Preserved Inotropic and Lusitropic Responses to Exercise-induced Adrenergic Stimulation in Patients With Compensated Hypertensive Left Ventricular Hypertrophy

1998 ◽  
Vol 31 (2) ◽  
pp. 322A
Author(s):  
M Inagaki
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Adrenergic Stimulation ◽  
Exercise Induced

RYR2 p.R169L mutation and left ventricular hypertrophy in a child with emotion-triggered sudden death

2020 ◽  
Vol 30 (7) ◽  
pp. 1039-1042
Author(s):  
Utkarsh Kohli ◽  
Lisa Kuntz ◽  
Hemal M. Nayak
Keyword(s):  
Ventricular Tachycardia ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Catecholaminergic Polymorphic Ventricular Tachycardia ◽  
Polymorphic Ventricular Tachycardia ◽  
Exercise Induced ◽  
In Vivo Effects

AbstractCatecholaminergic polymorphic ventricular tachycardia is a rare (prevalence: 1/10,000) channelopathy characterised by exercise-induced or emotion-triggered ventricular arrhythmias. There is an overall paucity of genotype-phenotype correlation studies in patients with catecholaminergic polymorphic ventricular tachycardia, and in vitro and in vivo effects of individual mutations have not been well characterised. We report an 8-year-old child who carried a mutation in the coding exon 8 of RYR2 (p.R169L) and presented with emotion-triggered sudden cardiac death. He was also found to have left ventricular hypertrophy, a combination which has not been reported before. We discuss the association between genetic variation in RYR2, particularly mutations causing replacement of arginine at position 169 of RYR2 and structural cardiac abnormalities.

scholarly journals Myocardial Metabolism in Endurance Exercise-Induced Left Ventricular Hypertrophy

2018 ◽  
Vol 11 (6) ◽  
pp. 928-930
Author(s):  
Meagan M. Wasfy ◽  
Courtney Foster Bibbo ◽  
Marcel Brown ◽  
James R. DeLuca ◽  
Francis Wang ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Endurance Exercise ◽  
Ventricular Hypertrophy ◽  
Myocardial Metabolism ◽  
Left Ventricular ◽  
Exercise Induced

scholarly journals PRESERVED MYOCARDIAL METABOLIC EFFICIENCY IN EXERCISE-INDUCED LEFT VENTRICULAR HYPERTROPHY

2016 ◽  
Vol 67 (13) ◽  
pp. 1639
Author(s):  
Meagan Murphy Wasfy ◽  
James R. DeLuca ◽  
Courtney Foster ◽  
Rory Weiner ◽  
Gregory Lewis ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Metabolic Efficiency ◽  
Exercise Induced

scholarly journals Exercise-induced subendocardial dysfunction in dogs with left ventricular hypertrophy.

1990 ◽  
Vol 66 (2) ◽  
pp. 329-343 ◽  
Author(s):  
L Hittinger ◽  
R P Shannon ◽  
S Kohin ◽  
W T Manders ◽  
P Kelly ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Exercise Induced

β-Adrenergic stimulation causes cardiocyte apoptosis: influence of tachycardia and hypertrophy

1998 ◽  
Vol 275 (3) ◽  
pp. H961-H968 ◽  
Author(s):  
Yukitaka Shizukuda ◽  
Peter M. Buttrick ◽  
David L. Geenen ◽  
Alain C. Borczuk ◽  
Richard N. Kitsis ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Myocardial Damage ◽  
Left Ventricular ◽  
Adrenergic Stimulation ◽  
Aortic Banding ◽  
Abdominal Aortic ◽  
Terminal Deoxynucleotide Transferase ◽  
Blood Pressures ◽  
And Control

To establish whether catecholamines per se in the absence of significant increases in systolic load induce myocardial damage via apoptosis, rats were treated with vehicle or isoproterenol (400 μg ⋅ kg−1 ⋅ h−1). Apoptotic cardiocytes (Apo) were identified in paraffin-embedded sections using terminal deoxynucleotide transferase-mediated dUTP nick end labeling. Results were confirmed using an independent ligase assay. Systolic blood pressures were comparable in isoproterenol-treated and control rats. Twenty-four hours of treatment with isoproterenol resulted in significant numbers of Apo compared with control [7.9 ± 2.5 vs. 0.3 ± 0.3 (SE) cm−2, P < 0.05]. A cohort of animals was subjected to ventricular pacing to induce a tachycardia equivalent to that induced by isoproterenol, and these animals did not show an increase in Apo. The left ventricular hypertrophy induced by 2 wk of abdominal aortic banding also increased Apo (∼7.2-fold); however, 24 h of isoproterenol infusion did not induce additional Apo in these rats. Thus catecholamines, in the absence of altered systolic load, induce Apo which is not mediated solely by tachycardia. Left ventricular hypertrophy secondary to abdominal aortic banding is associated with Apo, but this does not increase sensitivity to isoproterenol-induced Apo.

Sign in / Sign up

Export Citation Format

Share Document