scholarly journals C-11 acetate has excellent reproducibility for quantification of myocardial oxidative metabolism

2014 ◽  
Vol 16 (5) ◽  
pp. 500-506 ◽  
Author(s):  
S. V. Nesterov ◽  
O. Turta ◽  
C. Han ◽  
M. Maki ◽  
I. Lisinen ◽  
...  
Keyword(s):  
Oxidative Metabolism ◽  
Myocardial Oxidative Metabolism ◽  
Excellent Reproducibility

Abstract 16976: Derangements in Cardiac Oxidative Metabolism in Humans With Dilated Cardiomyopathy

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Daniel Clark ◽  
Giovanni E Davogustto ◽  
Susan P Bell ◽  
RAVINDER MALLUGARI ◽  
William S Bradham ◽  
...  
Keyword(s):  
Myocardial Perfusion ◽  
Dilated Cardiomyopathy ◽  
Oxidative Metabolism ◽  
Myocardial Perfusion Reserve ◽  
Normal Subjects ◽  
Rate Pressure Product ◽  
Gadolinium Contrast ◽  
Perfusion Reserve ◽  
Demand Rate ◽  
Myocardial Oxidative Metabolism

Introduction: Dilated cardiomyopathy (DCM) is associated with impaired myocardial perfusion reserve and impaired myocardial oxidative metabolism. However, the association between myocardial perfusion reserve and oxidative metabolism, is not fully understood. Hypothesis: Reduced myocardial perfusion reserve is associated with reduced myocardial oxidative metabolism. Methods: Using non-invasive cardiac imaging, we studied 8 DCM patients and 14 normal subjects. Myocardial perfusion reserve index (MPRI) was calculated using cardiac magnetic resonance as the normalized rate of myocardial signal augmentation following gadolinium contrast injection between rest and regadenoson induced stress. Resting oxidative metabolism was calculated as the myocardial mono-exponential decay rate (Kmono) of [ 11 C]acetate by positron emission tomography normalized per unit demand (rate-pressure product, RPP) (Kmono/RPP). Results: MPRI was lower in DCM compared to controls (1.25 ± 0.22 vs 1.59 ± 0.49, p=0.038). Similarly, Kmono/RPP was lower in DCM compared with normal subjects (0.6x10e-3 ± 0.15 x10e-3 vs 1.2x10e-3 ± 0.9x10e-3, p<0.0001). There was a linear relation between Kmono and RPP in normal subjects. However, DCM patients showed no increase in Kmono regardless of RPP (Figure 1A). Kmono/RPP was not significantly related to MPRI in either group (Figure 1B). Conclusions: Patients with DCM exhibit markedly impaired myocardial oxidative metabolism compared to normal subjects. However, this impairment was not quantitatively related to impaired myocardial perfusion reserve. Of the various mechanisms that could explain decrease in oxidative metabolism in DCM, these data suggest that reduced myocardial perfusion is not the principal driver of impaired oxidative metabolism.

Increased myocardial lactate oxidation in lambs with aortopulmonary shunts at rest and during exercise

1998 ◽  
Vol 275 (5) ◽  
pp. H1503-H1512 ◽  
Author(s):  
Gertie C. M. Beaufort-Krol ◽  
Janny Takens ◽  
Marieke C. Molenkamp ◽  
Gioia B. Smid ◽  
Koos J. Meuzelaar ◽  
...  
Keyword(s):  
Oxidative Metabolism ◽  
Myocardial Hypertrophy ◽  
Conscious State ◽  
Exercise Group ◽  
Lactate Oxidation ◽  
Lactate Release ◽  
Exogenous Glucose ◽  
Lactate Uptake ◽  
And Control ◽  
Myocardial Oxidative Metabolism

