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.

Syncope caused by complete heart block and ventricular arrhythmia as early manifestation of systemic lupus erythematosus in a pregnant patient: a case report

Lupus ◽  
2018 ◽  
Vol 27 (10) ◽  
pp. 1729-1731 ◽  
Author(s):  
C H Lo ◽  
J C C Wei ◽  
C F Tsai ◽  
L C Li ◽  
S W Huang ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Ventricular Tachycardia ◽  
Ventricular Arrhythmia ◽  
Clinical Features ◽  
Lupus Erythematosus ◽  
Pregnant Patient ◽  
Polymorphic Ventricular Tachycardia ◽  
Av Block ◽  
Systemic Lupus ◽  
Complete Av Block

Systemic lupus erythematosus (SLE) can affect all heart structures including the conduction system, with either reversible or permanent derangement. However, only a few cases of adult SLE and complete atrioventricular (AV) block have been reported. We describe a young pregnant woman who initially presented with complete AV block on electrocardiography before the diagnosis of SLE. Syncope subsequently developed during the postpartum period due to frequent nonsustained polymorphic ventricular tachycardia, suggesting lupus myocarditis. The ventricular arrhythmia was successfully treated by intravenous corticosteroids, lidocaine and implantation of a permanent pacemaker. This may represent the first report of complete AV block with polymorphic ventricular tachycardia, which was identified before the other clinical features of SLE fully manifested. SLE should be considered if a patient presents with complete AV block without other clinical features. It may warn for early diagnosis and appropriate treatment of SLE including lupus-related heart disease.

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.

scholarly journals Incidence and Clinical Management of Atrial Arrhythmias in Patients with Catecholaminergic Polymorphic Ventricular Tachycardia

2021 ◽  
Author(s):  
Gurukripa Kowlgi ◽  
John Giudicessi ◽  
Walid Barake ◽  
Konstantinos Siontis ◽  
Johan Bos ◽  
...  
Keyword(s):  
Ventricular Tachycardia ◽  
Ventricular Arrhythmias ◽  
Catecholaminergic Polymorphic Ventricular Tachycardia ◽  
Polymorphic Ventricular Tachycardia ◽  
Atrial Arrhythmias ◽  
Single Center ◽  
Ablation Therapy ◽  
Inappropriate Shocks ◽  
Drug Intolerance

Background: Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a genetic arrhythmia syndrome characterized by adrenergically-triggered ventricular arrhythmias, syncope, and sudden cardiac death. Several small studies suggest that atrial arrhythmias (AAs) are common in patients with CPVT. Objective: To determine the incidence and type of AAs observed within a large, single-center cohort of CPVT cases as well as the efficacy and durability of AA-directed management. Methods: In this retrospective study, the electronic medical record of 129 patients (52% female; average age at diagnosis 20.8  15.3 years) with CPVT (95% with a putative CPVT1-causative RYR2 variant) between 01/2000 and 09/2019 were reviewed for electrocardiographic evidence of AAs. Clinical features and efficacy of pharmacologic and ablation therapy were assessed. Results: Overall, 10/129 (7.8%) CPVT patients, all RYR2 variant-positive, had evidence of an AA (atrial fibrillation/flutter in 6, atrial tachycardia in 3, and supraventricular tachycardia in 1). The median age at AA diagnosis was 23 (14.2-35.5) years. 8/10 of patients experienced symptoms attributed to their AA, including inappropriate shocks. All patients were trialed on anti-arrhythmics, including -blockers, and/or flecainide. Owing to drug failure (1/10), drug intolerance (1/10), or patient preference (2/10); 4/10 patients received an ablation. Over a median follow-up of 23.5 (4.5-63) months, no AA recurrences were observed. Conclusion: Compared to prior studies, the incidence of AAs in this large, single-center referral cohort of CPVT patients was substantially lower (7.8% vs. 26%-35%). Although larger multi-center studies are needed to confirm, this study suggests that ablation is efficacious and durable in CPVT-associated AAs.

scholarly journals Arrhythmias from the Right Ventricular Moderator Band: Diagnosis and Management

2020 ◽  
Vol 8 (4) ◽  
pp. 294-299
Author(s):  
Megan Barber ◽  
Jason Chinitz ◽  
Roy John
Keyword(s):  
Ventricular Tachycardia ◽  
Right Ventricle ◽  
Ventricular Arrhythmias ◽  
Structural Heart Disease ◽  
Conduction System ◽  
Polymorphic Ventricular Tachycardia ◽  
Management Options ◽  
Premature Ventricular Contractions ◽  
Moderator Band ◽  
The Right

The moderator band in the right ventricle is being increasingly recognised as a source for arrhythmias in the absence of identifiable structural heart disease. Because it carries part of the conduction system from the right ventricle septum to the free wall, it is a source of Purkinje-mediated ventricular arrhythmias that manifest as premature ventricular contractions (PVC) or repetitive ventricular tachycardia. More importantly, short coupled PVCs triggering polymorphic ventricular tachycardia and VF have been localised to the moderator band and ablation of these Purkinje mediated PVCs can effectively prevent recurrent VF. The exact mechanism of arrhythmogenesis is still debated but stretch, fibrosis and ion channel alterations might be responsible. Arrhythmias originating in this region of the right ventricle may thus be another cause for idiopathic VF that is potentially treatable with catheter-based ablation techniques. Recognition of the typical PVC morphology can point to the moderator band as the source of idiopathic VF and an opportunity for timely intervention. The available data on the anatomy, electrophysiology and management options are reviewed.

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.

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