Marker Of Plaque Vulnerability Research Articles

Risk Functions and the Primary Prevention of Cardiovascular Disease

Cardiovascular risk functions are regarded as the best tools for establishing priorities in primary prevention. Since the original Framingham risk chart fell into disuse because it greatly overestimated the real risk, the adjusted REGICOR and SCORE functions have become widely available in Spain, although the REGICOR function is the only one that has been validated for use in the Spanish population. Risk estimates have been shown to be useful for decision-making, particularly on the treatment of hypercholesterolemia. However, the fact that the majority of cardiovascular events occurs in individuals classified as being at a medium risk is evidence for the poor discriminative ability of classical risk factors. Despite the use of new parameters proposed for estimating cardiovascular risk, such as the C-reactive protein level, the detection of coronary calcification, the carotid intima-media thickness and the ankle-brachial index, there has been no improvement in the predictive capacity of classical risk factors. The most promising alternative seems to be the identification of "vulnerable patients" using markers of vulnerable plaque (ie, unstable or high-risk plaque), vulnerable blood (ie, with a tendency for thrombosis), and vulnerable myocardium (ie, electrically unstable or with a tendency for arrhythmia). In this article, we discuss whether the combined use of cardiovascular risk functions, novel risk markers and noninvasive tests can be effective in increasing the accuracy of patient selection for the primary prevention of cardiovascular disease.

New Methods for Time-resolved Fluorescence Spectroscopy Data Analysis Based on the Laguerre Expansion Technique

A new deconvolution method for the analysis of time-resolved laser-induced fluorescence spectroscopy (TR-LIFS) data is introduced and applied for tissue diagnosis. The intrinsic TR-LIFS decays are expanded on a Laguerre basis, and the computed Laguerre expansion coefficients (LEC) are used to characterize the sample fluorescence emission. The method was applied for the diagnosis of atherosclerotic vulnerable plaques. At a first stage, using a rabbit atherosclerotic model, 73 TR-LIFS in-vivo measurements from the normal and atherosclerotic aorta segments of eight rabbits were taken. The Laguerre deconvolution technique was able to accurately deconvolve the TR-LIFS measurements. More interesting, the LEC reflected the changes in the arterial biochemical composition and provided discrimination of lesions rich in macrophages/foam-cells with high sensitivity (> 85%) and specificity (> 95%). At a second stage, 348 TR-LIFS measurements were obtained from the explanted carotid arteries of 30 patients. Lesions with significant inflammatory cells (macrophages/foam-cells and lymphocytes) were detected with high sensitivity (> 80%) and specificity (> 90%), using LEC-based classifiers. This study has demonstrated the potential of using TR-LIFS information by means of LEC for in vivo tissue diagnosis, and specifically for detecting inflammation in atherosclerotic lesions, a key marker of plaque vulnerability.

Atherosclerosis Neovascularization and Imaging

Neovascularization in atherosclerotic plaques is particularly prominent in complicated lesions, and has been recently identified as a marker of plaque vulnerability. This observation has led to a growing interest in the development of imaging techniques with the ability to visualize and quantify the extent of plaque neovascularization. Such feature may play an important role in identifying those lesions more prone to destabilization and rupture, and in the guidance and monitoring of therapeutic interventions. Several modalities have emerged as potential candidates for imaging neovessels in atherosclerotic lesions. They include magnetic resonance imaging, x-ray computed tomography, positron emission tomography, single photon emission computed tomography, ultrasound, or near-infrared optical imaging. These techniques differ in their achievable spatial and temporal resolution, availability, cost, reproducibility, degree of intrusiveness, capability to image atherosclerotic plaques in various vascular territories and ability to discern different plaque components, specifically the presence of neovessels. Molecular imaging, a rapidly evolving multidisciplinary field devoted to the visualization of specific physiopathologic processes at the cellular or molecular level, appears particularly well suited for this purpose because of its ability to target and visualize individual molecules specific to neoangiogenesis. In this manuscript we will review current evidence on the potential application of the various modalities, with a particular emphasis in molecular imaging.

