharmacology · doi:10.1097/01.fjc.0000205984.13395.9e · Cited by 102
Akar, F. G., Wu, R. C., Deschenes, I., Armoundas, A. A., Piacentino, V., Houser, S. R., & Tomaselli, G. F. (2004) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00673.2003 · Cited by 88
The human embryonic stem cell-derived cardiomyocyte as a pharmacological model
Harding, S. E., Ali, N. N., Brito-Martins, M., & Gorelik, J. (2007) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2006.08.008 · Cited by 84
CHEN, Y., PAN, N., CHENG, C., HIGA, S., CHEN, Y., & CHEN, S. (2009) · Journal of Cardiovascular Electrophysiology · doi:10.1111/j.1540-8167.2009.01480.x · Cited by 49
Lacroix, D. (2002) · Cardiovascular Research · doi:10.1016/s0008-6363(02)00236-5 · Cited by 37
Arrhythmogenic and metabolic remodelling of failing human heart
Gloschat, C. R., Koppel, A. C., Aras, K. K., Brennan, J. A., Holzem, K. M., & Efimov, I. R. (2016) · The Journal of Physiology · doi:10.1113/jp271992 · Cited by 23
Metadata
- Authors
- Beuckelmann, D. J., Näbauer, M., & Erdmann, E.
- Venue
- Circulation Research
- Published
- 1993-08
- Volume
- 73
- Issue
- 2
- Pages
- 379-385
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2155032388
- Cited by
- 733
- References
- 0
- FWCI
- 16.18
- Type
- journal article
- Language
- en
- Open access
- closed
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
