Coronary microvascular dysfunction after myocardial infarction: increased coronary zero flow pressure both in the infarcted and in the remote myocardium is mainly related to left ventricular filling pressure.
OBJECTIVE
To investigate the underlying mechanisms of a decreased coronary flow reserve after myocardial infarction (MI) by analysing the characteristics of the diastolic hyperaemic coronary pressure-flow relationship.


METHODS
Prospective study.


METHODS
Tertiary care hospital.


METHODS
68 patients with a recent MI and 27 patients with stable angina pectoris (AP; control group).


METHODS
The intercept with the pressure axis (the zero flow pressure or Pzf) and slope index of the pressure-flow relationship (SIPF) were calculated from the simultaneously recorded hyperaemic intracoronary blood flow velocity and aortic pressure after successful coronary stenting.


RESULTS
A stepwise increase in Pzf from AP (14.6 (8.0) mm Hg), over non-Q-wave MI (22.5 (9.1) mm Hg), to Q-wave MI (37.1 (12.9) mm Hg; p<0.001) was observed. Similar changes in Pzf were found in a reference artery perfusing the non-infarcted myocardium. Multivariate analysis showed that in both regions the left ventricular end-diastolic pressure (LVEDP) was the most important determinant of the Pzf. The SIPF was not statistically different in the treated vessel between patients with MI and AP, but was increased in MI patients with a markedly increased LVEDP.


CONCLUSIONS
After an MI, the coronary pressure-flow relationship is shifted to the right both in the infarcted and in the non-infarcted remote myocardium, as shown by the increased Pzf. The correlation with Pzf suggests that elevated left ventricular filling pressures contribute to the impediment of myocardial perfusion in patients with infarction.
Van Herck
P L
PL
Department of Cardiology, Antwerp University Hospital, Edegem, Belgium. paul.van.herck@uza.be
Carlier
S G
SG
Claeys
M J
MJ
Haine
S E
SE
Gorissen
P
P
Miljoen
H
H
Bosmans
J M
JM
Vrints
C J
CJ
D001783:Blood Flow Velocity / Q000502:physiology; D001794:Blood Pressure; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000503:physiopathology; D003326:Coronary Circulation / Q000502:physiology*; D023921:Coronary Stenosis / Q000209:etiology / Q000503:physiopathology; D003331:Coronary Vessels / Q000502:physiology; D003971:Diastole; D005260:Female; D006801:Humans; D008297:Male; D008833:Microcirculation; D008875:Middle Aged; D009203:Myocardial Infarction / Q000503:physiopathology* / Q000628:therapy; D011446:Prospective Studies; D015607:Stents; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology*