Comparison of normal values of Duplex indices of vertebral arteries in young and elderly adults

<p>Abstract</p> <p>Background</p> <p>Considering the role of aging in brain atrophy and cerebral vascular demand, we carried out this study to clarify the role of aging in duplex indices of vertebral arteries.</p> <p>Methods</p> <p>From June 2005 to June 2006, 96 volunteers with age range of 20 to 95 years, were evaluated with color doppler for duplex indices of vertebral arteries. Sever hemodynamic stenosis was excluded in all of these patients. These volunteers were subdivided in two groups: younger and older than 60 year old. In all of these patients we measured diameter, peak systolic velocity (PSV), resistive index (RI), and flow volume (FV) of vertebral arteries in right and left sides.</p> <p>Results</p> <p>There was no significant difference in diameter, PSV, RI and FV between two groups. We have clarified that in patients younger than 60 year old, comparing right and left vertebral arteries, PSV and FV were higher in left side.</p> <p>Conclusion</p> <p>Duplex indices of vertebral arteries are age independent in adults.</p

Carotid Plaque Age Is a Feature of Plaque Stability Inversely Related to Levels of Plasma Insulin

C-declination curve (a result of the atomic bomb tests in the 1950s and 1960s) to determine the average biological age of carotid plaques.C content by accelerator mass spectrometry. The average plaque age (i.e. formation time) was 9.6±3.3 years. All but two plaques had formed within 5–15 years before surgery. Plaque age was not associated with the chronological ages of the patients but was inversely related to plasma insulin levels (p = 0.0014). Most plaques were echo-lucent rather than echo-rich (2.24±0.97, range 1–5). However, plaques in the lowest tercile of plaque age (most recently formed) were characterized by further instability with a higher content of lipids and macrophages (67.8±12.4 vs. 50.4±6.2, p = 0.00005; 57.6±26.1 vs. 39.8±25.7, p<0.0005, respectively), less collagen (45.3±6.1 vs. 51.1±9.8, p<0.05), and fewer smooth muscle cells (130±31 vs. 141±21, p<0.05) than plaques in the highest tercile. Microarray analysis of plaques in the lowest tercile also showed increased activity of genes involved in immune responses and oxidative phosphorylation.C, can improve our understanding of carotid plaque stability and therefore risk for clinical complications. Our results also suggest that levels of plasma insulin might be involved in determining carotid plaque age

Multi-Organ Expression Profiling Uncovers a Gene Module in Coronary Artery Disease Involving Transendothelial Migration of Leukocytes and LIM Domain Binding 2: The Stockholm Atherosclerosis Gene Expression (STAGE) Study

Environmental exposures filtered through the genetic make-up of each individual alter the transcriptional repertoire in organs central to metabolic homeostasis, thereby affecting arterial lipid accumulation, inflammation, and the development of coronary artery disease (CAD). The primary aim of the Stockholm Atherosclerosis Gene Expression (STAGE) study was to determine whether there are functionally associated genes (rather than individual genes) important for CAD development. To this end, two-way clustering was used on 278 transcriptional profiles of liver, skeletal muscle, and visceral fat (n = 66/tissue) and atherosclerotic and unaffected arterial wall (n = 40/tissue) isolated from CAD patients during coronary artery bypass surgery. The first step, across all mRNA signals (n = 15,042/12,621 RefSeqs/genes) in each tissue, resulted in a total of 60 tissue clusters (n = 3958 genes). In the second step (performed within tissue clusters), one atherosclerotic lesion (n = 49/48) and one visceral fat (n = 59) cluster segregated the patients into two groups that differed in the extent of coronary stenosis (P = 0.008 and P = 0.00015). The associations of these clusters with coronary atherosclerosis were validated by analyzing carotid atherosclerosis expression profiles. Remarkably, in one cluster (n = 55/54) relating to carotid stenosis (P = 0.04), 27 genes in the two clusters relating to coronary stenosis were confirmed (n = 16/17, P<10−27and−30). Genes in the transendothelial migration of leukocytes (TEML) pathway were overrepresented in all three clusters, referred to as the atherosclerosis module (A-module). In a second validation step, using three independent cohorts, the A-module was found to be genetically enriched with CAD risk by 1.8-fold (P<0.004). The transcription co-factor LIM domain binding 2 (LDB2) was identified as a potential high-hierarchy regulator of the A-module, a notion supported by subnetwork analysis, by cellular and lesion expression of LDB2, and by the expression of 13 TEML genes in Ldb2–deficient arterial wall. Thus, the A-module appears to be important for atherosclerosis development and, together with LDB2, merits further attention in CAD research

Is Carotid Atherosclerosis More Important in Patients with Mitral Annular Calcification than in Those without?

It has been suggested that mitral annular calcification (MAC) may be a manifestation of generalized atherosclerosis. However, how the incidence and extent of coronary artery disease (CAD) are affected by the coexistence of carotid atherosclerosis (CAS) in patients with versus without MAC have not yet been studied. We studied 101 patients with echocardiographic MAC and 52 controls without MAC to investigate the clinical impact of CAS on the frequency and severity (defined as the number of obstructed vessels) of CAD in patients with MAC. Carotid Doppler ultrasonographic examination was performed on all patients before coronary angiography. In patients with both MAC and CAS, the incidences of CAD and multivessel disease (greater than or equal to 2 vessel or left main coronary artery disease) were significantly higher than in the control group with CAS alone (91% versus 68%, P = 0.008 and 76% versus 44%, P = 0.004, respectively). On the other hand, among study and control patients without CAS, although the frequencies of CAD and multivessel disease were higher in patients with MAC, interestingly, the differences were not statistically significant (37% versus 58% and 15% versus 26%, respectively, P>0.05 for both). Stepwise multiple logistic regression analysis revealed that CAS (P<0.001), MAC (P<0.01) and, to a limited extent hypertension (P = 0.054), were independent predictors for the presence of CAD. In conclusion, the coexistence of CAS is more important in patients with MAC than in those without as it provides valuable information about the incidence and severity of underlying CAD. In cases with MAC but without CAS, MAC could be caused by factors other than atherosclerosis.WoSScopu