Three-dimensional activation sequence of cesium-induced ventricular arrhythmias

1997 ◽  
Vol 273 (3) ◽  
pp. H1377-H1385 ◽  
Author(s):  
Y. Murakawa ◽  
K. Sezaki ◽  
T. Yamashita ◽  
Y. Kanese ◽  
M. Omata
Keyword(s):  
Ventricular Tachycardia ◽  
Ventricular Arrhythmia ◽  
Purkinje Cells ◽  
Ventricular Arrhythmias ◽  
Three Dimensional ◽  
Cesium Chloride ◽  
Recording System ◽  
Anesthetized Dogs ◽  
Myocardial Muscle ◽  
Activation Sequence

To investigate the electrophysiological and electrocardiographic characteristics of ventricular arrhythmia due to abnormal repolarization, we studied the three-dimensional activation sequence of cesium-induced ventricular tachycardia (VT) in 10 anesthetized dogs using a 384-channel recording system. Seventeen monomorphic VT (mVT) and eight polymorphic VT (pVT) episodes induced by cesium chloride (2 or 3 mM/kg) were analyzed. Only a single arrhythmogenic focus was detected in most beats of VT, whereas two competing foci were temporarily observed in two episodes of pVT. The site of arrhythmogenic focus of mVT was the endocardium (5 of 17), the midmyocardium (4 of 17), or undetermined (8 of 17). Both endocardial and midmyocardial arrhythmogenic foci were also found in pVT, and most pVT (6 of 8) were associated with the transition of the site of arrhythmogenic focus. These results are consistent with the view that both myocardial muscle fibers and Purkinje cells can cause ventricular arrhythmia due to abnormal repolarization and that changing the site of arrhythmogenic focus is the main mechanism of pVT.

P1603Nicorandil suppresses ischemia-induced cardiac interstitial norepinephrine enhancement and ventricular arrhythmia in hypertrophic hearts

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Kobara ◽  
N Naseratun ◽  
Y Watanabe ◽  
H Toba ◽  
T Nakata
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Ventricular Tachycardia ◽  
Ventricular Arrhythmia ◽  
Ventricular Arrhythmias ◽  
Sham Group ◽  
Cardiac Tissue ◽  
Norepinephrine Release ◽  
Norepinephrine Concentration ◽  
Ischemic Period

Abstract Background Myocardial infarction (MI) is a major cause of death in western countries and Japan, and hypertension is a major risk factor of MI. In hypertensive heart, acute myocardial infarction often leads to lethal ventricular arrhythmia. Nicorandil, an ATP sensitive potassium channel (KATP) opener, is usually used in the treatment of acute myocardial infarction. The effects of nicorandil on ischemic myocyte are fully defined. On the other hand, KATP in neuroterminals is known to regulate norepinephrine release, but the effect of nicorandil on ischemic norepinephrine release in cardiac tissue has remained unexplored. Purpose We examined whether nicorandil suppressed norepinephrine release via neuronal KATP and ventricular arrhythmia during acute ischemia in pressure overload-induced hypertrophic hearts. Methods SD Rats were divided into two groups; abdominal aortic constriction (AAC) group and sham-operated (Sham) group. Four weeks after constriction, cardiac geometry and function were examined using echocardiography. Then, myocardial ischemia was induced by the left anterior descending artery occlusion for 100 minutes in the presence or absence of intravenous infusion of nicorandil. Cardiac interstitial norepinephrine concentration in ischemic region was measured using the microdialysis method and concentration of cyclic AMP, a second messenger of norepinephrine, in cardiac tissue was measured by ELISA. Ventricular arrhythmias were monitered by ECG during whole ischemic period. Results Four weeks after constriction, remarkable left ventricular wall thickening was observed in AAC group. Before ischemia, ventricular arrhythmia was not found in both groups. Number of ventricular arrhythmia, including ventricular tachycardia and ventricular fibrillation, was increased in early ischemic period (- 40 min) in both groups, and was grater in AAC group. Before ischemia, interstitial norepinephrine concentration in cardiac tissue was higher level in AAC group than in Sham group. Ischemia obviously increased norepinephrine concentration in both groups time dependently and AAC further increased norepinephrine than Sham group. Concentration of cyclic AMP in cardiac tissue was raised in early ischemic period (- 40 min) and then gradually decreased. Nicorandil significantly suppressed the number of ventricular arrhythmias, and abolished the ventricular tachycardia and fibrillation without hemodynamic alterations. Nicorandil also attenuated norepinephrine and cAMP enhancement in acute ischemic period in both groups. Conclusion Ischemia-induced ventricular arrhythmia was more frequent and severe in hypertrophic hearts and interstitial norepinephrine enhancement may play a role in this ischemic arrhythmia. Nicorandil suppressed ischemia-induced interstitial norepinephrine release by neuronal KATP opening, which attenuated ventricular arrhythmias in normal and hypertrophic hearts.