Assessment of plaque vulnerability by angioscopic classification of plaque color

Background The disruption of yellow plaque and subsequent thrombosis is regarded as the mechanism of acute coronary syndrome. However, there are limited reports on the assessment of plaque vulnerability. Therefore, we tested whether the angioscopically determined yellow color intensity of plaque is associated with the prevalence of thrombosis on the plaque. Methods The angioscopic images of 843 patients who underwent catheterization and angioscopic examination from November 1999 to July 2003 for the diagnosis of coronary artery diseases were analyzed. Suspected culprit vessel was observed by angioscopy, and the yellow color intensity (1, light yellow; 2, yellow; 3, intensive yellow) of all yellow plaques (n = 1253) detected in the nonstenotic (diameter stenosis <50%) coronary segments was determined, as well as whether there was thrombosis on the plaques. Results The number of detected yellow plaques was 345, 721, and 187 for color grade 1, 2, and 3, respectively. The prevalence of thrombosis detected by angioscopy (15%, 26%, and 52% on the plaque of color grade 1, 2, and 3, respectively, P < .0001) was significantly higher on the plaque of higher yellow color grade. Conclusions The yellow color intensity of plaque determined by angioscopy was strongly related with the prevalence of thrombosis on the plaque. The yellow color intensity may be a marker of plaque vulnerability.

Prognostic Value of Myeloperoxidase in Patients With Chest Pain

Brennan, Marie-Luise; Penn, Marc S.; Van Lente, Frederick; Nambi, Vijay; Shishenbor, Mehdi H.; Aviles, Ronnier J.; Goormastic, Marlene; Pepoy, Michael L.; McErlean, Ellen S.; Topol, Eric J.; Nissen, Steven E.; Hazen, Stanley L.

841-2 Periadventitial fat inflammation correlates with plaque inflammation in patients with coronary plaque ruptures: New marker of plaque vulnerability?

841-2 Periadventitial fat inflammation correlates with plaque inflammation in patients with coronary plaque ruptures: New marker of plaque vulnerability?

Risk stratification and management of sudden cardiac death: a new paradigm.

Risk Stratification and Management of SCD. Management of SCD is undergoing radical change in direction. It is becoming increasingly appreciated that besides depressed left ventricular systolic function and the conventional risk stratification tools, new markers for plaque vulnerability, enhanced thrombogenesis, specific genetic alterations of the autonomic nervous system, cardiac sarcolemmal and contractile proteins, and familial clustering may better segregate patients with atherosclerotic coronary artery disease who are at high risk for SCD from those who may suffer from nonfatal ischemic events. Better understanding of pathophysiologic processes, such as postmyocardial infarction remodeling, the transition from compensated hypertrophy to heart failure, and the increased cardiovascular risk of coronary artery disease in the presence of diabetes or even a prediabetic state will help to improve both risk stratification and management. The rapidly developing fields of microchips technology and proteomics may allow rapid and cost-effective mass screening of multiple risk factors for SCD. The ultimate goal is to identify novel methods for risk stratification, risk modification, and prevention of SCD that could be applied to the general public at large.

Relationship between coronary artery remodeling and plaque vulnerability.

In vivo studies with intravascular ultrasound have shown that complex plaque anatomy and plaque rupture are more frequent in the presence of marked outward remodeling. A large lipid core and a high macrophage count are recognized histological markers for plaque vulnerability. The link between plaque vulnerability in terms of these markers and remodeling in coronary arteries has not been explored. In 88 male subjects who died suddenly with coronary artery disease, 108 plaques were studied. The percent remodeling was calculated. Lesions with remodeling > or = 0% were considered to have positive remodeling, and those in which remodeling was < 0% were considered to have negative remodeling. Percent lipid core and macrophage count at the plaque were assessed. Of 108 plaque sites, 64 (59.2%) had undergone no remodeling or positive remodeling, and 44 (40.7%) had negative remodeling (vessel shrinkage). Lesions with positive remodeling, compared with lesions with vessel shrinkage, had a larger lipid core (percent mean lipid core was 39.0 +/- 21.0% versus 22.3 +/- 23.1%, respectively; P < 0.0001) and a higher macrophage count (mean macrophage count was 15.6 +/- 12.3 versus 8.9 +/- 11.6, respectively; P = 0.005). We have shown that coronary artery plaques with positive remodeling have a higher lipid content and macrophage count, both markers of plaque vulnerability. These results may explain why plaque rupture is often apparent at sites with only modest luminal stenoses (but marked positive remodeling).