Sudden cardiac death (SC D ),m ostcom m only seen in coronary heart disease, is a kind of sud-den death caused by series of cardiac param eters, w hich usually com bines w ith m yocardial infarction. H ow ever, som e SC D s (including early m yocardial infarction) happen suddenly and cause death in a very short tim e. In these circum stances, typical m orphological changes are lack in m acroscopic or m icroscopic fields, w hich m ake such SC D s becom e the em phasis and difficulty in the present research. SC D caused by m yocardial infarction and abnorm alities of cardiac conduction system (C C S ) is related to atheroscle-rosis of coronary artery closely. T his paper review s cardiac dysfunction caused by m yocardial infarction and diseases of C C S from m orphology and m olecular biology, and explores potential relationship be-tw een them . T his paper aim s to provide clues to the m echanism of m yocardial infarction related sudden death and possible assistance for forensic diagnosis of SC D .

Objective To study the changes of hippocampal caspase-3 and PSD-95 expression levels in the mice exposed to ketamine 30 mg/(kg·d)for three months. Methods Forty C57BL/6 mice were randomly divided into two groups,and the chronic ketamine addiction model was established by giving mice a three month course of daily intraperitoneal injections of ketamine. Immunohistochemical study and Western blot-ting were applied to observe the expression of caspase-3 and PSD-95 protein. Results There were more expression of caspase-3 and less of PSD-95 in ketamine group as detected by immuohistochemistry. Western blotting results showed caspase-3 active fragment level significantly increased com-pared to saline group,but PSD-95 protein level was decreased. Conclusion The increased level of caspase-3 protein and reduced expression of PSD-95 are observed after long-term ketamine administration. These findings may provide an evidence for the neurotoxicity in mouse hippocampus of chronic ketamine addition as a recreational drug.