Cesium chloride induced ventricular arrhythmias in dogs: three-dimensional activation patterns and their relation to the cesium dose applied

2000 ◽  
Vol 95 (2) ◽  
pp. 152-162 ◽  
Author(s):  
Julia C. Senges ◽  
Laurence D. Sterns ◽  
Kirsten D. Freigang ◽  
Alexander Bauer ◽  
Rüdiger Becker ◽  
...  
Keyword(s):  
Ventricular Arrhythmias ◽  
Three Dimensional ◽  
Cesium Chloride ◽  
Activation Patterns

scholarly journals Short‐Term Variability of the QT Interval Can be Used for the Prediction of Imminent Ventricular Arrhythmias in Patients With Primary Prophylactic Implantable Cardioverter Defibrillators

2020 ◽  
Vol 9 (23) ◽  
Author(s):  
Agnieszka Smoczyńska ◽  
Vera Loen ◽  
David J. Sprenkeler ◽  
Anton E. Tuinenburg ◽  
Henk J. Ritsema van Eck ◽  
...  
Keyword(s):  
Ventricular Tachycardia ◽  
Ventricular Arrhythmia ◽  
Qt Interval ◽  
Ventricular Arrhythmias ◽  
Sustained Ventricular Tachycardia ◽  
Control Group ◽  
Implantable Cardioverter Defibrillators ◽  
Short Term ◽  
Cardioverter Defibrillators ◽  
Holter Recordings

Background Short‐term variability of the QT interval (STV QT ) has been proposed as a novel electrophysiological marker for the prediction of imminent ventricular arrhythmias in animal models. Our aim is to study whether STV QT can predict imminent ventricular arrhythmias in patients. Methods and Results In 2331 patients with primary prophylactic implantable cardioverter defibrillators, 24‐hour ECG Holter recordings were obtained as part of the EU‐CERT‐ICD (European Comparative Effectiveness Research to Assess the Use of Primary Prophylactic Implantable Cardioverter Defibrillators) study. ECG Holter recordings showing ventricular arrhythmias of >4 consecutive complexes were selected for the arrhythmic groups (n=170), whereas a control group was randomly selected from the remaining Holter recordings (n=37). STV QT was determined from 31 beats with fiducial segment averaging and calculated as , where D n represents the QT interval. STV QT was determined before the ventricular arrhythmia or 8:00  am in the control group and between 1:30 and 4:30  am as baseline. STV QT at baseline was 0.84±0.47 ms and increased to 1.18±0.74 ms ( P <0.05) before the ventricular arrhythmia, whereas the STV QT in the control group remained unchanged. The arrhythmic patients were divided into three groups based on the severity of the arrhythmia: (1) nonsustained ventricular arrhythmia (n=32), (2) nonsustained ventricular tachycardia (n=134), (3) sustained ventricular tachycardia (n=4). STV QT increased before nonsustained ventricular arrhythmia, nonsustained ventricular tachycardia, and sustained ventricular tachycardia from 0.80±0.43 ms to 1.18±0.78 ms ( P <0.05), from 0.90±0.49 ms to 1.14±0.70 ms ( P <0.05), and from 1.05±0.22 ms to 2.33±1.25 ms ( P <0.05). This rise in STV QT was significantly higher in sustained ventricular tachycardia compared with nonsustained ventricular arrhythmia (+1.28±1.05 ms versus +0.24±0.57 ms [ P <0.05]) and compared with nonsustained ventricular arrhythmia (+0.34±0.87 ms [ P <0.05]). Conclusions STV QT increases before imminent ventricular arrhythmias in patients, and the extent of the increase is associated with the severity of the ventricular arrhythmia.

scholarly journals Description of Ventricular Arrhythmia after Taking Herbal Medicines in Middle-Aged Couples

2020 ◽  
Vol 2020 ◽  
pp. 1-4
Author(s):  
Mohammad Ali Zakeri ◽  
Vahid Mohammadi ◽  
Gholamreza Bazmandegan ◽  
Maryam Zakeri
Keyword(s):  
Cardiac Arrest ◽  
Heart Disease ◽  
Ventricular Tachycardia ◽  
Sudden Cardiac Death ◽  
Ventricular Arrhythmia ◽  
Cardiac Death ◽  
Ventricular Arrhythmias ◽  
Herbal Medicines ◽  
Medicinal Herbs ◽  
History Of

Medicinal herbs and some derivatives have been used in the treatment of heart disease which is rarely responsible for ventricular arrhythmias and cardiac arrest. Ventricular tachycardia (VT) increases the risk of sudden cardiac death (SCD). However, only a few reports are available about the cardiac ventricular arrhythmia followed by taking herbal medicines. We present two patients (a couple) without a history of heart disease who referred to the hospital with ventricular arrhythmia.

