Separation between vasodilation and positive inotropism by assessment of myocardial energetics in patients with dilated cardiomyopathy

1989 ◽  
pp. 257-265
Author(s):  
Ch. Holubarsch ◽  
G. Hasenfuss ◽  
M. Allgeier ◽  
H. W. Heiss ◽  
Hj. Just
Keyword(s):  
Dilated Cardiomyopathy ◽  
Positive Inotropism ◽  
Myocardial Energetics

Separation between vasodilation and positive inotropism by assessment of myocardial energetics in patients with dilated cardiomyopathy

1989 ◽  
Vol 84 (1) ◽  
pp. 257-265
Author(s):  
Ch. Holubarsch ◽  
G. Hasenfuss ◽  
M. Allgeier ◽  
H. W. Heiss ◽  
Hj. Just
Keyword(s):  
Dilated Cardiomyopathy ◽  
Positive Inotropism ◽  
Myocardial Energetics

scholarly journals Mitochondrial CaMKII causes metabolic reprogramming, energetic insufficiency, and dilated cardiomyopathy

2020 ◽  
Author(s):  
Elizabeth D. Luczak ◽  
Yuejin Wu ◽  
Jonathan M. Granger ◽  
Mei-ling A. Joiner ◽  
Nicholas R. Wilson ◽  
...  
Keyword(s):  
Dilated Cardiomyopathy ◽  
Mechanical Performance ◽  
Left Ventricular ◽  
Metabolic Reprogramming ◽  
Ventricular Dilation ◽  
Over Expression ◽  
Calmodulin Kinase ◽  
Left Ventricular Dilation ◽  
Myocardial Energetics ◽  
Camkii Activation

AbstractDespite the clear association between myocardial injury, heart failure and depressed myocardial energetics, little is known about upstream signals responsible for remodeling myocardial metabolism after pathological stress. We found increased mitochondrial calmodulin kinase II (CaMKII) activation and left ventricular dilation in mice one week after myocardial infarction (MI) surgery. In contrast, mice with genetic mitochondrial CaMKII inhibition were protected from left ventricular dilation and dysfunction after MI. Mice with myocardial and mitochondrial CaMKII over-expression (mtCaMKII) had severe dilated cardiomyopathy and decreased ATP that caused elevated cytoplasmic resting (diastolic) Ca2+ concentration and reduced mechanical performance. We mapped a metabolic pathway that allowed us to rescue disease phenotypes in mtCaMKII mice, providing new insights into physiological and pathological metabolic consequences of CaMKII signaling in mitochondria. Our findings suggest myocardial dilation, a disease phenotype lacking specific therapies, can be prevented by targeted replacement of mitochondrial creatine kinase, or mitochondrial-targeted CaMKII inhibition.

Influence of Enoximone on Myocardial Energetics in Patients with Idiopathic Dilated Cardiomyopathy

1989 ◽  
Vol 14 (Supplement) ◽  
pp. S75
Author(s):  
Gerd Hasenfuss ◽  
Christian Holubarsch ◽  
H. Wolfgang Heiss ◽  
Thomas Meinertz ◽  
Thomas Hofmann ◽  
...  
Keyword(s):  
Dilated Cardiomyopathy ◽  
Idiopathic Dilated Cardiomyopathy ◽  
Myocardial Energetics

Effects of Pimobendan on Hemodynamics and Myocardial Energetics in Patients with Idiopathic Dilated Cardiomyopathy

1989 ◽  
Vol 14 (Supplement) ◽  
pp. S36
Author(s):  
Gerd Hasenfuss ◽  
Christian Holubarsch ◽  
H. Wolfgang Heiss ◽  
Martin Allgeier ◽  
Hanjorg Just
Keyword(s):  
Dilated Cardiomyopathy ◽  
Idiopathic Dilated Cardiomyopathy ◽  
Myocardial Energetics

Effects of Pimobendan on Hemodynamics and Myocardial Energetics in Patients with Idiopathic Dilated Cardiomyopathy

1989 ◽  
Vol 14 ◽  
pp. S36 ◽  
Author(s):  
Gerd Hasenfuss ◽  
Christian Holubarsch ◽  
H. Wolfgang Heiss ◽  
Martin Allgeier ◽  
Hanjorg Just
Keyword(s):  
Dilated Cardiomyopathy ◽  
Idiopathic Dilated Cardiomyopathy ◽  
Myocardial Energetics
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