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Grateful grape seeds

In this study, we choose MMCIMT and plaque score as the ultrasound indices to observe the effect of the intervention of GSPE on atherosclerosis and predict the incidence rate of ischemic vascular events. To determinate the lesion properties and degree, carotid artery ultrasound provide a simple, non-invasive, cost-effective and easily reproducible approach for visualizing and quantifying atherosclerotic lesions. On the same hand, there was evidence which proved that the mean maximum estimate was a more precise estimate of an individual’s atherosclerosis or cardiovascular risk status. [20] , [21] Separate characterization of plaque and IMT is prudent in order to derive better information on vascular risk. [22] In present study, we observed that GSPE could statistically decrease plaque thickness after treatment of six months, and with the long time treatment, the superior efficacy on carotid plaque occurred.

Atherosclerosis is the important pathologic basis of cerebral- and cardio-vascular disease. Atherosclerosis, and it’s devastating complications of cerebral and myocardial infarction and gangrene of the extremities, is the leading cause of death worldwide. [13] It is reported that there are more than 20 million people experience a sudden cardiac event (acute coronary syndromes and/or sudden cardiac death) every year, and a large portion of this population has no prior symptom. [14] Drugs are the foundation of treatment for atherosclerotic diseases, which can prevent the occurrence of restenosis after interventional therapy and the new generation of narrowing in other parts. However, the clinical use of statins is recommended for the patients with abnormal lipid profile. And the reports on the adverse effects of statins, especially liver damage, is becoming more drastic. The urgent demand for prevention and treatment of atherosclerosis remains unresolved, especially in the significant proportion of patients who had serious atherosclerosis and plaque formation with multiple lipid measurement in the normal range.

Values presented as mean ± SD or n (%) unless other indicated. Baseline characteristics were similar and well-balanced between treatment groups. BMI: body mass index; BP: blood pressure; GSPE: grape seed proanthocyanidin extract; HDL-C: high density lipoprotein-cholesterol; LDL-C: low density lipoprotein-cholesterol; MMCIMT: mean maximum carotid intima-media thickness; TC: total cholesterol; TG: triglyceride.

The percentage of vulnerable plaque was similar between groups at baseline ( Table 1 , P = 0.17). Six months after treatment, the total number of plaque decreased by 13 and the number of unstable plaques decreased by 22 in the GSPE group, while the two parameters remained stable in control group. After treatment of 12 months, the change in the GSPE group compared with baseline was statistically different. In the control group, the total number of plaque increased by 21 and the number of unstable plaque increased by 18. After treatment of 24 months, 39 plaques disappeared and unstable plaques reduced by 54 in the GSPE group; and in the control group, the total number of plaque increased by 38 and the number of unstable plaque increased by 33, the difference became significantly greater between groups ( Figure 3 ).

Table 2.

As anticipated, after treatment, GSPE resulted in significant reduction in MMCIMT progression (4.2% decrease after six months, 4.9% decrease after 12 months and 5.8% decrease after 24 months) and plaque score (10.9% decrease after six months, 24.1% decrease after 12 months and 33.1% decrease after 24 months) for the primary outcome, while MMCIMT and plaque score were stable and even increased with the time going on in control group. The number of plaques and unstable plaques also decreased after treatment of GSPE. Furthermore, the carotid plaque can disappear after treatment with GSPE. The incidence rate for transitory ischemic attack (TIA), arterial revascularization procedure, and hospital readmission for unstable angina in GSPE group were statistically significant lower (P = 0.02, 0.08, 0.002, respectively) compared with the control group.

GSPE can inhibit the development of CIMT, regress the carotid plaque and promote the stabilization of carotid plaque, and as the treatment of prolonged, the anti-atherosclerotic effect of GSPE becomes more apparent. Finally, after 24-month treatment, GSPE can reduce the cardiovascular event significantly. In the light of our results, we can speculate that GSPE could be an effective therapeutic candidate for the primary prevention programs for the asymptomatic patient with atherosclerotic lesion. Future in vivo studies are required to investigate the mechanism.

Researchers paid more attention to this issue. Yamakoshi, et al. [8] found that grape seed proanthocyanidin extract (GSPE) can significantly reduce atherosclerotic plaque formation in the wall of the aortic arch and the thoracic aorta using the New Zealand rabbit atherosclerosis model, so, it was reasoned that GSPE may provide a new means in the prevention and treatment of atherosclerosis. A series of studies were conducted using GSPE to demonstrate its cardioprotective ability in animals. [8] – [10] GSPE can protect endothelial function, resist myocardial oxidative stress damage, inhibit low density lipoprotein oxidation and anti-inflammation. Additionally, our previous animal experiment has demonstrated that GSPE can slow down the development of atherosclerotic plaques. However, clinical trials about the effect of GSPE on atherosclerotic plaques have not been reported. In this study, we examined the effect of GSPE on carotid intima-media thickness (CIMT) and carotid plaque in clinical use.

3.4. GSPE decreased ischemic vascular events

This is the first report of the effects of GSPE on carotid plaque and CIMT, and it presents a valuable method to prevent the progression of atherosclerotic plaque and protect the patients without high risks. One important point should also be mentioned, that in our study, vascular events significantly decreased compared with the control group after 24-month treatment with GSPE. Meanwhile, no noteworthy adverse effects were reported.

It is well established that atherosclerosis is a bland proliferative process. [15] Endothelial denuding injury led to platelet aggregation and release of platelet-derived growth factor that would trigger the proliferation of smooth muscle cells in the arterial intima, and form the nidus of the atherosclerotic plaque. Extensive atherosclerosis may be associated with increased blood thrombogenicity, and vulnerable plaques are much more thrombogenic than stable ones. Previous studies have showed that proanthocyanidin inhibited thrombogenesis in vivo and inhibited ADP-induced platelet aggregation and arterial thrombus formation, enhance platelet-derived NO release, modulate the activity of some enzymes systems including cyclooxygenase and lipooxygenase and decrease superoxide production. [16] , [17] In our study, GSPE showed a great effect on plaque stability, the mechanism may involve direct protective effect on platelets and blood vessels.