Sudden cardiac death （SCD）, most commonly seen in coronary heart disease, is a kind of sudden death caused by series of cardiac parameters, which usually combines with myocardial infarction. However, some SCDs （including early myocardial infarction） happen suddenly and cause death in a very short time. In these circumstances, typical morphological changes are lack in macroscopic or microscopic fields, which make such SCDs become the emphasis and difficulty in the present research. SCD caused by myocardial infarction and abnormalities of cardiac conduction system （CCS） is related to atherosclerosis of coronary artery closely. This paper reviews cardiac dysfunction caused by myocardial infarction and diseases of CCS from morphology and molecular biology, and explores potential relationship between them. This paper aims to provide clues to the mechanism of myocardial infarction related sudden death and possible assistance for forensic diagnosis of SCD.
Coronary Disease ; Death, Sudden, Cardiac/etiology* ; Heart Conduction System/physiopathology* ; Humans ; Myocardial Infarction/physiopathology*

OBJECTIVETo explore the relationship between electrocardiographic (ECG) and genetic mutations of patients with hypertrophic cardiomyopathy (HCM), and early ECG changes in HCM patients.

METHODSClinical, 12-lead ECG and echocardiographic examination as well as genetic examinations were made in a three-generation Chinses HCM pedigree with 8 family members (4 males). The clinical characterization and ECG parameters were analyzed and their relationship with genotypes in the family was explored.

RESULTSFour missense mutations (MYH7-H1717Q, MYLK2-K324E, KCNQ1-R190W, TMEM70-I147T) were detected in this pedigree. The proband carried all 4 mutations and 5 members carried 2 mutations. Corrected QTc interval of KCNQ1-H1717Q carriers was significantly prolonged and was consistent with the ECG characterization of long QT syndrome. MYLK2-K324E and KCNQ1-R190W carriers presented with Q wave and(or) depressed ST segment, as well as flatted or reversed T waves in leads from anterolateral and inferior ventricular walls. ECG results showed ST segment depression, flat and inverted T wave in the gene mutation carriers with normal echocardiographic examination results. ECG and echocardiographic results were normal in TMEM70-I147T mutation carrier.

CONCLUSIONSThe combined mutations of the genes associated with cardiac ion channels and HCM are linked with the ECG phenotype changes in this HCM pedigree. The variations in ECG parameters due to the genetic mutation appear earlier than the echocardiography and clinical manifestations. Variation in ECG may become one of the indexes for early diagnostic screening and disease progression of the HCM gene mutation carriers.

Brugada Syndrome ; Cardiac Conduction System Disease ; Cardiac Myosins ; Cardiomyopathy, Hypertrophic ; Echocardiography ; Electrocardiography ; Exons ; Genetic Testing ; Genotype ; Humans ; KCNQ1 Potassium Channel ; Long QT Syndrome ; Mutation ; Mutation, Missense ; Myosin Heavy Chains ; Myosin-Light-Chain Kinase ; Pedigree ; Phenotype

OBJECTIVE: To explore the change of the amplitude of P wave, T wave and ST segment of 12 lead electrocardiogram (ECG) in children with breath holding spell.
 METHODS: A total of 29 children (24 males and 5 females) with breath holding spell in Second Xiangya Hospital, Central South University were enrolled for this study from October, 2009 to September, 2015. Their ages ranged from 3 months to 6 years, with an average of 1.82±1.27 years old. The control group consisted of 30 age-matched and gender-matched healthy children. All subjects were underwent electrocardiography by the SR-1000A comprehensive automatic electrocardiograph analyzer, and the changes of the ECG parameters were compared between the two groups.
 RESULTS: Compared with the control group, the amplitude of P-wave of V5 lead was decreased [(44.10±23.98) vs (58.30±21.19) μV, P<0.05], the amplitude of T-wave of V6 lead was increased [(423.80±122.6) vs (350.00±105.73) μV, P<0.05], the amplitude of ST segment of II lead was increased [(84.80±39.97) vs (57.30±38.77) μV, P<0.05], the amplitude of ST segment of aVR lead was increased [(-77.60±37.41) vs (-51.00±33.46) μV, P<0.05], the amplitude of ST segment of aVL lead was increased [(35.20±28.24) vs (17.70±33.90) μV, P<0.05], the amplitude of ST segment of V5 lead was increased [(111.00±59.36) vs (69.00±36.33) μV, P<0.05], the amplitude of ST segment of V6 lead was increased [(79.30±45.51) vs (51.30±33.19) μV, P<0.05]. 
 CONCLUSION The children with breath holding spell have autonomic nerve dysfunction. The amplitude of ST segment changes is sensitive.
Breath Holding ; Brugada Syndrome ; Cardiac Conduction System Disease ; Electrocardiography ; Female ; Heart Conduction System ; Humans ; Infant ; Male

Acute Coronary Syndrome ; therapy ; Angina, Unstable ; Arrhythmias, Cardiac ; Brugada Syndrome ; Cardiac Conduction System Disease ; Heart Conduction System ; abnormalities ; Humans ; Myocardial Infarction

