Insights from Novel Noninvasive CT and ECG Imaging Modalities on Electromechanical Myocardial Activation in a Canine Model of Ischemic Dyssynchronous Heart Failure

2016 ◽  
Vol 27 (12) ◽  
pp. 1454-1461 ◽  
Author(s):  
FADY DAWOUD ◽  
KARL H. SCHULERI ◽  
DAVID D. SPRAGG ◽  
B. MILAN HORÁČEK ◽  
RONALD D. BERGER ◽  
...  
Keyword(s):  
Heart Failure ◽  
Canine Model ◽  
Imaging Modalities ◽  
Dyssynchronous Heart Failure

scholarly journals Cardiac Resynchronization Therapy Improves Altered Na Channel Gating in Canine Model of Dyssynchronous Heart Failure

2013 ◽  
Vol 6 (3) ◽  
pp. 546-554 ◽  
Author(s):  
Takeshi Aiba ◽  
Andreas S. Barth ◽  
Geoffrey G. Hesketh ◽  
Yasmin L. Hashambhoy ◽  
Khalid Chakir ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Resynchronization Therapy ◽  
Channel Gating ◽  
Canine Model ◽  
Cardiac Resynchronization ◽  
Na Channel ◽  
Resynchronization Therapy ◽  
Dyssynchronous Heart Failure

Abstract 271: A Novel Functional Role for Plasma miR-30d in Dyssynchronous Heart Failure

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Kirsty Danielson ◽  
Yonathan Melman ◽  
Bridget Simonson ◽  
Andreas Barth ◽  
Khalid Chakir ◽  
...  
Keyword(s):  
Heart Failure ◽  
Functional Role ◽  
Lateral Wall ◽  
Canine Model ◽  
Cardiac Resynchronization ◽  
Tissue Samples ◽  
Diagnostic Strategies ◽  
Qrt Pcr ◽  
Dyssynchronous Heart Failure

Introduction: We have previously shown that plasma miR-30d level is an independent predictor of echocardiographic response to cardiac resynchronization therapy (CRT) in patients with dyssynchronous heart failure (DHF). We now test the hypothesis that miR-30d is dynamically regulated in cardiomyocytes (CMs) and plays a functional role in DHF. Methods: miR-30d levels were assessed in a canine model of DHF and CRT using qRT-PCR, and potential miR-30d targets were identified using a bioinformatics approach. miR-30d targets were validated in the canine model and in CMs in culture. The regulation and functional role of miR-30d was investigated in CMs in culture using microscopy, western blotting and qRT-pCR. Results: miR-30d is enriched in the coronary sinus compared to peripheral blood in human patients, suggesting a cardiac origin (n=7, p<0.05). In tissue samples from the canine model of DHF, miR-30d levels are highest in the lateral wall, in concert with the greatest wall stress, and decreases with CRT (n=5, p<0.05). Bioinformatics analysis using differential gene expression data and in silico miR target prediction algorithms identified integrin and PI3/Akt signaling pathways as targets of miR-30d. Several targets including MAP4K4 and lims1 were further validated in tissue as well as in cultured CMs (n=4, p<0.05). miR-30d appears to be expressed in CMs, packaged into exosomes and micovesicles, and released in response to pathological rotational stress (n=2). Over-expression of miR-30d in CMs induces cellular hypertrophy with a unique expression signature of cardiac hypertrophy markers most consistent with physiological hypertrophy (n=3, p<0.05). Overexpression of miR-30d appears to be cardioprotective by abrogating TNF-induced increase in MAP4K4 expression (n=4, p<0.05). Conclusions: miR-30d is dynamically regulated in DHF and appears to play an important role in CM biology. Further insight into the role of ‘stretch’-regulated microRNAs such as miR-30d may pave the way for novel therapeutic and diagnostic strategies.

