Validation study of a novel method for the 3D reconstruction of coronary bifurcations.

Quantitative Coronary Angiography (QCA) is an important tool in the study of coronary artery disease. Validation of this technique is crucial for their ongoing development and refinement although it is difficult due to several factors such as potential sources of error. The present work aims to a further validation of a new semi-automated method for three-dimensional (3D) reconstruction of coronary bifurcations arteries based on X-Ray Coronary Angiographies (CA). In a dataset of 40 patients (79 angiographic views), we used the aforementioned method to reconstruct them in 3D space. The validation was based on the comparison of these 3D models with the true silhouette of 2D models annotated by an expert using specific metrics. The obtained results indicate a good accuracy for the most parameters (≥ 90 %). Comparison with similar works shows that our new method is a promising tool for the 3D reconstruction of coronary bifurcations and for application in everyday clinical use.

Late Na(+) current and protracted electrical recovery are critical determinants of the aging myopathy.

The aging myopathy manifests itself with diastolic dysfunction and preserved ejection fraction. We raised the possibility that, in a mouse model of physiological aging, defects in electromechanical properties of cardiomyocytes are important determinants of the diastolic characteristics of the myocardium, independently from changes in structural composition of the muscle and collagen framework. Here we show that an increase in the late Na(+) current (INaL) in aging cardiomyocytes prolongs the action potential (AP) and influences temporal kinetics of Ca(2+) cycling and contractility. These alterations increase force development and passive tension. Inhibition of INaL shortens the AP and corrects dynamics of Ca(2+) transient, cell contraction and relaxation. Similarly, repolarization and diastolic tension of the senescent myocardium are partly restored. Thus, INaL offers inotropic support, but negatively interferes with cellular and ventricular compliance, providing a new perspective of the biology of myocardial aging and the aetiology of the defective cardiac performance in the elderly.