PubMed Health⌕ Search

Biomedical subjects

Audrius Simaitis

Publications and source records attributed to Audrius Simaitis.

3 recordsLinked to original sources

[Relationship of paradoxical vasoconstriction induced by acetylcholine to risk factors for ischemic heart disease].

Acetylcholine test is widely used for the investigation of endothelium function. Acetylcholine induces paradoxical vasoconstriction, if endothelium of coronary artery is damaged. The aim of this study was to investigate the endothelium dysfunction among the patients who have complaints of the chest pain and at the same time no significant changes are found in their coronary arteries by angiography. The impact of the risk factors (smoking, hypertension, positive family history, and hypercholesterolemia) to the lack of endothelium function was studied as well. Intracoronary acetylcholine test was performed for 100 patients (52 males and 48 females). Acetylcholine was given in two steps (10(-6) mol/l and 3.3x10(-6) mol/l) followed by the 300 microg of nitroglycerin. The change of the diameter in comparison with baseline was assessed in left anterior descending and left circumflex arteries. Vasoconstriction of more than 5% from baseline was interpreted as endothelium dysfunction. Coronary vessels from 8 patients reacted to the acetylcholine infusion by vasodilatation and in 92 patients paradoxical vasoconstriction of more than 5% was induced. However, such risk factors as smoking, hypertension, positive family history, and acute coronary syndrome in the past had negative impact to the endothelium dysfunction (p<0.05). The more risk factors patient had, the more expressed his reaction to acetylcholine was (p<0.05). The smaller diameter of segment was, the more expressed contraction to acetylcholine it exhibited (p<0.05). Left coronary artery mainly was unresponsive to the acetylcholine.

Acetylcholine↗

[Effect of high doses of atorvastatin on the endothelial function of the coronary arteries].

OBJECTIVE: The aim of this study is to investigate the role of high doses of atorvastatin (80 mg per day) in the treatment of endothelium dysfunction of the coronary arteries. MATERIAL AND METHODS: Intracoronary acethylcholine test was performed for 28 (16 in treatment group and 12 in control group) patients who had normal coronary angiogram or minimal lesions (stenosis <50%) and symptomatic coronary heart disease. Acetylcholine was given into left coronary artery in three stages (2 min each) at estimated intracoronary concentrations 10(-6) mol/l, 3.3x10(-6) mol/l,and 10(-5) mol/l. Treatment group patients were given atorvastatin 80 mg per day. Intracoronary acetylcholine test was repeated after six months. The target segment was the segment that exhibited the maximal constrictive response at baseline in a given patient. RESULTS: Total cholesterol was reduced by 40.6+/-11.2% (p<0.001), low density lipoproteins cholesterol by 55.4+/-14% (p<0.001), triglycerides by 29.6% (p<0.05) and high density lipoproteins cholesterol was increased by 24.7% (p<0.05) in atorvastatin group after 6 months of therapy. No significant lipid changes were observed in the control group. Sixteen target segments in the treatment group and 12 segments in the control group were selected for primary efficacy parameter. The vasoconstrictor reaction to acetylcholine was similar at baseline in both groups: -16.8%+/-11.6% of diameter in atorvastatin group and -14.2%+/-13.7% in control group (p=0.58) at dose 10(-6) mol/l, -43.5%+/-21.2% in atorvastatin group and -41.2%+/-22.4% in control group (p=0.79) at dose 3.3x10(-6) mol/l, -64.5%+/-12.4% in atorvastatin group and -57.4%+/-15.6% in control group (p=0.35) at dose 10(-5) mol/l. Treatment with high doses of atorvastatin markedly decreased acetylcholine - induced vasoconstriction: -6.5%+/-14.5% of diameter in atorvastatin group versus -18.3%+/-14.0% in control group (p=0.04) at dose 10(-6) mol/l, -19.7%+/-22.8% in atorvastatin group versus -40.0%+/-25.0% in control group (p=0.034) at dose 3.3x10(-6) mol/l, -29.9%+/-21.3% in atorvastatin group (6 segments) versus -48.7%+/-19.0% in control group (3 segments, p=0.24) at dose 10(-5) mol/l. CONCLUSION: Treatment with high doses of atorvastatin significantly improves endothelium-mediated response to acetylcholine in the coronary arteries of the patients with minimal lesions.

Acetylcholine↗

[Oxidative stress and endothelial dysfunction].

Growing numbers of morbidity and mortality due to the Coronary Heart Disease (CHD) is recognized as the more increasing challenge in the world. The initial stage of atherosclerosis, early diagnosis and treatment of CHD are the main objectives of current research. Endothelium dysfunction, the earliest expression of the atherosclerotic process is associated with subtle biochemical changes that gradually are transformed into the structural changes of the arterial wall. The theory of free radicals is the most common among the atherosclerosis explanations. Overproduction or impaired neutralization of the free radicals accounts for oxidative stress that is causing substantial damage to the low density lipoproteins, nitric oxyde (NO), endothelium cells, tissue cells and finally leads to the endothelium dysfuction. Pathophysiology of oxidative stress and its role in the endothelium dysfunction are discussed in this paper. Positive role of various medications (statins, angiotensin converting enzym inhibitors, aldosteron antagonists, estrogens, antioxidants, b-blockers with vasodilatative properties) to the oxidative stress and consequently to the endothelium dysfuction are discussed as well.

Age Factors↗