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  • Title: Late ventricular remodeling in non-reperfused acute myocardial infarction in humans is predicted by angiotensin II type 1 receptor density on blood platelets.
    Author: Maczewski M, Borys M, Kacprzak P, Gdowski T, Kowalewski M, Wojciechowski D.
    Journal: Int J Cardiol; 2008 Jun 23; 127(1):57-63. PubMed ID: 17651844.
    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 (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.
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