Late ventricular remodeling in non-reperfused acute myocardial infarction in humans is predicted by angiotensin II type 1 receptor density on blood platelets

Mączewski, Michał; Borys, Marcin; Kacprzak, Paweł; Gdowski, Tomasz; Kowalewski, Marek; Wojciechowski, Dariusz

doi:10.1016/j.ijcard.2007.04.074

« Previous Next »International Journal of Cardiology
Volume 127, Issue 1 , Pages 57-63, 23 June 2008

Late ventricular remodeling in non-reperfused acute myocardial infarction in humans is predicted by angiotensin II type 1 receptor density on blood platelets

Michał Mączewski
- Department of Clinical Physiology, Medical Centre of Postgraduate Education, Warszawa, Poland
- Department of Cardiology, Wolski Hospital, Warszawa, Poland
- Corresponding author. Department of Clinical Physiology, Medical Centre of Postgraduate Education, Marymoncka 99, 01-813 Warszawa, Poland. Tel.: +48 22 5693 841; fax: +48 22 5693 712.
Marcin Borys
- Department of Cardiology, Wolski Hospital, Warszawa, Poland
Paweł Kacprzak
- Department of Cardiology, Wolski Hospital, Warszawa, Poland
Tomasz Gdowski
- Department of Cardiology, Wolski Hospital, Warszawa, Poland
Marek Kowalewski
- Department of Cardiology, Wolski Hospital, Warszawa, Poland
Dariusz Wojciechowski
- Department of Cardiology, Wolski Hospital, Warszawa, Poland

Received 17 July 2006; received in revised form 12 April 2007; accepted 23 April 2007. published online 28 July 2007.

Abstract

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 (AT₁R) density in target tissues. We have recently shown that AT₁R 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 AT₁R density on blood platelets (a presumable marker of cardiovascular AT₁R 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 AT₁R density above median (N=17) as compared to those with AT₁R 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 AT₁R 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-AT₁R groups: over 85% patients received ACE-inhibitor, β-blocker and statin.

Conclusions

High AT₁R density on blood platelets (a presumable marker of cardiovascular AT₁R 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.

Keywords: Remodeling, Myocardial infarction, Angiotensin II, Renin–angiotensin system, Heart failure