Direct demonstration of preload dependency of myocardial flow reserve in human failing heart by ¹⁵O–H₂O positron emission tomography

Abstract

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 < 0.05). therefore, MFR was significantly reduced in CHF patients than in controls (2.30 ± 1.30 vs. 4.03 ± 0.90, 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 patients.