Aim:To investigate the effect of smoking and smoking cessation on cardio-ankle vascular index (CAVI). Methods: The subjects were 82 smokers (77 men, 64 10 years) and 20 non-smokers (18 men, 61 7 years). CAVI was measured every 3 months and CAVI severity was classified into 3 levels. Decreased, unchanged, and increased CAVI severity levels were coded as "improvement," "no change," and "exacerbation," respectively. Smoking status was coded as "success" for complete abstinence, "partial success" for a reduced number of cigarettes, and "failure" for an unchanging number of cigarettes. Results: Compared with non-smokers, smokers showed a higher CAVI (p 0.05) prior to smoking cessation. Post-cessation, CAVI improved from 9.4 to 8.6 (p 0.01) in "success" cases (n 22), and the significant pre-cessation difference from non-smokers (n 20, CAVI 8.8) disappeared. With regard to the change in CAVI severity of each smoking status, "improvement" occurred in 17%, 24%, and 68% of "failure" (n 35), "partial success" (n 25), and "success" (n 22) groups, respectively, and the "success" group was significantly higher than the other two groups. Conclusion: The study showed that CAVI was increased by smoking, and complete smoking cessation improved CAVI. J Atheroscler Thromb, 2010; 17:517-525.
Aim:The aim of this study was to clarify the relationship between CAVI and serum cystatin C levels to understand the role of arterial stiffness in the presence of renal insufficiency.
SummaryThe cardio-ankle vascular index (CAVI) has been proposed as a new noninvasive marker of arterial stiffness independent of blood pressure. Arterial stiffness is closely related to afterload, and elevated afterload aggravates heart failure. We hypothesized that CAVI is a potential marker of afterload in patients with heart failure. Thirty patients who were admitted because of acute heart failure were identified retrospectively from a review of clinical records. Plasma brain natriuretic peptide (BNP) levels, CAVI, cardiothoracic ratio (CTR), and echocardiographic parameters obtained during acute and chronic phases of heart failure were analyzed. Left ventricular ejection fraction (LVEF) increased significantly and CTR, BNP and CAVI decreased significantly after treatment of heart failure. A significant negative correlation was observed between the change in CAVI and change in LVEF in all subjects (r = -0.3272, P < 0.05). To examine the relationship between CAVI and LVEF, we divided the patients into two subgroups (∆CAVI < -0.5; CAVI decrease group, ∆CAVI ≥ -0.5; CAVI non-decrease group). CAVI was significantly improved after heart failure treatment only in the CAVI decrease group. LVEF decreased significantly in both groups, but the P value was smaller in the CAVI decrease group than in the CAVI non-decrease group. The change in LVEF correlated significantly with the change in CAVI in the CAVI decrease group (r = -0.4201, P < 0.05), whereas no significant correlation was found in the CAVI non-decrease group. CAVI correlates inversely with LVEF after heart failure treatment. Our results suggest that CAVI might partially reflect the afterload in patients with heart failure. (Int Heart J 2013; 54: 216-221) Key words: Left ventricle ejection fraction, Afterload H eart failure is the inability of the heart to supply adequate blood flow and therefore oxygen to peripheral tissues and organs. It is estimated that there are more than 15 million new cases of heart failure each year worldwide. The overall prevalence of heart failure is increasing because of aging of the population. 1) Heart failure is the leading cause of hospitalization of patients over 65 years of age. Despite many new advances in drug therapy and cardiac assist devices, the prognosis for chronic heart failure remains very poor.Cardiac dysfunction induces changes in vascular function, cardiac output, and neurohumoral status. These changes serve as compensatory mechanisms to help maintain cardiac output (primarily by the Frank-Starling mechanism) and arterial blood pressure (by systemic vasoconstriction). However, these compensatory changes over months and years can worsen cardiac function. This compensation is at the expense of an increase in systemic vascular resistance that increases the afterload on the left ventricle, which can further depress its output. An increase in afterload shifts the Frank-Starling curve downward and to the right. The increased afterload reduces the velocity of fiber shortening. Because the period of time available for ...
Aim: Recent clinical studies using intra-vascular ultrasound have clarified that coronary artery plaque already exists in subjects with normal coronary artery which is diagnosed by coronary angiography; furthermore, culprit lesion on acute coronary syndrome often occurs in mild to moderate angiographical stenotic lesion. The aim of this study is to clarify relationship between metabolic syndrome and early stage coronary atherosclerosis using a 3-dimensional intra-vascular ultrasound. Methods: 70 subjects with normal coronary artery diagnosed by coronary angiography were enrolled. Proxymal range of left anterior descending coronary artery was observed by intra-vascular ultrasound using autopullback methods. Results: Subjects with metabolic syndrome had significantly high percent plaque volume (31 8% vs 21 8%, p 0.0001) and frequently detected abnormal plaque quality such as eccentricity, calcification and lipid pool into plaque than those without metabolic syndrome. Multivariate analysis showed that serum adiponectin concentration was the most strongest variable for percent plaque volume (t value 3.0, p 0.01). On the other hand, subjects with hypoadiponectinemia were detected high incidence of mild calcification into plaque.
Aim: 7-Ketocholesterol concentrations can be measured in a blood sample; however, the relationship between blood 7-ketocholesterol concentrations and atherosclerotic disease is not well-known. The aim of this study was to clarify the clinical significance of serum 7-ketocholesterol concentrations (s-7KCHO) in the progression of coronary atherosclerosis. Methods: One hundred and thirty-nine subjects with coronary artery disease (CAD, subjects with stable angina pectoris or acute myocardial infarction) and 43 subjects with normal coronary arteries were enrolled in the study. s-7KCHO was measured using gas chromatography mass spectrometry. Results: s-7KCHO was significantly higher in subjects with CAD than in those with normal coronary arteries (normal coronary artery: 19.0 11.3 ng/mL, CAD: 32.4 23.1 ng/mL, p 0.01). Furthermore, patients with multiple vessel disease had significantly higher s-7KCHO than those with single vessel disease. Multivariate analysis revealed that s-7KCHO was an independent variable for CAD (p 0.01). In CAD subjects, the presence of acute myocardial infarction, number of affected vessels, and high sensitive C-reactive protein concentrations strongly correlated with s-7KCHO (p 0.01, 0.05, 0.05, respectively). Conclusion: These results indicate that high s-7KCHO is closely associated with the progression of coronary atherosclerosis and inflammation.
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