The Effect of Statins on RyR and RyR- Associated Disease

2021 ◽  
Author(s):  
Mohsin Haseeb ◽  
Paul D. Thompson
Keyword(s):  
Skeletal Muscle ◽  
Ventricular Tachycardia ◽  
Adverse Effects ◽  
Ventricular Arrhythmia ◽  
Ventricular Arrhythmias ◽  
English Language ◽  
Genetic Diseases ◽  
Polymorphic Ventricular Tachycardia ◽  
Sufficient Information ◽  
Apparent Reduction

Objective: We sought to review the effects of statins on the ryanodine receptor (RyR) and on RyR-associated diseases, with an emphasis on catecholaminergic polymorphic ventricular tachycardia (CPVT). Background: Statins can affect skeletal muscle and produce statin associated muscle symptoms (SAMS), but have no adverse effects on cardiac muscle. These contrasting effects may be due to differences in how statins affect the skeletal (RyR1) and cardiac (RyR2) RyR. Methods: We searched PubMed to identify English language articles reporting the pathophysiology of the RyR, the effect of statins on RyR function and on RyR associated genetic diseases. Results: We selected 150 articles for abstract review, 96 of which provided sufficient information to be included and were reviewed in detail. Fifteen articles highlighted the interaction of statins with the RyR. Nine identified the interaction of statins with RyR1; 6 addressed the interaction of statins with RyR2; 13 suggested that statins reduce ventricular arrhythmias (VA); 7 suggested that statins increase the risk of malignant hyperthermia (MH). In general statins increase RyR1 and decrease RyR2 activity. We identified no articles examining the effect of statins on CPVT, a condition often caused by defects in RyR2. Conclusion: Statins appear to increase the risk of MH and decrease the risk of ventricular arrhythmia. The effect of statins on CPVT has not been directly examined, but statins' reduction in RyR2 function and their apparent reduction in VA suggest that they may be beneficial in this condition.

scholarly journals Noninvasive reconstruction of the three-dimensional ventricular activation sequence during pacing and ventricular tachycardia in the canine heart

2012 ◽  
Vol 302 (1) ◽  
pp. H244-H252 ◽  
Author(s):  
Chengzong Han ◽  
Steven M. Pogwizd ◽  
Cheryl R. Killingsworth ◽  
Bin He
Keyword(s):  
Ventricular Tachycardia ◽  
Clinical Medicine ◽  
Three Dimensional ◽  
Left Ventricular ◽  
Canine Heart ◽  
Cardiovascular Research ◽  
Computed Tomography Images ◽  
Electrical Imaging ◽  
Ectopic Beats ◽  
Activation Sequence

Single-beat imaging of myocardial activation promises to aid in both cardiovascular research and clinical medicine. In the present study we validate a three-dimensional (3D) cardiac electrical imaging (3DCEI) technique with the aid of simultaneous 3D intracardiac mapping to assess its capability to localize endocardial and epicardial initiation sites and image global activation sequences during pacing and ventricular tachycardia (VT) in the canine heart. Body surface potentials were measured simultaneously with bipolar electrical recordings in a closed-chest condition in healthy canines. Computed tomography images were obtained after the mapping study to construct realistic geometry models. Data analysis was performed on paced rhythms and VTs induced by norepinephrine (NE). The noninvasively reconstructed activation sequence was in good agreement with the simultaneous measurements from 3D cardiac mapping with a correlation coefficient of 0.74 ± 0.06, a relative error of 0.29 ± 0.05, and a root mean square error of 9 ± 3 ms averaged over 460 paced beats and 96 ectopic beats including premature ventricular complexes, couplets, and nonsustained monomorphic VTs and polymorphic VTs. Endocardial and epicardial origins of paced beats were successfully predicted in 72% and 86% of cases, respectively, during left ventricular pacing. The NE-induced ectopic beats initiated in the subendocardium by a focal mechanism. Sites of initial activation were estimated to be ∼7 mm from the measured initiation sites for both the paced beats and ectopic beats. For the polymorphic VTs, beat-to-beat dynamic shifts of initiation site and activation pattern were characterized by the reconstruction. The present results suggest that 3DCEI can noninvasively image the 3D activation sequence and localize the origin of activation of paced beats and NE-induced VTs in the canine heart with good accuracy. This 3DCEI technique offers the potential to aid interventional therapeutic procedures for treating ventricular arrhythmias arising from epicardial or endocardial sites and to noninvasively assess the mechanisms of these arrhythmias.

