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

OBJECTIVETo investigate the relationship between abnormal ECG and pathologic changes in the cardiac conduction system (CCS).

METHODPathological changes of the CCS in 12 cases with abnormal ECG out of 16 pre-death ECG were observed.

RESULTS(1) Among 7 cases of sudden cardiac death, ECG monitoring recorded bradyarrhythmia in 6 cases, tachyarrhythmia 6 cases, bradycardia-tachycardia syndrome 2 cases, conduction block 6 cases, atrial premature beats 6 cases, ventricular premature beats 6 cases, and ST-T changes 4 cases. (2) The histopathological findings in the CCS were noted in all cases. Of these 12 cases, three had signs of fatty infiltration, and/or fibrous 4 cases, three of amyloidosis, one of chronic inflammatory changes, two of acute inflammatory changes, two of developmental anomalies, two of hemorrhages and one of LAD stenosis. (3) Acute inflammation changes in the CCS corresponded to tachyarrhythmia and multiple ventricular premature beats, whereas chronic inflammation and degenerative changes in the CCS were often related to bradyarrhythmia, bradycardia-tachycardia syndrome and conduction block. (4) The CCS changes alone could lead to ST-T changes in ECG.

CONCLUSIONThe pathological changes in the CCS are related to ECG changes, and attributed to the pathological bases of arrhythmia.

Adolescent ; Adult ; Aged ; Arrhythmias, Cardiac ; pathology ; physiopathology ; Child ; Electrocardiography ; Female ; Heart Conduction System ; pathology ; physiopathology ; Humans ; Male ; Middle Aged ; Young Adult

OBJECTIVE: To explore relationship between increase of fibrous and fatty in atrioventricular node (AVN) and narrowing of the AVN artery. To analyze the cause of pathological fibrosis and fatty infiltration in AVN. METHODS: One hundred and nineteen cases of sudden cardiac death determined by autopsy were selected and the histological sections were examined with Image-pro plus software to calculate the AVN area, AVN artery inside-diameter, AVN artery lumen area(LA) , AVN artery perimeter area(PA), fibrous area and fatty area. All cases were divided into two groups: narrowing of artery group and normal control group. The changes of the PA/LA value and the fibrous and fatty contents were evaluated. RESULTS: The PA/LA value is the highest in 21-40 age group. The difference of the fatty contents and total interstitial tissue was statistical significance in the two groups under 40 years of age. CONCLUSION There is some relationship between the narrowing of the AVN artery and the increase of interstitial contents in AVN.
Adolescent ; Adult ; Age Factors ; Atrioventricular Node/pathology* ; Child ; Coronary Stenosis/pathology* ; Coronary Vessels/pathology* ; Death, Sudden, Cardiac/etiology* ; Female ; Fibrosis ; Forensic Pathology ; Heart Conduction System/pathology* ; Humans ; Lipid Metabolism ; Male ; Middle Aged ; Retrospective Studies ; Young Adult

Under conditions of Na+ channel hyperactivation with aconitine, the changes in action potential duration (APD) and the restitution characteristics have not been well defined in the context of aconitine-induced arrhythmogenesis. Optical mapping of voltage using RH237 was performed with eight extracted rabbit hearts that were perfused using the Langendorff system. The characteristics of APD restitution were assessed using the steady-state pacing protocol at baseline and 0.1 microM aconitine concentration. In addition, pseudo-ECG was analyzed at baseline, and with 0.1 and 1.0 microM of aconitine infusion respectively. Triggered activity was not shown in dose of 0.1 microM aconitine but overtly presented in 1.0 microM of aconitine. The slopes of the dynamic APD restitution curves were significantly steeper with 0.1 microM of aconitine than at baseline. With aconitine administration, the cycle length of initiation of APD alternans was significantly longer than at baseline (287.5 +/- 9.6 vs 247.5 +/- 15.0 msec, P = 0.016). The functional reentry following regional conduction block appears with the progression of APD alternans. Ventricular fibrillation is induced reproducibly at pacing cycle length showing a 2:1 conduction block. Low-dose aconitine produces arrhythmogenesis at an increasing restitution slope with APD alternans as well as regional conduction block that proceeds to functional reentry.
Aconitine/*pharmacology ; Action Potentials/*drug effects ; Animals ; Arrhythmias, Cardiac/*chemically induced/*physiopathology ; Cardiac Pacing, Artificial ; Electrocardiography ; Heart/physiopathology ; Heart Conduction System/physiology ; Myocardium/*pathology ; Rabbits ; Sodium Channels/drug effects/metabolism ; Ventricular Fibrillation/physiopathology