This study was aimed to establish an experimental mouse model of combined transgenic inhibition of both multifunctional Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) and inward rectifier potassium current (Ik1), and to observe whether the specific inhibition of both CaMKII and Ik1 can bring about any effects on cardiac remodeling. Mice were divided into 4 groups: wild type (WT), CaMKII inhibited (AC3-I), Ik1 inhibited (Kir2.1-AAA) and combined inhibition of both CaMKII and Ik1 (AC3-I+Kir2.1-AAA). Mice in each group received electrocardiogram (ECG) and echocardiography examination. ECG in the condition of isoproterenol (ISO) injection was also checked. The whole cell patch clamp technique was used to measure Ik1 and the transient outward potassium current (Ito) from enzymatically isolated myocytes of left ventricle. In the condition of basal status, no significant changes of heart rate, PR interval and QRS interval were observed. No mouse showed ventricular arrhythmias in all of the 4 groups. After ISO injection, each group presented no significant ventricular arrhythmias either. The indexes measured by M-mode (motion-mode) and two-dimensional echocardiography had no significant differences among the four groups. Ik1 in AC3-I group was significantly higher than those in other three groups (P < 0.01) because of the results brought about by CaMKII inhibition. Among the latter three groups, both Kir2.1-AAA group and AC3-I+Kir2.1-AAA group had a significant reduced Ik1 compared with that of WT group, which was due to the Ik1 inhibition (P < 0.01). Ito in AC3-I group was higher than that of the other three groups (P < 0.01), but there were no significant differences in Ito among WT, Kir2.1-AAA and AC3-I+Kir2.1-AAA groups. Thus, combined transgenic myocardial CaMKII and Ik1 inhibition eliminated the up-regulation of Ik1 in CaMKII inhibited mice, and had no effects on cardiac remodeling including heart structure and function as well as arrhythmias at the basic and ISO conditions. The results of this study may provide a basis for the further investigation of combined inhibition of CaMKII and Ik1 in pathogenic cardiac remodeling.
Animals ; Arrhythmias, Cardiac ; Brugada Syndrome ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; physiology ; Cardiac Conduction System Disease ; Disease Models, Animal ; Electrocardiography ; Heart ; physiology ; Heart Conduction System ; abnormalities ; Heart Ventricles ; Isoproterenol ; Mice ; Mice, Transgenic ; Patch-Clamp Techniques ; Potassium Channels, Inwardly Rectifying ; physiology ; Up-Regulation ; Ventricular Remodeling

PURPOSE: Recent studies show positive association of early repolarization (ER) with the risk of life-threatening arrhythmias in patients with coronary artery disease (CAD). This study was to investigate the relationships of ER with myocardial scarring and prognosis in patients with CAD. MATERIALS AND METHODS: Of 570 consecutive CAD patients, patients with and without ER were assigned to ER group (n=139) and no ER group (n=431), respectively. Myocardial scar was evaluated using cardiac single-photon emission computed tomography. RESULTS: ER group had previous history of myocardial infarction (33% vs. 15%, p<0.001) and lower left ventricular ejection fraction (57+/-13% vs. 62+/-13%, p<0.001) more frequently than no-ER group. While 74 (53%) patients in ER group had myocardial scar, only 121 (28%) patients had in no-ER group (p<0.001). During follow up, 9 (7%) and 4 (0.9%) patients had cardiac events in ER and no-ER group, respectively (p=0.001). All patients with cardiac events had ER in inferior leads and horizontal/descending ST-segment. Patients with both ER in inferior leads and horizontal/descending ST variant and scar had an increased adjusted hazard ratio of cardiac events (hazard ratio 16.0; 95% confidence interval: 4.1 to 55.8; p<0.001). CONCLUSION: ER in inferior leads with a horizontal/descending ST variant was associated with increased risk of cardiac events. These findings suggest that ER in patients with CAD may be related to myocardial scar rather than pure ion channel problem.
Aged ; Arrhythmias, Cardiac/physiopathology ; Cicatrix/*physiopathology ; Coronary Artery Disease/*pathology/*physiopathology ; Death, Sudden, Cardiac/pathology ; Female ; Heart Conduction System/abnormalities/physiopathology ; Humans ; Male ; Middle Aged ; Myocardium/*pathology ; Prognosis

Adult ; Arrhythmias, Cardiac ; diagnosis ; physiopathology ; Brugada Syndrome ; Cardiac Conduction System Disease ; Electrocardiography ; Female ; Heart Conduction System ; abnormalities ; physiopathology ; Humans ; Young Adult

Arrhythmias, Cardiac ; Brugada Syndrome ; Cardiac Conduction System Disease ; Heart ; Heart Conduction System ; abnormalities ; Humans ; Magnetic Resonance Spectroscopy

The early cardiac biological pacemaker studies were mostly around HCN channel, and how to build a biological pacemaker through the enhanced If current. In recent years, however, people found that the genes of Tbx3 could play an important role in the development of cardiac conduction system, especially in processes of the maturity of the sinoatrial node and maintenance of its function. And the Tbx3 can further optimize the biological pacemaker. Therefore, it could be a new therapeutic focus in biological pacemaker and treatment of cardiac conduction system disease. This paper summarizes some of the latest research progress of the Tbx3 in biological pacemaker in recent years. We hope that this review could provide theoretical basis for the clinical applications of Tbx3.
Arrhythmias, Cardiac ; genetics ; Biological Clocks ; Brugada Syndrome ; Cardiac Conduction System Disease ; Heart ; physiopathology ; Heart Conduction System ; abnormalities ; Humans ; Sinoatrial Node ; T-Box Domain Proteins ; genetics

Arrhythmias, Cardiac ; diagnosis ; Brugada Syndrome ; Cardiac Conduction System Disease ; Coronary Vessels ; pathology ; Heart Conduction System ; abnormalities ; Humans ; Male ; Middle Aged