scholarly journals Levosimendan improves cardiac function and myocardial efficiency in rats with right ventricular failure

2017 ◽  
Vol 8 (1) ◽  
pp. 204589321774312 ◽  
Author(s):  
Mona S. Hansen ◽  
Asger Andersen ◽  
Lars P. Tolbod ◽  
Nils H. Hansson ◽  
Roni Nielsen ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Cardiac Function ◽  
Right Ventricular ◽  
Glucose Uptake ◽  
Myocardial Oxygen Consumption ◽  
External Work ◽  
Myocardial Glucose Uptake ◽  
Positron Emission ◽  
Myocardial Efficiency ◽  
Rv Function

Levosimendan is an inotropic and vasodilator drug, which is known to improve cardiac function in animal models of right ventricular (RV) failure. The effects of levosimendan on oxygen consumption and myocardial efficiency in the failing RV is unknown. We investigated the effects of levosimendan on RV function, myocardial oxygen consumption, myocardial external efficiency (MEE), and myocardial metabolism in rats with RV hypertrophy and failure. RV hypertrophy and failure were induced by pulmonary trunk banding in rats. Rats were randomized to seven weeks of treatment with vehicle (n = 16) or levosimendan (3 mg/kg/day) (n = 13). Control animals without pulmonary banding received vehicle treatment (n = 11). RV MEE and RV metabolism were evaluated by echocardiography, 11C-acetate positron emission tomography (PET), 18F-FDG PET, and invasive pressure measurements. We found that levosimendan improved RV MEE (26 ± 3 vs. 14 ± 1%, P < 0.01) by increasing RV external work (0.62 ± 0.06 vs. 0.30 ± 0.03 mmHgċmL, P < 0.001) without affecting RV myocardial oxygen consumption ( P = 0.64). The improvement in RV MEE was not associated with a change in RV myocardial glucose uptake (1.3 ± 0.1 vs. 1.0 ± 0.1 µmol/g/min, P = 0.44). In conclusion, in the hypertrophic and failing RV of the rat, levosimendan improves RV function without increasing myocardial oxygen consumption leading to improved MEE. The improvement in RV MEE was not associated with a change in myocardial glucose uptake. This study emphasizes the potential therapeutic value of chronic levosimendan treatment RV failure. It extends previous observations on the effect profile of levosimendan and motivates clinical testing of levosimendan in RV failure.

scholarly journals Noninvasive Detection of Early Metabolic Left Ventricular Remodeling in Systemic Hypertension

Cardiology ◽  
2015 ◽  
Vol 133 (3) ◽  
pp. 157-162 ◽  
Author(s):  
Yasmin S. Hamirani ◽  
Bijoy K. Kundu ◽  
Min Zhong ◽  
Andrew McBride ◽  
Yinlin Li ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Pressure Overload ◽  
Positron Emission Tomography Imaging ◽  
Left Ventricular ◽  
Systemic Hypertension ◽  
Myocardial Glucose Uptake ◽  
Positron Emission ◽  
Metabolic Remodeling

Objectives: Hypertension (HTN) is a common cause of left ventricular hypertrophy (LVH). Sustained pressure overload induces a permanent myocardial switch from fatty-acid to glucose metabolism. In this study, we tested the hypothesis that metabolic remodeling, characterized by increased myocardial glucose uptake, precedes structural and functional remodeling in HTN-induced LVH. Methods: We recruited 31 patients: 11 with HTN only, 9 with HTN and LVH and 11 normotensive controls without LVH. Transthoracic echocardiography was performed to assess the function, mass, wall thickness and diastolic function of the left ventricle. Positron emission tomography imaging was performed, and the rate of myocardial 2-deoxy-2-[18F]fluoro-D-glucose uptake, Ki, was determined using a 3-compartment kinetic model. Results: The mean Ki values were significantly higher in HTN patients than in those with HTN and LVH (p < 0.001) and in controls (p = 0.003). The unexpected decrease in Ki with LVH may be secondary to a decreased Ki with diastolic dysfunction (DD), 0.039 ± 0.032 versus 0.072 ± 0.013 (p = 0.004). There was also a significant stepwise decrease in Ki with increasing DD grade (p = 0.04). Conclusion: Glucose metabolic remodeling is detectable in hypertensive patients before the development of LVH. Furthermore, lower glucose uptake rates are observed in patients with DD. The mechanism for this last finding requires further investigation.

Myocardial oxygen consumption, cardiac work, and myocardial efficiency in children

1996 ◽  
Vol 155 (6) ◽  
pp. 436-439 ◽  
Author(s):  
Zenshiro Onouchi ◽  
Kenji Hamaoka ◽  
Koichi Sakata ◽  
Yali Liu ◽  
Fumiaki Suto ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Myocardial Oxygen Consumption ◽  
Cardiac Work ◽  
Myocardial Efficiency

scholarly journals SGLT2 Inhibition Does Not Affect Myocardial Fatty Acid Oxidation or Uptake, But Reduces Myocardial Glucose Uptake and Blood Flow in Individuals With Type 2 Diabetes– a Randomized Double-Blind, Placebo-Controlled Crossover Trial

2020 ◽  
Author(s):  
Katrine M. Lauritsen ◽  
Bent R.R. Nielsen ◽  
Lars P. Tolbod ◽  
Mogens Johannsen ◽  
Jakob Hansen ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Oxygen Consumption ◽  
Glucose Uptake ◽  
Acid Oxidation ◽  
Double Blind ◽  
Double Blind Placebo ◽  
Myocardial Glucose Uptake ◽  
Pet Ct ◽  
Sglt2 Inhibition

Sodium-glucose cotransporter 2 (SGLT2) inhibition reduces cardiovascular morbidity and mortality in individuals with type 2 diabetes. Beneficial effects have been attributed to increased ketogenesis, reduced cardiac fatty acid oxidation and diminished cardiac oxygen consumption. We therefore studied whether SGLT2 inhibition altered cardiac oxidative substrate consumption, efficiency, and perfusion. <p>13 individuals with type 2 diabetes were studied after four weeks treatment with empagliflozin and placebo in a randomized, double-blind, placebo-controlled crossover study. Myocardial palmitate and glucose uptake were measured with <sup>11</sup>C-palmitate and <sup>18</sup>F-FDG PET/CT. Oxygen consumption and myocardial external efficiency (MEE) were measured with <sup>11</sup>C-acetate PET/CT. Resting and adenosine stress myocardial blood flow (MBF) and myocardial flow reserve (MFR) were measured using <sup>15</sup>O-H<sub>2</sub>O PET/CT. </p> <p>Empagliflozin did not affect myocardial FFA uptake but reduced myocardial glucose uptake by 57% (p<0.001). Empagliflozin did not change myocardial oxygen consumption or MEE. Empagliflozin reduced resting MBF by 13% (p<0.01), but did not significantly affect stress MBF or MFR.</p> <p>In conclusion, SGLT2 inhibition did not affect myocardial FFA uptake, but channeled myocardial substrate utilization from glucose towards other sources and reduced resting MBF. However, the observed metabolic and hemodynamic changes were modest and most likely contribute only partially to the cardioprotective effect of SGLT2 inhibition. </p>

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