scholarly journals Imaging of Myocardial Oxidative Metabolism in Heart Failure

Author(s):  
Masanao Naya ◽  
Nagara Tamaki
2014 ◽  
Vol 16 (5) ◽  
pp. 500-506 ◽  
Author(s):  
S. V. Nesterov ◽  
O. Turta ◽  
C. Han ◽  
M. Maki ◽  
I. Lisinen ◽  
...  

2008 ◽  
Vol 10 (11) ◽  
pp. 1117-1122 ◽  
Author(s):  
Heikki Ukkonen ◽  
Ian G. Burwash ◽  
William Dafoe ◽  
Robert A. de Kemp ◽  
Haissam Haddad ◽  
...  

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Daniel Clark ◽  
Giovanni E Davogustto ◽  
Susan P Bell ◽  
RAVINDER MALLUGARI ◽  
William S Bradham ◽  
...  

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.


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 ◽  
...  

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.


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

Sign in / Sign up

Export Citation Format

Share Document