Cardiac expression of placental growth factor predicts the improvement of chronic phase left ventricular function in patients with acute myocardial infarction.
OBJECTIVE
Our aim was to investigate cardiac expression of placental growth factor (PlGF) and its clinical significance in patients with acute myocardial infarction (AMI).


BACKGROUND
Placental growth factor is known to stimulate wound healing by activating mononuclear cells and inducing angiogenesis. The clinical significance of PlGF in AMI is not yet known.


METHODS
Fifty-five AMI patients and 43 control subjects participated in the study. Peripheral blood sampling was performed on days 1, 3, and 7 after AMI. Blood was also sampled from the coronary artery (CAos) and the coronary sinus (CS), before and after acute coronary recanalization. Cardiac expression of PlGF was analyzed in a mouse AMI model.


RESULTS
In AMI patients, peripheral plasma PlGF levels on day 3 were significantly higher than in control subjects. Plasma PlGF levels just after recanalization were significantly higher in the CS than the CAos, which indicates cardiac production and release of PlGF. Peripheral plasma levels of PlGF on day 3 were negatively correlated with the acute phase left ventricular ejection fraction (LVEF), positively correlated with both acute phase peak peripheral monocyte counts and chronic phase changes in LVEF. Placental growth factor messenger ribonucleic acid expression was 26.6-fold greater in a mouse AMI model than in sham-operated mice, and PlGF was expressed mainly in endothelial cells within the infarct region.


CONCLUSIONS
Placental growth factor is rapidly produced in infarct myocardium, especially by endothelial cells during the acute phase of myocardial infarction. Placental growth factor might be over-expressed to compensate the acute ischemic damage, and appears to then act to improve LVEF during the chronic phase.
Iwama
Hajime
H
First Department of Medicine, Nara Medical University, Kashihara, Nara, Japan.
Uemura
Shiro
S
Naya
Noriyuki
N
Imagawa
Kei-ichi
K
Takemoto
Yasuhiro
Y
Asai
Osamu
O
Onoue
Kenji
K
Okayama
Satoshi
S
Somekawa
Satoshi
S
Kida
Yoshitomi
Y
Takeda
Yukiji
Y
Nakatani
Kimihiko
K
Takaoka
Minoru
M
Kawata
Hiroyuki
H
Horii
Manabu
M
Nakajima
Tamio
T
Doi
Naofumi
N
Saito
Yoshihiko
Y
D000818:Animals; D001772:Blood Cell Count; D016022:Case-Control Studies; D003331:Coronary Vessels; D042783:Endothelial Cells / Q000378:metabolism; D005260:Female; D006801:Humans; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008875:Middle Aged; D009000:Monocytes / Q000473:pathology; D009203:Myocardial Infarction / Q000378:metabolism / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism*; D000072483:Placenta Growth Factor; D011237:Predictive Value of Tests; D011257:Pregnancy Proteins / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D020127:Recovery of Function; D013318:Stroke Volume; D016277:Ventricular Function, Left
C000608036:PGF protein, human; C000608037:Pgf protein, mouse; D011257:Pregnancy Proteins; D012333:RNA, Messenger; D000072483:Placenta Growth Factor