Free fatty acids are the major fuels for the myocardium, but during a higher load carbohydrates are preferred. Previously, we demonstrated that myocardial net lactate uptake was higher in lambs with aortopulmonary shunts than in control lambs. To determine whether this was caused by an increased lactate uptake and oxidation or by a decreased lactate release, we studied myocardial lactate and glucose metabolism with13C-labeled substrates in 36 lambs in a fasting, conscious state. The lambs were assigned to two groups: a resting group consisting of 8 shunt and 9 control lambs, and an exercise group (50% of peak O2consumption) consisting of 9 shunt and 10 control lambs. Myocardial lactate oxidation was higher in shunt than in control lambs (mean ± SE, rest: 10.33 ± 2.61 vs. 0.17 ± 0.82, exercise: 38.05 ± 8.87 vs. 16.89 ± 4.78 μmol ⋅ min−1⋅ 100 g−1; P < 0.05). There was no difference in myocardial lactate release between shunt and control lambs. Oxidation of exogenous glucose, which was approximately zero at rest, increased during exercise in shunt and control lambs. The contribution of glucose and lactate to myocardial oxidative metabolism increased during exercise compared with at rest in both shunt and control lambs. We conclude that myocardial lactate oxidation is higher in shunt than in control lambs, both at rest and during exercise, and that the contribution of carbohydrates in myocardial oxidative metabolism in shunt lambs is higher than in control lambs. Thus it appears that this higher contribution of carbohydrates occurs not only in the case of pressure-overloaded hearts but also in myocardial hypertrophy due to volume overloading.

Functional recovery after reperfusion is predicated on recovery of myocardial oxidative metabolism

1993 ◽  
Vol 125 (4) ◽  
pp. 939-949 ◽  
Author(s):  
Carla J. Weinheimer ◽  
Michael A. Brown ◽  
Ryuji Nohara ◽  
Julio E. Perez ◽  
Steven R. Bergmann
Keyword(s):  
Functional Recovery ◽  
Oxidative Metabolism ◽  
Myocardial Oxidative Metabolism

Abnormal in vivo myocardial energy substrate uptake in diet-induced type 2 diabetic cardiomyopathy in rats

2010 ◽  
Vol 298 (5) ◽  
pp. E1049-E1057 ◽  
Author(s):  
Sébastien L. Ménard ◽  
Etienne Croteau ◽  
Otman Sarrhini ◽  
Roselle Gélinas ◽  
Pascal Brassard ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Fatty Acid ◽  
Mrna Expression ◽  
Oxidative Metabolism ◽  
Left Ventricular ◽  
Glucose Clamp ◽  
Left Ventricular Ejection ◽  
Myocardial Oxidative Metabolism

The purpose of this study was to determine in vivo myocardial energy metabolism and function in a nutritional model of type 2 diabetes. Wistar rats rendered insulin-resistant and mildly hyperglycemic, hyperinsulinemic, and hypertriglyceridemic with a high-fructose/high-fat diet over a 6-wk period with injection of a small dose of streptozotocin (HFHFS) and control rats were studied using micro-PET (μPET) without or with a euglycemic hyperinsulinemic clamp. During glucose clamp, myocardial metabolic rate of glucose measured with [18F]fluorodeoxyglucose ([18F]FDG) was reduced by ∼81% ( P < 0.05), whereas myocardial plasma nonesterified fatty acid (NEFA) uptake as determined by [18F]fluorothia-6-heptadecanoic acid ([18F]FTHA) was not significantly changed in HFHFS vs. control rats. Myocardial oxidative metabolism as assessed by [11C]acetate and myocardial perfusion index as assessed by [13N]ammonia were similar in both groups, whereas left ventricular ejection fraction as assessed by μPET was reduced by 26% in HFHFS rats ( P < 0.05). Without glucose clamp, NEFA uptake was ∼40% lower in HFHFS rats ( P < 0.05). However, myocardial uptake of [18F]FTHA administered by gastric gavage was significantly higher in HFHFS rats ( P < 0.05). These abnormalities were associated with reduced Glut4 mRNA expression and increased Cd36 mRNA expression and mitochondrial carnitine palmitoyltransferase 1 activity ( P < 0.05). HFHFS rats display type 2 diabetes complicated by left ventricular contractile dysfunction with profound reduction in myocardial glucose utilization, activation of fatty acid metabolic pathways, and preserved myocardial oxidative metabolism, suggesting reduced myocardial metabolic efficiency. In this model, increased myocardial fatty acid exposure likely occurs from circulating triglyceride, but not from circulating plasma NEFA.

Reduction of myocardial oxidative metabolism in dilated cardiomyopathy but not in remote areas in myocardial infarction

2004 ◽  
Vol 1264 ◽  
pp. 271-274
Author(s):  
Kazuyuki Noriyasu ◽  
Takahiro Tsukamoto ◽  
Koichi Morita ◽  
Hiroyuki Kageyama ◽  
Megumi Mabuchi ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Dilated Cardiomyopathy ◽  
Oxidative Metabolism ◽  
Remote Areas ◽  
Myocardial Oxidative Metabolism
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