We investigated whether the presence of J wave on the surface electrocardiography (sECG) could be a potential risk factor for ventricular fibrillation (VF) during acute myocardial infarction (AMI). We performed a retrospective study of 317 patients diagnosed with AMI in a single center from 2009 to 2012. Among the enrolled 296 patients, 22 (13.5%) patients were selected as a VF group. The J wave on the sECG was defined as a J point elevation manifested through QRS notching or slurring at least 1 mm above the baseline in at least two leads. We found that the incidence of J wave on the sECG was significantly higher in the VF group. We also confirmed that several conventional risk factors of VF were significantly related to VF during AMI; time delays from the onset of chest pain, blood concentrations of creatine phosphokinase and incidence of ST-segment elevation. Multiple logistic regression analysis demonstrated that the presence of J wave and the presence of a ST-segment elevation were independent predictors of VF during AMI. This study demonstrated that the presence of J wave on the sECG is significantly related to VF during AMI.
Arrhythmias, Cardiac/*diagnosis ; Creatine Kinase/blood ; *Electrocardiography ; Female ; Heart Conduction System/*abnormalities ; Humans ; Male ; Middle Aged ; Myocardial Infarction/*diagnosis/pathology ; Retrospective Studies ; Risk Factors ; Ventricular Fibrillation/*diagnosis/pathology/physiopathology

Sudden cardiac death accounts for majority of deaths in human. Evident cardiac lesions that may explain the cause of death can be detected in comprehensive postmortem investigation in most sudden cardiac death. However, no cardiac morphological abnormality is found in a considerable number of cases although the death is highly suspected from cardiac anomaly. With the advances in the modern molecular biology techniques, it has been discovered that many of these sudden deaths are caused by congenital ion channelopathies in myocardial cell, i.e., Brugada syndrome, long QT syndrome, catecholaminergic polymorphic ventricular tachycardia, and short QT syndrome, etc. This article presents the molecular genetics, electrocardiographic abnormalities, clinical manifestations, and mechanisms leading to sudden cardiac death with emphasis on the role of postmortem genetic testing in certification of cause of death. It may provide helpful information in investigating sudden cardiac death due to ion channelopathies in medico-legal practice.
Arrhythmias, Cardiac/genetics* ; Autopsy/methods* ; Brugada Syndrome/genetics* ; Cause of Death ; Channelopathies/genetics* ; Death, Sudden, Cardiac/pathology* ; Electrocardiography ; Forensic Pathology ; Genetic Testing ; Heart Conduction System/physiopathology* ; Humans ; Ion Channels/genetics* ; Long QT Syndrome/genetics* ; Mutation ; Tachycardia, Ventricular/genetics*

Arrhythmias, Cardiac ; diagnosis ; genetics ; pathology ; Brugada Syndrome ; diagnosis ; genetics ; pathology ; Channelopathies ; diagnosis ; genetics ; pathology ; DNA Mutational Analysis ; Electrocardiography ; Genetic Testing ; Heart Conduction System ; physiopathology ; Humans ; Infant ; Long QT Syndrome ; diagnosis ; genetics ; pathology ; Muscle Proteins ; genetics ; Mutation ; NAV1.5 Voltage-Gated Sodium Channel ; genetics ; Sodium Channels ; genetics ; Sudden Infant Death ; etiology