Adiponectin mediates he effects of cardiometabolic risk profile on the coronary microcirculation in patients with idiopathic LV systolic dysfunction.
Abstract
Data di Pubblicazione:
2008
Abstract:
Purpose. Adiponectin (ADN), a biologically active protein produced
by the adipose
tissue, has protective vascular effects. Accordingly,
ADN plasma levels are reduced in
patients with coronary artery
disease (CAD) while in heart failure ADN tends to
increase.
We hypothesized that ADN plasma levels could mediate the effects
of
atherogenic risk profile on the coronary microcirculation
of patients with early LV
systolic dysfunction (ILVDys) not
secondary to established CAD.
Methods. Plasma ADN was measured in 55 patients (age 59±1
yrs, 36 males, BMI
26.9±0.49 Kg/m
2
, mean±sem)
with angiographically normal coronary arteries, LV
systolic
dysfunction (LVEF 39.8±1.3 % range 22-54 %) but
without overt heart failure
(NYHA class I-II) and in 40
age- and BMI-matched healthy controls by using a
specific Elisa
(Linco Res). BMI, cholesterol and glucose profiles were assessed
in all.
In a subset of 25 patients coronary microvascular function
was studied by PET and
13
N-Ammonia as a flow tracer. Myocardial
blood flow (MBF) was measured at rest
and during i.v. dipyridamole
(Dip) (0.56 mg/Kg in 4 min).
Results. ADN was 6.6±0.34 µg/ml in controls and
10.9±0.85 in ILVDys patients
(p<0.001). In patients
ADN levels were inversely related with BMI (p=0.009) and
directly
related with age (p=0.007), HDL Cholesterol (p=0.003) and MBF
Dip (0.020).
Patients showing more severe coronary microvascular
dysfunction (MBF Dip<1.42
ml/min/g, median value in patients)
had significantly depressed ADN (9.7±2.3 vs
13.7±1.6,
p=0.021) as compared with the remaining patients.
Conclusions. This is the first study which associates adiponectin
plasma levels with
atherogenic risk profile and coronary microvascular
function in patients with idiopathic
LV dysfunction. These results
suggest that adiponectin signal is strongly involved in
mediating
coronary vascular function independently of the presence of
overt CAD or
heart failure.
Tipologia CRIS:
01.05 Abstract in rivista
Elenco autori:
Neglia, Danilo; Cabiati, Manuela; Giannessi, Daniela; DEL RY, Silvia; Maltinti, Maristella; L'Abbate, Antonio; Caselli, Chiara
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