Intravenous Quercetin Significantly Reduces Mortality in STEMI: Presented at HF2008
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Intravenous Quercetin Significantly Reduces Mortality in STEMI: Presented at HF2008

By Chris Berrie

MILAN, Italy -- June 15, 2008 -- Intravenous (IV) quercetin reduces infarct size, improves left ventricular function, and significantly lowers cardiac mortality in patients with ST-segment elevation myocardial infarction (STEMI), according to a prospective, randomised study presented here on June 15 at the Heart Failure 2008 Congress.

In patients with acute STEMI, reduced survival has been linked to infarct size and left ventricular enlargement. Therefore, as Alexander Parkhomenko, MD, Institute of Cardiology, National Scientific Centre, Kiev, Ukraine, indicated, demonstrations that this IV, carrier form of the nitric-oxide remodelling, lipoxygenase inhibitor quercetin has anti-ischemic actions and limits left ventricular remodelling provided promise for its addition to standard therapy for these patients.

The main inclusion criteria for this study were patients aged 21 years or older who were admitted to the hospital within 12 hours of onset of STEMI symptoms and who had Killip ranking of class II or III and a left ventricle ejection fraction (LVEF) <=40%. The main exclusion criteria were for standard comorbidities, including decompensated diabetes and severe renal insufficiency (serum creatinine >=265 mcmol/L).

Nearly all 57 patients enrolled were receiving antiplatelet (100%), heparin (99%), and beta-blocker (98%) therapy, with 76% also on acetylcholine esterase inhibitors. Patients were randomised to receive either placebo (n = 32; mean age, 55.5 years; male, 93.7%) or the quercetin IV infusion (n = 25; mean age, 57.3 years; male, 96.0%) over 5 days, with quercetin started at least 30 minutes before reperfusion.

There were no significant differences in baseline clinical characteristics across the treatment groups, including for echocardiography. Patients exhibited similar peak levels of creatine kinase (CK) muscle and brain (MB) and time to peak of CK-MB; the treatment groups were thus similar for baseline infarct size.

Following calculations for mass of myocardial necrosis (dynamics of serum CK-MB), there was a significant 25% reduction seen between control and quercetin-treated patients (60.8 g/eq vs 45.6 g/eq, respectively; P < .01). This was seen as a significant shortening of the CK-MB normalisation times (43.1 vs 30.2 hours; P < .05).

From a median baseline LVEF of 34.5% across all patients, by day 10 the quercetin group saw a significant 21.8% increase in LVEF (P < .01); the increase in the placebo group of 11.3% did not reach significance over this baseline. Similarly, at median follow-up of 6.7 years, the patients in the quercetin group showed a significantly reduced primary endpoint of cardiovascular death at 120 months (P = .04 vs placebo).

As Prof. Parkhomenko summarised, "In these patients with systolic heart failure, we have good data concerning myocardial protection, even while using all of the modern approaches. … Reducing the final infarct size, we see an improvement in function; the injection fraction; and, extremely important, we have a very good long-term survival rate improvement." Furthermore, he added, "This is a safe inhibitor; it is not toxic."

[Study title: Long-Term Prognosis in Patients With Acute ST-Segment Elevation Myocardial Infarction and Acute Heart Failure: Prospective Randomised Study. Poster Session 2. Abstract P264.]

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