Key result
Intravenous adenosine stress revealed no significant correlation between myocardial and peripheral perfusion reserve across different patient populations (r = -0.07, p = 0.47).
Why the study?
Does peripheral perfusion reserve correlate with myocardial perfusion reserve during adenosine stress [13N]ammonia PET in patients with various cardiac conditions?
Cross-Sectional (n=58)
No
Does peripheral perfusion reserve correlate with myocardial perfusion reserve during adenosine stress [13N]ammonia PET in patients with various cardiac conditions?
Effect estimate: r = -0.07
p-value: p=0.47
Peripheral perfusion reserve does not correlate with myocardial perfusion reserve during intravenous adenosine stress, suggesting functional differences in response between the two vascular beds.
Peripheral perfusion reserve should not proxy myocardial perfusion reserve; leaves open bed-specific adenosine responses in larger cohorts.
INTRODUCTION: [13N]ammonia PET allows quantification of myocardial perfusion. The similarity between peripheral flow and myocardial perfusion is unclear. We compared perfusion flow in the myocardium with the upper limb during rest and adenosine stress [13N]ammonia PET to establish whether peripheral perfusion reserve (PPR) correlates with MPR. METHODS: [13N]ammonia myocardial perfusion PET-scans of 58 patients were evaluated (27 men, 31 women, age 64 ± 13 years) and were divided in four subgroups: patients with coronary artery disease (CAD, n = 15), cardiac syndrome X (SX, n = 14), idiopathic dilating cardiomyopathy (DCM, n = 16), and normal controls (NC, n = 13). Peripheral limb perfusion was measured in the muscular tissue of the proximal upper limb and quantified through a 2-tissue-compartment model and the PPR was calculated (stress/rest ratio). MPR was also calculated by a 2-tissue-compartment model. The PPR results were compared with the MPR findings. RESULTS: Mean myocardial perfusion increased significantly in all groups as evidenced by the MPR (CAD 1.99 ± 0.47; SX 1.39 ± 0.31; DCM 1.72 ± 0.69; NC 2.91 ± 0.78). Mean peripheral perfusion also increased but not significantly and accompanied with great variations within and between groups (mean PPR: CAD 1.30 ± 0.79; SX 1.36 ± 0.71; DCM 1.60 ± 1.22; NC 1.27 ± 0.63). The mean difference between PPR and MPR for all subpopulations varied widely. No significant correlations in flow reserve were found between peripheral and myocardial microcirculatory beds in any of the groups (Total group: r = -0.07, SEE = 0.70, CAD: r = 0.14, SEE = 0.48, SX: r = 0.17, SEE = 0.30, DCM: r = -0.11, SEE = 0.71, NC: r = -0.19, SEE = 0.80). CONCLUSION: No correlations between myocardial and peripheral perfusion (reserve) were found in different patient populations in the same PET session. This suggests a functional difference between peripheral and myocardial flow in the response to intravenously administered adenosine stress.
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Scholtens et al. (2011) conducted a cross-sectional in Coronary artery disease, cardiac syndrome X, idiopathic dilating cardiomyopathy (n=58). Intravenous adenosine stress vs. Rest was evaluated on Correlation between myocardial perfusion reserve (MPR) and peripheral perfusion reserve (PPR) (r = -0.07, p=0.47). Intravenous adenosine stress revealed no significant correlation between myocardial and peripheral perfusion reserve across different patient populations (r = -0.07, p = 0.47).
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