Key result
Pravastatin 10 mg decreased the coronary sinus-arterial concentration gradients of MMP-2 (69 vs 213 ng/ml) and MMP-9 (14 vs 119 ng/ml) in patients with acute myocardial infarction (P<0.05).
Why the study?
Does pravastatin 10 mg reduce cardiac production of MMP-2 and MMP-9 in patients with acute myocardial infarction?
Observational (n=30)
Does pravastatin 10 mg reduce cardiac production of MMP-2 and MMP-9 in patients with acute myocardial infarction?
Absolute Event Rate: 69% vs 213%
p-value: p=<0.05
Pravastatin attenuates the enhanced cardiac production of MMP-2 and MMP-9 in patients with acute myocardial infarction, suggesting a potential mechanism for preventing post-infarction left ventricular remodeling.
Suggests pravastatin may limit MMP-driven remodeling after AMI; hypothesis-generating and requires randomized confirmation before practice change.
Previous experimental studies have demonstrated that MMPs (matrix metalloproteinases) contribute to LV (left ventricular) remodelling. We hypothesized that cardiac MMPs are activated in patients with AMI (acute myocardial infarction) and, if so, MMP production may be attenuated by statins (3-hydroxy-3-methylglutaryl-CoA reductase inhibitors) through their cardiovascular protective actions. We studied 30 patients, ten control patients with stable angina pectoris and 20 patients with AMI, in whom LV catheterization at the chronic stage was performed 22+/-12 days (value is mean+/-S.D.) after the onset of AMI. Blood samples were collected from the CS (coronary sinus) and a peripheral artery. In patients with AMI, the levels of MMP-2 and MMP-9 were significantly (P<0.05) higher in the CS than the peripheral artery (MMP-2, 853+/-199 compared with 716+/-127 ng/ml; MMP-9, 165+/-129 compared with 98+/-82 ng/ml), whereas no significant differences were observed in the patients with angina pectoris. The CS-arterial concentration gradients of MMP-2 and MMP-9 correlated positively with BNP (brain natriuretic peptide) levels (MMP-2, R=0.68, P<0.01; MMP-9, R=0.59, P<0.05) and LV end-diastolic volume index (MMP-2, R=0.70, P<0.01; MMP-9, R=0.70, P<0.01). When patients with AMI treated with 10 mg of pravastatin or without (n=10 in each group) were compared, this statin therapy significantly (P<0.05) decreased the CS-arterial concentration gradients of MMP-2 (69+/-43 compared with 213+/-185 ng/ml) and MMP-9 (14+/-27 compared with 119+/-84 ng/ml). In conclusion, the enhanced production of cardiac MMP-2 and MMP-9 is associated with LV enlargement and elevated BNP levels in patients with AMI. A pleiotropic effect of statins appears to be associated with the modulation of cardiac MMP activation, which may be potentially beneficial in the attenuation of post-infarction LV remodelling.
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Yasuda et al. (2006) conducted an observational in Acute myocardial infarction and stable angina pectoris (n=30). Pravastatin vs. Without pravastatin was evaluated on Coronary sinus-arterial concentration gradient of MMP-2 (p=<0.05). Pravastatin 10 mg decreased the coronary sinus-arterial concentration gradients of MMP-2 (69 vs 213 ng/ml) and MMP-9 (14 vs 119 ng/ml) in patients with acute myocardial infarction (P<0.05).
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