Dipyridamole-induced abnormal Tl-201 lung uptake in patients with normal myocardial perfusion: a marker of increased left ventricular filling pressures.
BACKGROUND
The mechanism of dipyridamole-induced abnormal increased T1-201 lung uptake in patients without coronary artery disease is poorly understood. The purpose of this study was to evaluate the relation between dipyridamole-induced abnormal T1-201 lung uptake and left ventricular (LV) diastolic indexes using Doppler, color M-mode and Tissue Doppler modalities at rest, and at dipyridamole stress echocardiograpy (DSE) in patients with normal myocardial perfusion and LV function.


RESULTS
18 consecutive patients (mean age 64 +/- 7 years) with normal myocardial perfusion and increased lung T1-201 uptake on dipyridamole stress-redistribution single photon emission computed tomography (SPECT) were included in our study. These patients were compared with 18 age-matched control patients with normal perfusion and normal T1-201 lung uptake. All patients underwent DSE. A good correlation was found between the T-201 lung uptake, the peak early velocity of mitral inflow (E, r = 0.57) and estimated pulmonary capillary wedge pressure (PCWP = 1.24[E/Ea] + 1.9, r = 0.68). In patients with increased L/H ratio compared to control group, the E and the PCWP were significantly higher at baseline 81 +/- 18 vs 68 +/- 11 (cm/s) and 13 +/- 3 vs 10.2 +/- 2 (mmHg). An additional significant increase of E to 91 +/- 23 (cm/s (P = 0.001)) and PCWP to 14.8 +/- 3 (P = 0.005) after dipyridamole administration was seen; in contrast to a nonsignificant change observed in control group. For the detection of a dipyridamole induced PCWP >12 mmHg, a L/H ratio of >/=50% had a sensitivity of 72% and a specificity of 83%, resulting in a positive and a negative predictive value of 81% and 75%, respectively.


CONCLUSIONS
A dipyridamole-induced abnormal T1-201 lung uptake in patients with normal myocardial perfusion and systolic function is predictive of elevated filling pressures at rest and in response to dipyridamole administration, probably reflecting an intrinsic resting diastolic dysfunction and a further abnormal response to vasodilatation.
Goland
Sorel
S
Institute of Cardiology, Kaplan Hospital, Rehovot, Israel. sorel_g@clalit.org.il
Shimoni
Sarah
S
Livschitz
Shay
S
Loutaty
Gaby
G
Azulay
Orli
O
Levy
Rosa
R
Caspi
Avraham
A
Arditi
Alex
A
D000368:Aged; D004176:Dipyridamole / Q000008:administration & dosage*; D004452:Echocardiography / Q000379:methods; D005080:Exercise Test / Q000379:methods*; D005260:Female; D006352:Heart Ventricles / Q000000981:diagnostic imaging* / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011877:Radionuclide Imaging; D019275:Radiopharmaceuticals / Q000493:pharmacokinetics; D012016:Reference Values; D013793:Thallium / Q000493:pharmacokinetics*; D016277:Ventricular Function, Left / Q000187:drug effects / Q000502:physiology
D019275:Radiopharmaceuticals; C027549:thallium chloride; D004176:Dipyridamole; D013793:Thallium