Contribution of myocyte apoptosis to myocardial infarction?
β Scribed by B. Bartling; J. Holtz; D. Darmer
- Publisher
- Springer
- Year
- 1998
- Tongue
- English
- Weight
- 242 KB
- Volume
- 93
- Category
- Article
- ISSN
- 0300-8428
No coin nor oath required. For personal study only.
π SIMILAR VOLUMES
The clinical implications of hemorrhagic versus nonhemorrhagic infarcts are currently unclear. Our study suggests that hemorrhage may not simply be a bystander but an active contributor to adverse left-ventricular remodeling following acute myocardial infarction.
## Abstract The longβlasting signal enhancement by GdβDTPA in areas of myocardial infarction has been conventionally explained by low perfusion and an enhanced Gd distribution volume. To test whether binding of Gd to myocardial constituents is an additional factor contributing to this effect, GdβDT
## Abstract Left ventricular (LV) remodeling and heart failure (HF) complicate acute myocardial infarction (AMI) even weeks to months after the initial insult. Apoptosis may represent an important pathophysiologic mechanism causing progressive myocardiocyte loss and LV dilatation even late after AM