In vitro Vasorelaxant Effect of Artemisia herba alba Asso. in Spontaneously Hypertensive Rats.

BACKGROUND: The present study aims to evaluate the in vitro vasorelaxant effect of Artemisia herba alba (Ah) aqueous extract. METHOD: Aortic rings were isolated from spontaneously hypertensive rats and incubated in aqueous Ah extract at the following doses: 3, 5, 10 and 20 mg/ml. Incubation of aqueous Ah extract for 30 minutes produced a significant shift of the dose response curve to Norepinephrine (NE) (10-8 to 10-5 M) (p<0.001). RESULTS: Endothelium ablation significantly reduced the vasorelaxant effect of aqueous Ah extract (p<0.001). In addition, inhibition of vascular nitric oxide by Nω-Nitro-L-Arginine Methyl (LNAME) produced a significant reduction in the vasorelaxant effect of aqueous Ah extract (p<0.001). CONCLUSION: We conclude that aqueous Ah extract at a dose of 20 mg/ml possess an in vitro vasorelaxant effect which seems to be dependent on the endothelium vasorelaxant factors involving nitric oxide synthesis.

Anti-platelet treatment of middle-sized abdominal aortic aneurysms.

The physiological transport in the aortic wall occurs mainly by centrifugal convection from the lumen to the adventitia through the arterial wall. Enlargement of an abdominal aortic aneurysm (AAA) is usually associated with the development of an intraluminal mural thrombus (ILT). The interface between the luminal side of the thrombus and flowing blood is a site of constant thrombus renewal, which is linked to platelet aggregation-induced fibrin generation and accumulation. In addition, red blood cells are entrapped causing an oxidative response. Through centrifugal convection are factors increasing the inflammatory and degenerative response transported from the ILT to media and adventitia. Two experimental studies on rats with experimental AAA have shown that aneurysmal progression can be impaired by antiplatelet agents. By a systematic literature search, 4 human cohorts were identified analysing the effect of antiplatelet treatment on the progression of AAA. The two largest cohorts couldn´t detect any significant difference. However, the cohorts included very small AAA, in which ILT seldom is present. In the two other trials, only testing AAA sized above 35 and 39 mm, respectively, use of low dose aspirin was associated with significantly lower expansion rates and less need for later surgical repair. Size-based subgroup analyses from relevant existing cohorts ought to be conducted for confirmation. Finally, low dose aspirin is recommend as general cardiovascular secondary prevention, however, large-scaled trials comparing low dose aspirin with more potent antiplatelets would be relevant.

Low-dose aspirin may prevent growth and later surgical repair of medium-sized abdominal aortic aneurysms.

Experimental data suggest that aspirin-induced platelet inhibition may retard growth of abdominal aortic aneurysms. In this article, whether low-dose aspirin use is associated with reduced aneurysm progression and subsequent need for surgery is examined. In this observational cohort study within a screening trial, 148 patients with small aneurysms (maximum diameter 30-48 mm) annually are followed. Patients were referred for surgery when the aneurysmal diameter exceeded 50 mm. Median follow-up time was 6.6 years. Among patients whose abdominal aortic aneurysms were initially 40 to 49 mm in size, the abdominal aortic aneurysm expansion rate for low-dose aspirin users compared with nonusers was 2.92 mm/y versus 5.18 mm/y (difference 2.27 mm/y, 95% CI, 0.42-4.11). No difference in expansion rates and risk ratios for operative repair was found for patients with abdominal aortic aneurysms <40 mm. For medium-sized abdominal aortic aneurysms, low-dose aspirin may prevent abdominal aortic aneurysm growth and need for subsequent repair, but residual confounding cannot be excluded.

Quest for novel cardiovascular biomarkers by proteomic analysis.

Atherosclerosis, and the resulting coronary heart disease and stroke, is the most common cause of death in developed countries. Atherosclerosis is an inflammatory process that results in the development of complex lesions or plaques that protrude into the arterial lumen. Plaque rupture and thrombosis result in the acute clinical complications of myocardial infarction (MI) and stroke. Although certain risk factors (dyslipidemias, diabetes, hypertension) and humoral markers of plaque vulnerability (C-reactive protein, interleukin-6, 10 and 18, CD40L) have been identified, a highly sensitive and specific biomarker or protein profile, which could provide information on the stability/vulnerability of atherosclerotic lesions, remains to be identified. In this review, we report several proteomic approaches which have been applied to circulating or resident cells, atherosclerotic plaques or plasma, in the search for new proteins that could be used as cardiovascular biomarkers. First, an example using a differential proteomic approach (2-DE and MS) comparing the secretome from control mammary arteries and atherosclerotic plaques is displayed. Among the different proteins identified, we showed that low levels of HSP-27 could be a potential marker of atherosclerosis. Second, we have revised several studies performed in cells involved in the pathogenesis of atherosclerosis (foam cells and smooth muscle cells). Another approach consists of performing proteomic analysis on circulating cells or plasma, which will provide a global view of the whole body response to atherosclerotic aggression. Circulating cells can bear information reflecting directly an inflammatory or pro-coagulant state related to the pathology. As an illustration, we report that circulating monocytes and plasma in patients with acute coronary syndromes has disclosed that mature Cathepsin D is increased both in the plasma and monocytes of these patients. Finally, the problems of applying proteomic approach directly to plasma will be discussed. The purpose of this review is to provide the reader with an overview of different proteomic approaches that can be used to identify new biomarkers in vascular diseases.