Arrhythmias, Cardiac ; pathology ; physiopathology ; Humans ; Purkinje Fibers

Sudden cardiac death (SCD) refers to sudden stop of breath and heartbeat and death within one hour caused by underlying cardiac diseases. Clinical manifestation of inherited arrhythmia is lethal arrhythmia without gross cardiac lesions, which can lead to SCD. The autopsy and pathological examination are difficult to identify the cause of death. Fatal mechanism of inherited arrhythmia is the change in the genes encoding for cardiac ion channel protein, which causes the dysfunctions of cardiac electrical activity. It is very important to detect genetic mutation by the technique of molecular biology in negative autopsy. This review presents the latest research on the relation between SCD and inherited arrhythmia, and the application of molecular autopsy used in identifying SCD due to inherited arrhythmia and its candidate gene.
Arrhythmias, Cardiac/pathology* ; Autopsy/methods* ; Cardiovascular Diseases/genetics* ; Death, Sudden, Cardiac/pathology* ; Humans ; Mutation ; Pathology, Molecular

The advancement of studies about the molecular biology and electronic physiology on sudden cardiac death was summarized in this article, including particularly cardiac concussion(commotio cordis), congenital long QT syndrome, and Brugada syndrome which probably resulting in fatal arrhythmia and sudden cardiac death. These corpses of fatal functional disorders often show the results of negative autopsy without obvious organic pathological changes. So when come across negative autopsy the medical examiner and the pathologist should be careful to investigate the inductive cause of sudden death, the history of disease, and the family history, then to rule out the possibility of the above disorders.
Arrhythmias, Cardiac/pathology* ; Death, Sudden, Cardiac/pathology* ; Forensic Medicine ; Heart Injuries/pathology* ; Humans ; Long QT Syndrome/pathology*

Arrhythmias, Cardiac ; etiology ; Coronary Vessels ; pathology ; Humans ; Male ; Mediastinal Cyst ; pathology ; Young Adult

Sudden unexplained nocturnal death syndrome （SUNDS） is always a difficulty in forensic medicine researches. Although the development of molecular genetics promotes the etiologic study of SUNDS, the pathogenesis of most such cases is still unclear. Sleep apnea syndrome （SAS） is one of the common forms of sleep disorders, and obstructive sleep apnea hypopnea syndrome （OSAHS） is the most common. In recent years, some domestic and international researches show that OSAHS is related to the development of cardiovascular disease, which may cause cardiac arrhythmia, even sudden death. This article reviews the relationship between SUNDS and OSAHS and aims to provide new ideas for the pathogenesis of SUNDS.
Arrhythmias, Cardiac ; Brugada Syndrome/pathology* ; Death, Sudden/etiology* ; Humans ; Male ; Sleep Apnea, Obstructive/pathology*

Due to the negative autopsy and without cardiac structural abnormalities, unexpected sudden cardiac death （USCD） is always a tough issue for forensic pathological expertise. USCD may be associated with parts of fatal arrhythmic diseases. These arrhythmic diseases may be caused by disorders of cardiac ion channels or channel-related proteins. Caveolin can combine with multiple myocardial ion channel proteins through its scaffolding regions and plays an important role in maintaining the depolarization and repolarization of cardiac action potential. When the structure and function of caveolin are affected by gene mutations or abnormal protein expression, the functions of the regulated ion channels are correspondingly impaired, which leads to the occurrence of multiple channelopathies, arrhythmia or even sudden cardiac death. It is important to study the effects of caveolin on the functions of ion channels for exploring the mechanisms of malignant arrhythmia and sudden cardiac death.
Arrhythmias, Cardiac/physiopathology* ; Autopsy ; Caveolins/metabolism* ; Channelopathies/genetics* ; Death, Sudden, Cardiac/pathology* ; Forensic Pathology ; Humans ; Ion Channels/metabolism* ; Mutation ; Myocardium

BACKGROUNDProlongation of the Tpeak-Tend (TpTe) interval as a measurement of transmural dispersion of repolarization (TDR) is an independent risk factor for chronic heart failure mortality. However, the cardiac resynchronization therapy's (CRT) effect on TDR is controversial. Therefore, this study aimed to evaluate CRTs acute and chronic effects on repolarization dispersion. Furthermore, we aimed to investigate the relationship between TpTe changes and ventricular arrhythmia.

METHODSThe study group consisted of 101 patients treated with CRT-defibrillator (CRT-D). According to whether TpTe was shortened, patients were grouped at immediate and 1-year follow-up after CRT, respectively. The echocardiogram index and ventricular arrhythmia were observed and compared in these subgroups.

RESULTSFor all patients, TpTe slightly increased immediately after CRT-D implantation, and then decreased at the 1-year follow-up (from 107 ± 23 to 110 ± 21 ms within 24 h, to 94 ± 24 ms at 1-year follow-up, F = 19.366,P< 0.001). No significant difference in the left ventricular reverse remodeling and ventricular tachycardia/ventricular fibrillation (VT/VF) episodes between the TpTe immediately shortened and TpTe immediately nonshortened groups. However, patients in the TpTe at 1-year shorten had a higher rate of the left ventricular (LV) reverse remodeling (65% vs. 44%, χ2 = 4.495, P = 0.038) and less VT/VF episodes (log-rank test, χ2 = 10.207, P = 0.001) compared with TpTe 1-year nonshortened group. TpTe immediately after CRT-D independently predicted VT/VF episodes at 1-year follow-up (hazard ratio [HR], 1.030; P = 0.001).

CONCLUSIONSPatients with TpTe shortened at 1-year after CRT had a higher rate of LV reverse remodeling and less VT/VF episodes. The acute changes of TpTe after CRT have minimal value on mechanical reverse remodeling and ventricular arrhythmia.

Aged ; Arrhythmias, Cardiac ; etiology ; Cardiac Resynchronization Therapy ; adverse effects ; Female ; Heart Ventricles ; pathology ; physiopathology ; Humans ; Male ; Middle Aged ; Retrospective Studies

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

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

Adolescent ; Adult ; Aged ; Arrhythmias, Cardiac ; diagnosis ; etiology ; Child ; Child, Preschool ; Ebstein Anomaly ; complications ; pathology ; Humans ; Infant ; Middle Aged ; Young Adult