Cardiac Energetics: From Emax to Pressure-Volume Area

1995 ◽  
Keyword(s):  
Cardiac Energetics

Thermodynamic inconsistency disproves the Suga-Sagawa theory of cardiac energetics

2021 ◽  
Author(s):  
Denis S. Loiselle ◽  
Andrew J. Taberner ◽  
Kenneth Tran ◽  
June-Chiew Han
Keyword(s):  
Cardiac Energetics ◽  
Thermodynamic Inconsistency

scholarly journals Normobaric hypoxia elevates free fatty acids and impairs cardiac energetics and diastolic function in normal human volunteers

2010 ◽  
Vol 12 (S1) ◽  
Author(s):  
Cameron J Holloway ◽  
Lowri E Cochlin ◽  
Ion Codreanu ◽  
Edward Bloch ◽  
Marzieh Fatemianl ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Diastolic Function ◽  
Normobaric Hypoxia ◽  
Cardiac Energetics ◽  
Human Volunteers ◽  
Normal Human

scholarly journals Increased myocardial fat supply improves cardiac energetics and function in heart failure

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
W Watson ◽  
P.G Green ◽  
S Neubauer ◽  
O.J Rider
Keyword(s):  
Heart Failure ◽  
Creatine Kinase ◽  
Ejection Fraction ◽  
Funding Source ◽  
Cardiac Energetics ◽  
Fat Emulsion ◽  
Euglycaemic Clamp ◽  
Fat Infusion ◽  
And Function ◽  
Glucose Supply

Abstract Introduction The failing heart is starved of energy, in part accounting for its contractile dysfunction. Reduced uptake of fat and sugar required for energy production has frequently been demonstrated in heart failure, therefore altering metabolism of glucose and/or fat is therefore attractive as a therapy. We hypothesized increasing glucose supply would be beneficial over increasing fat supply so measured ATP usage (via PCr/ATP ratio and flux through creatine kinase) and cardiac function during fat emulsion infusion or euglycaemic hyperinsulinaemic clamp. Methods 11 patients with a diagnosis of heart failure and nonischaemic cardiomyopathy were recruited, mean age 66 (range 49–80), mean BMI 27.7 (range 21.3–37.5), F:M 3:8, 3 diabetic and 8 non-diabetic. On the first visit they had a baseline cardiac magnetic resonance (CMR), collecting cardiac volumes and function, then were randomised to receive either fat infusion or euglycaemic clamp. Following an hour of infusion, CMR was repeated followed by 31P cardiac magnetic resonance spectroscopy, then a dobutamine stress sequence at 65% maximum heart rate. They received the alternate infusion at the next visit. Results Data was normally distributed. Baseline ejection fraction was 37±9%. PCr/ATP ratio was greater with the fat infusion compared to euglycaemic clamp (1.82±0.26 vs 1.68±0.24, p=0.04). Fat emulsion infusion also brought about a greater ejection fraction increase over the baseline, compared to the euglycaemic clamp in which there was little difference (+5.3±5.3% vs −0.6±3.1%, p=0.004). Calculated cardiac work was greater in the fat infusion group than the Insulin/glucose group (682±156 L.mmHg/min vs 581±85 L.mmHg/min, p=0.009). There was no significant difference in creatine kinase first order rate constant (fat infusion 0.2±0.09/s vs euglycaemic clamp 0.16±0.07/s, p=0.32) nor creatine kinase flux (fat infusion 1.85±0.92 μmol/g/s vs euglycaemic clamp 1.46±0.58 μmol/g/s, p=0.22). The increment in cardiac output on stress over baseline was not significantly different between arms (fat infusion +3.39±3.07 L/min vs euglycaemic clamp +3.08±2.57 L/min, p=0.42). The PCr/ATP ratio showed positive correlation with the stress ejection fraction (R2=0.656, p=0.001), but not with resting ejection fraction. Conclusions Increased supply of fat to the myocardium brought about improved contractility and cardiac energetics compared to an increased glucose supply. The increase in PCr/ATP ratio would imply (given ATP concentrations are kept constant in the myocardium) there is a greater availability of phosphocreatine, suggesting increased mitochondrial ATP synthesis. These results were unexpected as it has traditionally been thought that increased glucose metabolism would yield greater cardiac function in the failing heart. These data suggest targeting myocardial fat metabolism may provide novel treatments for cardiac dysfunction. Figure 1 Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): British Heart Foundation

scholarly journals Differences in Cardiac Energetics Between Patients With Familial and Nonfamilial Hypertrophic Cardiomyopathy

Circulation ◽  
2000 ◽  
Vol 101 (12) ◽  
Author(s):  
Wulf-Ingo Jung ◽  
Thomas Hoess ◽  
Michael Bunse ◽  
Stefan Widmaier ◽  
Ludger Sieverding ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Cardiac Energetics

Cardiac Energetics and Adenosine Formation

1995 ◽  
pp. 169-177
Author(s):  
Jürgen Schrader ◽  
Ulrich Decking ◽  
Thomas Stumpe
Keyword(s):  
Cardiac Energetics

scholarly journals Non‐invasive integrative analysis of cardiac energetics, translation to human heart in vivo

