Direct Demonstration of Preload Dependency of Myocardial Flow Reserve in Human Failing Heart by 15 O–H 2 O Positron Emission Tomography
Kagawa University Second Department of Internal Medicine 1750–1, Miki, kita Kagawa 761–0793 Japan 1750–1, Miki, kita Kagawa 761–0793 Japan International Journal of Angiology
08/2005; 14(3):133-137. DOI: 10.1007/s00547-005-2037-7
Although myocardial flow reserve (MFR) in congestive heart failure (CHF) has been reported to be impaired, the mechanism has
not been fully shown in humans. Therefore, we performed positron emission tomography to measure myocardial blood flow (MBF)
in patients with CHF and compared it with hemodynamic parameters. Sixteen normal coronary patients with CHF and ten normal
controls were enrolled. 15O-labeled water positron emission tomography was performed at rest and during peak hyperemia induced by adenosine triphosphate.
MFR was calculated as the ratio of peak hyperemic to baseline MBF. All CHF patients underwent cardiac catheterization. Baseline
MBF was similar between CHF patients and normal controls (0.73 0.25 vs. 0.80 0.12 mL/min/g, p = NS). Hyperemic MBF was significantly reduced in CHF patients than in controls (1.68 1.09 vs. 3.21 0.69 mL/min/g, p p < 0.05). There was no significant correlation between baseline MBF and either pulmonary capillary wedge pressure or left
ventricular end-diastolic pressure, while both hyperemic MBF and MFR significantly correlated with both pulmonary capillary
wedge pressure (r = −0.67 and r = −0.75, respectively) and left ventricular end-diastolic pressure (r = −0.51 and r = −0.60, respectively). Despite elevated preload, MBF at rest in CHF patients was compensated to the similar level as that
in controls. However, this compensation may exhaust vasodilatory reserve in the failing human heart. Thus, preload at rest
is a determinant of myocardial vasodilator reserve and preload reduction may ameliorate coronary vasodilator response in CHF
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