Abstract 302: Sex Differences In Nonlinear Dynamics And Their Circadian Variation In Control Dogs And In A New Arrhythmogenic Canine Model Of Heart Failure

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Yujie Zhu ◽  
Steven M Pogwizd
Keyword(s):  
Nonlinear Dynamics ◽  
Heart Failure ◽  
Sex Differences ◽  
Sex Difference ◽  
Circadian Variation ◽  
Holter Monitoring ◽  
Canine Model ◽  
Nonlinear Parameters ◽  
Arrhythmogenic Substrate ◽  
Males And Females

Introduction: Females can be more arrhythmogenic than males, and this sex difference can persist with development of chronic heart failure (CHF). The aim of this study was to investigate sex differences in the arrhythmogenic substrate in control dogs and in a new arrhythmogenic canine model of CHF. Methods: CHF was induced in 30 dogs by aortic insufficiency and aortic constriction. Holter monitoring assessed VT and PVCs from 30 dogs, as well as traditional HRV measures and nonlinear dynamics (including correlation dimension (CD), detrended fluctuations analysis α1 (DFAα1), and Shannon entropy (SE)) at baseline, 240 days (240d) and 720 days (720d) after CHF induction. Results: At baseline, females had lower LF/HF (0.27±0.03 vs 0.33±0.02, p=0.04), CD (1.60±0.17 vs 2.21±0.15, p=0.01), DFAα1 (0.62±0.03 vs 0.72±0.03, p=0.03), and SE (2.99±0.02 vs 3.10±0.03, p=0.03 vs males). Females lacked circadian variation in LF/HF, DFAα1, and SE while males had circadian variation in all of these. Of 11 dogs with frequent runs of VT and PVCs, 95% and 91% of total VT runs and total PVCs, respectively, were in females. With CHF, all these linear and nonlinear parameters progressively declined in males and females. CHF females had less decline in LF/HF than males so that by 720 days there was no more sex difference (0.24±0.06, 0.17±0.03 in females vs 0.22±0.05, 0.18±0.01 in males at 240d, 720d). However, for nonlinear parameters of CD, DFAα1, and SE, CHF females had lower values than males (CD: 1.56±0.21, 0.99±0.32 vs 1.87±0.24, 1.50±0.34; DFAα1: 0.51±0.05, 0.43±0.04 vs 0.54±0.07, 0.48±0.04; and SE 2.93±0.08, 2.76±0.08 vs 3.01±0.11, 2.91±0.04 in females vs males at 240d, 720d). With CHF, circadian variation in CD, DFAα1, and SE were lost in both males and females. Conclusions: There are sex differences in the arrhythmogenic substrate in control dogs and in this new arrhythmogenic canine model of moderate CHF. At baseline, females have lower sympathetic stimulation, reduced cardiac chaos, and loss of circadian variation in nonlinear dynamics. With CHF, sex differences in nonlinear dynamics persist; this reflects a loss of complexity and fractal properties that could contribute to increased arrhythmias in female CHF dogs.

scholarly journals Pirfenidone Prevents the Development of a Vulnerable Substrate for Atrial Fibrillation in a Canine Model of Heart Failure

Circulation ◽  
2006 ◽  
Vol 114 (16) ◽  
pp. 1703-1712 ◽  
Author(s):  
Ken W. Lee ◽  
Thomas H. Everett ◽  
Dulkon Rahmutula ◽  
Jose M. Guerra ◽  
Emily Wilson ◽  
...  
Keyword(s):  
Heart Failure ◽  
Atrial Fibrillation ◽  
Canine Model

scholarly journals P-413 The site of stimulation is more important than av delay variation for optimization of resynchronization therapy: Insights from a canine model of heart failure

EP Europace ◽  
2003 ◽  
Vol 4 (Supplement_2) ◽  
pp. B163-B163
Author(s):  
B. Thibault ◽  
A. Ducharme ◽  
E. Deblazio ◽  
Y.F. Shi ◽  
M. Dubuc ◽  
...  
Keyword(s):  
Heart Failure ◽  
Canine Model ◽  
Resynchronization Therapy ◽  
Site Of Stimulation ◽  
Av Delay ◽  
Delay Variation

Spontaneous and inducible ventricular arrhythmias in a canine model of chronic heart failure: relation to haemodynamics and sympathoadrenergic activation

1992 ◽  
Vol 13 (11) ◽  
pp. 1562-1572 ◽  
Author(s):  
H. N. SABBAH ◽  
A. D. GOLDBERGN ◽  
W. SCHOELS ◽  
T. KONO ◽  
C. WEBB ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Ventricular Arrhythmias ◽  
Canine Model

Effect of YM435, a Novel Dopamine DA1 Receptor Agonist, in a Canine Model of Acute Congestive Heart Failure

1998 ◽  
Vol 30 (5) ◽  
pp. 733-737 ◽  
Author(s):  
Takeyuki Yatsu ◽  
Yukinori Arai ◽  
Katsumi Sudoh ◽  
Masayuki Shibasaki ◽  
Wataru Uchida ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Receptor Agonist ◽  
Canine Model
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