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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ABSTRACT: The purposes of this study were to examine the effects of angiotensin-converting enzyme inhibitors (ACEI) or angiotensin receptor blockers (ARB) on myocardial flow reserve in patients with acute myocardial infarction (AMI) in the subacute phase using oxygen-15 positron emission tomography (PET) and to elucidate the relationship between the myocardial flow reserve and remodeling in the chronic phase. Sixty patients who had been treated with coronary angioplasty within 12 h after the onset of AMI were enrolled. Patients were divided into an enalapril (ACEI) group and a candesartan (ARB) group. The myocardial flow reserve was measured by oxygen-15 water PET in the subacute phase from the 20th to the 30th day after the onset of AMI. Left ventriculography was performed to measure the left ventricular ejection fraction in the chronic phase about 6 months after the onset. Ten patients (33%) in the enalapril group and 4 patients (13%) in the candesartan group stopped taking their respective medications within a few days of starting, because of side effects such as cough or hypotension. Thus, the prevalence of medication intolerance was higher in the enalapril group. The myocardial flow reserve in the subacute phase and the left ventricular ejection fraction in the chronic phase were lower in the enalapril group (2.08 +/- 0.30 and 42 +/- 6%) than in the candesartan group (2.25 +/- 0.20 and 49 +/- 5%) (p < 0.05). The myocardial flow reserve significantly correlated with the left ventricular ejection fraction in all patients (r = 0.45, p < 0.01). The myocardial flow reserve assessed by PET in the subacute phase after AMI was found to be related to left ventricular remodeling in the chronic phase.
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