ABSTRACT
Human heart rhythm is mainly regulated and controlled by the sinoatrial node. Fibrosis plays an important regulating role in adjusting the structural and functional integrity of the sinoatrial node pacemaker complex. In physiological state, the fibrosis degree of sinoatrial node is negatively correlated with heart rate, positively correlated with age and heart size, and can maintain a relatively stable heart rate. Pathological fibrosis of sinoatrial node can induce various types of arrhythmias which can result in sudden death. Determination of the mechanisms related to sinoatrial node pathological fibrosis could provide a target for clinical treatment of sinoatrial node fibrosis and diagnosis basis for forensic pathologists. This paper reviews the main mechanism of sinoatrial node pathological fibrosis, including abnormal activation of cardiac fibroblast cells in sinoatrial node, hyperplasia of epicardial adipose tissue, calcium clock disorder, artery stenosis, etc., introduces the test methods, diagnostic criteria as well as its role in sudden cardiac death and discusses the potential application, to provide reference for relevant research and application.
Subject(s)
Humans , Arrhythmias, Cardiac , Fibrosis , Heart Rate , Sinoatrial NodeABSTRACT
Four fresh corpses of infant are used in this research. Three-dimensional microvasculatures of the sinoatrial node and atrioventricular node were studied by means of the observation of vascular casts with SEM. The results showed that the vascular bed of the sinoatrial node was consisted of the microvascular networks. It was oval in shape. The central artery penetrated this node, through its longitudinal axis and divided progressively into arterioles and precapillary arterioles and finally, they branched into capillary networks at the superficial part of the node. The postcapillary venules were characterized by draining blood in accordance with area. The microvascular construction of atrioventricular node was an oblate microvascular network in shape. There was a layer of delicate capillary networks at its superficial part. In the depth of the capillary networks, the venous plexus which was thick and sinusoidal in shape was observed through the meshes. The artery of atrioventricular node entered the node from one side of it. In the node, the artery ramified by degrees to periphery into precapillary arterioles, which penetrated venous plexus and connected with capillary networks in the superficial part of the node. There were evidently narrow rings, whick were impression of the muscle sphincters at the origin of thep ostcapillary venules.