Cardiomyocyte differentiation from embryonic and adult stem cells.

In recent years multiple reports indicating that embryonic as well as adult stem cells can differentiate to cardiomyocytes have ignited discussions on whether these stem cells could lead to new therapies for patients with heart disease. Recent developments have been made in the generation of cardiomyocytes from both embryonic and adult stem cells, and progress towards clinical applications in patients with heart failure has been made. Nevertheless, controversies surrounding safety and transdifferentiation issues will need to be overcome before these stem cell approaches can reach their full potential.

Functional role for toll-like receptors in atherosclerosis and arterial remodeling.

Purpose Of Review: Activation of inflammatory cascades is causally related to the development of atherosclerotic disease. Toll-like receptors are innate immune receptors that recognize pathogen-associated molecular patterns. In this review the pathways by which toll-like receptors might play a role in the development and progression of atherosclerosis will be discussed according to recent literature.

Atherosclerotic plaque burden, plaque vulnerability and arterial remodeling: the role of inflammation.

Atherosclerotic narrowing of the arterial lumen is caused by gradual plaque growth and arterial remodeling. Expansive remodeling retards and constrictive remodeling accelerates narrowing of the lumen by plaque accumulation. In the acute phase luminal narrowing may be accelerated by rupture of a vulnerable plaque and subsequent thrombus formation.

Is there a role for implantable cardioverter defibrillators in long QT syndrome?

The congenital familial long QT syndrome (LQTS) is characterized by QT interval prolongation on ECG and potentially life-threatening polymorphic ventricular arrhythmias. Antiadrenergic therapy, i.e.

Brain death-induced alterations in myocardial workload and high-energy phosphates: a phosphorus 31 magnetic resonance spectroscopy study in the cat.

Background: Hemodynamic deterioration resulting from brain death-induced myocardial left ventricular dysfunction may preclude heart donation. A reduced myocardial high-energy phosphate content, assessed by biopsy specimens, has been suggested to be responsible for this phenomenon. By applying phosphorus 31 magnetic resonance spectroscopy, in vivo myocardial high-energy phosphate metabolism can be studied continuously.