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Philippe Henri Diolez ◽  
Veronique Deschodt-Arsac ◽  
Mathilde Chapolard ◽  
Meleze Hocini ◽  
Pierre Jais ◽  
...  
Keyword(s):  
Human Heart ◽  
Integrative Analysis ◽  
Cardiac Energetics ◽  
Non Invasive

Cardiac energetics alteration in chronic hypoxia rat model: a non invasive in vivo 31P magnetic resonance spectroscopy experimental study

2021 ◽  
Author(s):  
Xiaohan Yuan ◽  
Xiaomei Zhu ◽  
Yang Chen ◽  
Wangyan Liu ◽  
Wen Qian ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Magnetic Resonance Spectroscopy ◽  
Right Ventricular ◽  
Myocardial Injury ◽  
Chronic Hypoxia ◽  
Volume Index ◽  
Control Group ◽  
Resonance Spectroscopy ◽  
Cardiac Energetics

Abstract Background: Energetics alteration plays a key role in the process of myocardial injury in chronic hypoxic diseases (CHD). 31P magnetic resonance spectroscopy (MRS) can investigate alterations in cardiac energetics in vivo. This study was aimed to characterize the potential value of 31P MRS in evaluating cardiac energetics alteration of chronic hypoxia rats (CHR).Methods: Twenty-four CHRs were induced by SU5416 combined with hypoxia, and six rats were raised as control group. 31P MRS was performed weekly and the ratio of concentrations of phosphocreatine (PCr) to adenosine triphosphate (ATP) (PCr/ATP) was obtained. The index of cardiac structure and systolic function parameters, including the right ventricular function (RVEF), right ventricular end-diastolic volume index (RVEDVi), right ventricular end-systolic volume index (RVESVi), the left ventricular function parameters were also measured.Results: The declension of resting cardiac PCr/ATP ratio in CHR was observed at the 1st week, compared to control group (2.90±0.35 vs. 3.31±0.45, p =0.045), while the RVEF，RVEDVi and RVESVi decreased at the 2nd week (p＜0.05). The PCr/ATP ratio displayed a significant correlation with RVEF(r = 0.605, p = 0.001)，RVEDVi and RVESVi (r = -0.661, r = -0.703; p＜0.001).Conclusions: 31P MRS can early detect the cardiac energetics alteration in CHR model before the onset of ventricular dysfunction. The decrease of PCr/ATP ratio likely revealed myocardial injury and cardiac dysfunction.

Abstract 15649: Pharmacological Inhibition of Aldose Reductase by AT001 Prevents Abnormal Cardiac Energy Metabolism and Improves Heart Function in an Animal Model of Diabetic Cardiomyopathy

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Keshav Gopal ◽  
Qutuba Karwi ◽  
Seyed Amirhossein Tabatabaei Dakhili ◽  
Riccardo Perfetti ◽  
Ravichandran Ramasamy ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Energy Metabolism ◽  
Fatty Acid Oxidation ◽  
Diabetic Cardiomyopathy ◽  
Acid Oxidation ◽  
Cardiac Energetics ◽  
Cardiac Efficiency ◽  
Oxidation Rates ◽  
Cardiac Energy Metabolism ◽  
Cardiac Energy

Introduction: Diabetic Cardiomyopathy (DCM) is a major cause of death in people with type 2 diabetes (T2D). Alterations in cardiac energy metabolism including increased fatty acid oxidation rates and reduced glucose oxidation rates are key contributing factors to the development of DCM. Studies have shown that Aldose Reductase (AR), an enzyme activated under hyperglycemic conditions, can modulate myocardial glucose and fatty acid oxidation, and promotes cardiac dysfunction. Hypothesis: Pharmacological inhibition of AR using a next-generation inhibitor AT-001, can mitigate DCM in mice by modulating cardiac energy metabolism and improving cardiac efficiency. Methods: Male human AR overexpressing (hAR-Tg) and C57BL/6J (Control) mice were subjected to experimental T2D (high-fat diet [60% kcal from lard] for 10-wk with a single intraperitoneal streptozotocin injection of 75 mg/kg) and treated for the last 3-wk with AT-001 (40mg/kg/day) or vehicle via oral gavage. Cardiac energy metabolism and in vivo cardiac function were assessed via isolated working heart perfusions and ultrasound echocardiography, respectively. Results: AT-001 treatment significantly improved cardiac energetics in a murine model of DCM (hAR-Tg mice with T2D). Particularly, AT-001-treated mice exhibited decreased cardiac fatty acid oxidation rates compared to the vehicle-treated mice (342 ± 53 vs 964 ± 130 nmol/min/g dry wt.). Concurrently, there was a significant decrease in cardiac oxygen consumption in the AT-001-treated compared to the vehicle-treated mice (41 ± 12 vs 60 ± 11 μmol/min/g dry wt.), suggesting increased cardiac efficiency. Furthermore, treatment with AT-001 prevented cardiac structural and functional abnormalities present in DCM, including diastolic dysfunction as reflected by an increase in the tissue Doppler E’/A’ ratio and decrease in E/E’ ratio. Moreover, AT-001 treatment prevented cardiac hypertrophy as reflected by a decrease in LV mass in AT-001-treated mice. Conclusions: AR inhibition with AT-001 prevents cardiac structural and functional abnormalities in a mouse model of DCM, and normalizes cardiac energetics by shifting cardiac metabolism towards a non-diabetic metabolic state.

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