scholarly journals Noninvasive imaging of three-dimensional cardiac activation sequence during pacing and ventricular tachycardia

Heart Rhythm ◽  
2011 ◽  
Vol 8 (8) ◽  
pp. 1266-1272 ◽  
Author(s):  
Chengzong Han ◽  
Steven M. Pogwizd ◽  
Cheryl R. Killingsworth ◽  
Bin He
Keyword(s):  
Ventricular Tachycardia ◽  
Noninvasive Imaging ◽  
Three Dimensional ◽  
Activation Sequence

scholarly journals SEARCH OF THE STRESS INDUSED VENTRICULAR TACHICARDIA REASONS — THE METABOLIC THERAPY OPPORTUNITIES

2018 ◽  
Vol 8 (5) ◽  
pp. 394-402
Author(s):  
T. V. Treshkur ◽  
A. A. Tatarinova ◽  
E. A. Ryngach
Keyword(s):  
Ventricular Tachycardia ◽  
Coronary Artery ◽  
Ventricular Arrhythmia ◽  
Ventricular Arrhythmias ◽  
Clinical Case ◽  
Stable Coronary Artery Disease ◽  
Antiarrhythmic Effect ◽  
Diagnostic Methods ◽  
Metabolic Therapy ◽  
Exercise Induced

A clinical case of a 56-year-old man is presented in which only ventricular tachycardia without clinical and ECG criteria of myocardial ischemia is recorded on the exercise test. The ventricular tachycardia was the only reason for stopping the test. This clinical case demonstrates all the difficulties in determining the genesis of ventricular arrhythmias induced by exercise. The purpose of the work was to show all the difficulties in determining the genesis of exercise-induced ventricular arrhythmia. The literature references related to the exercise-induced ventricular arrhythmia differentiation is rather poor. It is only known that if a patient develops and progresses ventricular arrhythmia, a tredmill test is considered questionable. Exerciseinduced ventricular arrhythmias especially ventricular tachycardia, are the most dangerous. Therefore, additional diagnostic methods were used to reveal the main disease as the background of ventricular tachycardia. Results of pharmacological test with nitroglycerine were the indication of the ischemic origin of ventricular tachycardia. Coronary angiography did not reveal coronary artery stenoses. Positron emission tomography revealed coronary microcirculation disturbance after which a decision about metabolic therapy with Mexicor was made. The correct choice of the drug (Mеxisor) was confirmed by the results of control studies — improvement of metabolism and antiarrhythmic effect. The article concludes that the choice of the treatment exercise-induced ventricular arrhythmia in patients with stable coronary artery disease should be individual and pathogenetic.

Triggered activity due to delayed afterdepolarizations in sites of focal origin of ischemic ventricular tachycardia

2004 ◽  
Vol 287 (5) ◽  
pp. H2078-H2084 ◽  
Author(s):  
Dezhi Xing ◽  
James B. Martins
Keyword(s):  
Ventricular Tachycardia ◽  
Three Dimensional ◽  
In Vitro Study ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Triggered Activity ◽  
Anesthetized Dogs ◽  
Delayed Afterdepolarizations ◽  
First Time

This study for the first time systematically evaluated the site of origin of focal ventricular tachycardia (VT) induced 1–3 h after acute coronary artery ligation in dogs. We determined whether delayed afterdepolarizations (DADs) and triggered activity (TA) are more often recorded from ischemic endocardium excised from focal sites of VT origin. A total of 145 α-chloralose-anesthetized dogs were studied: in 54 dogs without inducible VT, normal or ischemic endocardium was investigated in vitro; in 91 dogs, inducible VT was studied by three-dimensional activation mapping, with in vitro study of 51 endocardial foci compared with 40 endocardial ischemic sites not of VT origin. Incidence of DADs (71% vs. 33%, P < 0.05) and TA (32% vs. 11%, P < 0.05) was greater in ischemic than in normal Purkinje tissues. Purkinje sites of origin of focal VT demonstrated the greatest frequency of DADs (92%, P < 0.05) and TA (75%, P < 0.05), with repetitive TA predominating. Similar results were obtained in endocardial sites of origin. Action potentials were mildly depolarized and prolonged in the focal sites of origin. These abnormalities were stable up to 2.5 h of recording. This study demonstrated that DADs and TA may underlie a majority of focal VTs in ischemic endocardium and Purkinje tissue.

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