Non-invasive assessment of coronary flow reserve in idiopathic dilated cardiomyopathy: hemodynamic correlations.
BACKGROUND
Impaired vasodilator myocardial blood flow response has been observed in dilated cardiomyopathy (DCMP). However, the mechanisms responsible for this blunted response are not clear. In the present study, we investigated whether the blunted vasodilator flow response is related to indices of left ventricular performance in patients with idiopathic dilated cardiomyopathy.


RESULTS
Eighteen DCMP patients and 12 healthy subjects (C) underwent transoesophageal echocardiography within 48 h from cardiac catheterization. Coronary flow velocity reserve (CFR) was measured in the proximal LAD as the ratio of the peak diastolic coronary flow velocity (Vd-M) after intravenous administration of adenosine to peak baseline diastolic flow velocity (Vd-R). Left ventricular (LV) mass index was positively correlated with baseline coronary diastolic velocity (r=0.415; p=0.043) and inversely correlated with coronary flow reserve (r=-0.570; p=0.003). The baseline coronary diastolic velocity was higher in DCMP vs C (56+/-13 cm/s vs 35+/-12 cm/s; p=0.04). In DCMP pts Vd-R positively correlated with end-diastolic wall stress (r=0.654; p=0.01). Vd increased in both C (96+/-32 cm/s; p<0.05 vs baseline) and DCMP patients (108+/-20 cm/s; p<0.01 vs baseline). The CFR was lower in DCMP patients vs C (1.93+/-0.78 vs 2.99+/-1.01; p=0.009). In DCMP pts CFR was negatively correlated with right atrial pressure (r=-0.595; p=0.015), LVEDP (r=-0.576; p=0.015), pulmonary capillary wedge pressure (PCWP: r=-0.772; p<0.001) and positively with ejection fraction (EF: r=0.683; p=0.003).


CONCLUSIONS
Pts with DCMP have lower CFR compared to controls. This blunted CFR is due to higher baseline coronary flow and reflects higher wall stress. The close relation between CFR and EF, PCWP and LVEDP suggests that not only a higher baseline Vd but also compressive forces due to left ventricular dysfunction might be responsible for the observed blunted adenosine-mediated coronary vasodilation.
Vanderheyden
Marc
M
Cardiovascular Center, Onze Lieve Vrouw Ziekenhuis, Moorselbaan 164, 9300 Aalst, Belgium. marc.vanderheyden@skynet.be
Bartunek
Jozef
J
Verstreken
Sofie
S
Mortier
Linda
L
Goethals
Marc
M
de Bruyne
Bernard
B
D000241:Adenosine / Q000494:pharmacology; D001783:Blood Flow Velocity / Q000187:drug effects / Q000502:physiology; D006328:Cardiac Catheterization; D002311:Cardiomyopathy, Dilated / Q000000981:diagnostic imaging / Q000503:physiopathology*; D016022:Case-Control Studies; D003326:Coronary Circulation / Q000187:drug effects / Q000502:physiology; D017548:Echocardiography, Transesophageal / Q000379:methods; D005260:Female; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D006801:Humans; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D011184:Postoperative Period; D018487:Ventricular Dysfunction, Left
D000241:Adenosine