In patients with coronary artery disease (CAD), coronary blood flow is usually impaired due to imbalanced vasoactive substances such as nitric oxide (NO) and endothelin-1 (ET-1). The study was designed to test the effects of Ginkgo biloba extract (GBE) on the distal left anterior descending coronary artery (LAD) blood flow and plasma NO and ET-1 levels. Eighty CAD patients were randomly assigned to GBE (n = 42) and control (n = 38) groups. The LAD blood flow was assessed non-invasively using Doppler echocardiography at baseline and after 2 weeks. GBE treatment demonstrated a significant improvement in maximal diastolic peak velocity (MDPV), maximal systolic peak velocity (MSPV) and diastolic time velocity integral (DTVI) compared with controls (14.61 +/- 4.51% vs 0.67 +/- 2.66%, 9.03 +/- 4.81% vs 0.34 +/- 2.67% and 14.69 +/- 5.08% vs 0.68 +/- 3.00%, respectively, p < 0.01). NO was increased by 12.42% (p < 0.01), whereas ET-1 was decreased by 5.82% (p < 0.01). The NO/ET-1 ratio was increased by 19.47% (p < 0.01). A linear correlation was confirmed between the percentage change in LAD blood flow and in NO, ET-1 or NO/ET-1 ratio following GBE treatment. The results suggest that GBE treatment in CAD patients led to an increase of LAD blood flow, which might at least be related partly to the restoration of the delicate equilibrium between NO and ET-1.
Ginkgo biloba extract (GBE) has well-documented cardioprotective effects on coronary flow and positive effects on vasodilation through endothelium-derived nitric oxide in experimental animals, but these impacts in patients with coronary artery disease (CAD) have not yet been investigated. We designed this study to test the effects of GBE on distal left anterior descending coronary artery (LAD) blood flow and endothelium-dependent brachial artery flow-mediated dilation (FMD) in patients with CAD. Eighty CAD patients were randomly assigned to either GBE or saline (control) groups. LAD blood flow and brachial artery FMD were measured non-invasively using high-resolution ultrasound before and after intravenous administration of GBE or saline. GBE significantly increased LAD blood flow in maximal diastolic peak velocity (MDPV), maximal systolic peak velocity (MSPV) and diastolic time velocity integral (DTVI) compared with the control group (16.14 +/- 10.93 % vs. 0.28 +/- 2.14 %, 9.14 +/- 8.23 % vs. 0.79 +/- 2.56 %, and 15.23 +/- 7.28 % vs. 0.42 +/- 2.43 %, respectively, p < 0.01). Brachial artery FMD was also increased by 69.75 % (from 3.95 +/- 1.49 % to 6.55 +/- 2.51 %, p < 0.01). A linear correlation was found between the percentage changes in MDPV, MSPV, or DTVI of LAD blood flow and the percentage change in brachial artery FMD following treatment with GBE (r = 0.612, 0.486, or 0.521, respectively, p < 0.01). In summary, our data demonstrate that GBE treatment in CAD patients leads to an increase of LAD blood flow in MDPV, MSPV and DTVI, and the increase response might relate to the improved endothelium-dependent vasodilatory capacity. CAD: coronary artery disease DTVI: diastolic time velocity integral FMD: flow-mediated dilation GBE: GINKGO BILOBA extract LAD: distal left anterior descending coronary artery MDPV: maximal diastolic peak velocity MSPV: maximal systolic peak velocity NO: nitric oxide TTDE: transthoracic Doppler echocardiography.
This study indicates that CRA blood flow is impaired in patients with CAD, and this may partly relate to endothelial dysfunction. Thus, endothelial function is likely to play an important role in the CRA microcirculation.
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