LONG-TERM FOLLOW-UP ASSESSMENT OF POTENTIAL ADVERSE EFFECTS AFTER RADIOFREQUENCY ABLATION IN AN INFANT (A CLINICAL CASE)

The article presents a long-term follow-up of the patient who underwent an intracardiac electrophysiological study (EPS) and radiofrequency ablation (RFA) of focal tachycardia at the age of 2 months. 12 years after the indexed procedure, Wolff-Parkinson-White (WPW) syndrome was diagnosed and required repeat RFA procedure. The atrial map of the first ablated zone was reconstructed using non-fluroscopic mapping system. EPS reported the absence of myocardial electrical activity reduction zones. There were no damages after the indexed ablation. Our findings suggested the normal electrical activity of the atrial tissue in the long-term period following the indexed RFA. This clinical case reports the absence of post-ablation necrosis and successful restoration of the electrical activity of the myocardium with the child’s growth.

A Meshfree Method for Simulating Myocardial Electrical Activity

An element-free Galerkin method (EFGM) is proposed to simulate the propagation of myocardial electrical activation without explicit mesh constraints using a monodomain model. In our framework the geometry of myocardium is first defined by a meshfree particle representation that is, a sufficient number of sample nodes without explicit connectivities are placed in and inside the surface of myocardium. Fiber orientations and other material properties of myocardium are then attached to sample nodes according to their geometrical locations, and over the meshfree particle representation spatial variation of these properties is approximated using the shape function of EFGM. After the monodomain equations are converted to their Galerkin weak form and solved using EFGM, the propagation of myocardial activation can be simulated over the meshfree particle representation. The derivation of this solution technique is presented along a series of numerical experiments and a solution of monodomain model using a FitzHugh-Nagumo (FHN) membrane model in a canine ventricular model and a human-heart model which is constructed from digitized virtual Chinese dataset.

Cell biology of cardiac mitochondrial phospholipids

Phospholipids are important structural and functional components of all biological membranes and define the compartmentation of organelles. Mitochondrial phospholipids comprise a significant proportion of the entire phospholipid content of most eukaroytic cells. In the heart, a tissue rich in mitochondria, the mitochondrial phospholipids provide for diverse roles in the regulation of various mitochondrial processes including apoptosis, electron transport, and mitochondrial lipid and protein import. It is well documented that alteration in the content and fatty acid composition of phospholipids within the heart is linked to alterations in myocardial electrical activity. In addition, reduction in the specific mitochondrial phospholipid cardiolipin is an underlying biochemical cause of Barth Syndrome, a rare and often fatal X-linked genetic disease that is associated with cardiomyopathy. Thus, maintenance of both the content and molecular composition of phospholipids synthesized within the mitochondria is essential for normal cardiac function. This review will focus on the function and regulation of the biosynthesis and resynthesis of mitochondrial phospholipids in the mammalian heart.Key words: phospholipid, metabolism, heart, cardiolipin, mitochondria.