M. Bottcher et al., Endothelium-dependent and -independent perfusion reserve and the effect ofL-arginine on myocardial perfusion in patients with syndrome X, CIRCULATION, 99(14), 1999, pp. 1795-1801
Citations number
42
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Background-Impaired vasodilatation capacity in patients with angina pectori
s and a normal coronary arteriogram (syndrome X [SX]) has been reported. Mo
st studies report on the response in epicardial vessels. This does not nece
ssarily reflect compromised myocardial microcirculation. Lack of the NO pre
cursor L-arginine has been suggested as a possible cause.
Methods and Results-Myocardial blood flow (MBF) was measured, using PET, at
rest (MBF-rest) and during intravenous dipyridamole (MBF-DIP) in 25 women
(mean age 53+/-7 years) with SX. Thirty healthy volunteers served as contro
ls. One group (A) consisted of 15 age-matched female volunteers (54+/-10 ye
ars). The other control group consisted of 15 young healthy women (B; 24+/-
5 years). In 12 SX patients, MBF-rest and MBF during cold presser testing w
ere also measured after infusion of L-arginine (6.7 g/min for 45 minutes).
The increase in MBF after cold presser testing was similar in the SX group
compared with controls. L-arginine did not affect MBF-rest (0.83+/-0.14 ver
sus 0.89+/-0.13 mL . g(-1) . min(-1)) or MBF after cold presser test (0.95/-0.10 versus 1.03+/-0.17 mL . g(-1) . min(-1)), In contrast, the hyperemic
response to DIP was blunted compared with the group A controls (1.68+/-0.4
9 versus 2.34+/-0.45 mt . g(-1) . min(-1), P<0.05); this resulted in a sign
ificant reduction of the coronary flow reserve in SX patients relative to c
ontrols (2.03+/-0.53 versus 2.96+/-0.63 mt . g(-1) . min(-1), P<0.01).
Conclusions-In patients with SX, the microcirculatory response to cold, ref
lecting the endothelium function, is normal and unaltered by intravenous L-
arginine. This suggests preserved microcirculatory endothelial function. Ho
wever, a markedly attenuated hyperemic flow and flow reserve after DIP sugg
est a dysfunction of the adenosine-mediated endothelium-independent vasodil
atation at the microcirculatory level in these patients.