Late ventricular remodeling in non-reperfused acute myocardial infarction in humans is predicted by angiotensin II type 1 receptor density on blood platelets.
BACKGROUND
Ventricular remodeling after myocardial infarction (MI) is largely dependent on renin-angiotensin system activity, which is determined by angiotensin II concentration and angiotensin II type 1 receptor (AT(1)R) density in target tissues. We have recently shown that AT(1)R density in the acute phase of MI determines post-MI ventricular remodeling at discharge (8 days). The aim of this study was to test whether this correlation is retained in a longer follow-up (6 months), in the same group of patients.


METHODS
In 48 patients with first acute MI who did not undergo reperfusion therapy, angiotensin AT(1)R density on blood platelets (a presumable marker of cardiovascular AT(1)R density) was assessed 13+/-5 h after the onset of MI, using radioligand binding assay. Echocardiographic indices of left ventricular function and dimensions were used as measures of ventricular remodeling.


RESULTS
6 months after the infarction patients who at baseline had AT(1)R density above median (N=17) as compared to those with AT(1)R density below median (N=20) had higher left ventricular end-systolic volume index (LVESVI, 41.3+/-2.7 vs. 33.2+/-2.3) and lower ejection fraction (LVEF 48.1+/-1.8 vs. 54.7+/-2.0). Moreover LVESVI positively and LVEF negatively correlated with AT(1)R density although the strength of these correlations was weaker than at discharge. Infarct size as reflected by a single troponin T measurement and post-MI therapy did not differ between high- and low-AT(1)R groups: over 85% patients received ACE-inhibitor, beta-blocker and statin.


CONCLUSIONS
High AT(1)R density on blood platelets (a presumable marker of cardiovascular AT(1)R density) drawn in the acute phase of MI predicts poorer left ventricular systolic function in 6-month follow up. This suggests that modern therapy offers suboptimal blockade of renin-angiotensin system activity in the setting of MI.
Maczewski
Michał
M
Department of Clinical Physiology, Medical Centre of Postgraduate Education, Warszawa, Poland; Department of Cardiology, Wolski Hospital, Warszawa, Poland. maczmich@cmkp.edu.pl
Borys
Marcin
M
Kacprzak
Paweł
P
Gdowski
Tomasz
T
Kowalewski
Marek
M
Wojciechowski
Dariusz
D
D000368:Aged; D000704:Analysis of Variance; D001792:Blood Platelets / Q000378:metabolism*; D016009:Chi-Square Distribution; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000503:physiopathology; D011237:Predictive Value of Tests; D044140:Receptor, Angiotensin, Type 1 / Q000097:blood*; D012044:Regression Analysis; D012307:Risk Factors; D020257:Ventricular Remodeling / Q000502:physiology*
D044140:Receptor, Angiotensin, Type 1