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Biomedical subjects

Eric Larose

Publications and source records attributed to Eric Larose.

6 recordsLinked to original sources
PubMed2006

Observation of multiple scattering of kHz vibrations in a concrete structure and application to monitoring weak changes.

In this paper, we present two experimental studies of mechanical wave propagation in a concrete building around 1 kHz. The first experiment is devoted to the observation of the coherent backscattering enhancement, which demonstrates the presence of multiple diffractions in the late part of the wave records. An application of multiple diffraction and reverberations is proposed in a second experiment. Thanks to their sensitivity to weak changes of the medium, the late records are used to monitor weak change in concrete wave velocity induced by thermal variations. The velocity change measurements have a precision of deltac/c=10(-4). Such a precision is difficult to obtain with direct waves. This experiment is the first step to other applications like stress, damage, aging, or crack monitoring in concrete structures.

Journal Article↗
PubMed2005

Passive retrieval of Rayleigh waves in disordered elastic media.

When averaged over sources or disorder, cross correlation of diffuse fields yields the Green's function between two passive sensors. This technique is applied to elastic ultrasonic waves in an open scattering slab mimicking seismic waves in the Earth's crust. It appears that the Rayleigh wave reconstruction depends on the scattering properties of the elastic slab. Special attention is paid to the specific role of bulk to Rayleigh wave coupling, which may result in unexpected phenomena, such as a persistent time asymmetry in the diffuse regime.

Journal Article↗
PubMed2005

Characterization of human atherosclerotic plaques by intravascular magnetic resonance imaging.

BACKGROUND: Development and validation of novel imaging modalities to assess the composition of human atherosclerotic plaques will improve the understanding of atheroma evolution and could facilitate evaluation of therapeutic strategies for plaque modification. Surface MRI can characterize tissue content of carotid but not deeper arteries. This study evaluated the usefulness of intravascular MRI (IVMRI) to discern the composition of human iliac arteries in vivo. METHODS AND RESULTS: Initial studies validated IVMRI against histopathology of human atherosclerotic arteries ex vivo. A 0.030-inch-diameter IVMRI detector coil was advanced into isolated human aortoiliac arteries and coupled to a 1.5-T scanner. Information from combined T1-, moderate T2-, and proton-density-weighted images differentiated lipid, fibrous, and calcified components with favorable sensitivity and specificity and allowed accurate quantification of plaque size. The validated approach was then applied to image iliac arteries of 25 human subjects in vivo, and results were compared with those of intravascular ultrasound (IVUS). IVMRI readily visualized inner and outer plaque boundaries in all arteries, even those with extensive calcification that precluded IVUS interpretation. It also revealed the expected heterogeneity of atherosclerotic plaque content that was noted during ex vivo validation. Again, IVUS did not disclose this heterogeneity. The level of interobserver and intraobserver agreement in the interpretation of plaque composition was high for IVMRI but poor for IVUS. CONCLUSIONS: IVMRI can reliably identify plaque composition and size in arteries deep within the body. Identification of plaque components by IVMRI in vivo has important implications for the understanding and modification of human atherosclerosis.

Adult↗
PubMed2004

Statins and endothelial dysfunction.

The endothelium integrates and modulates critical functions of the arterial wall. As well as regulating vasomotion, it controls inflammation, coagulation, and thrombosis. Many of these actions are mediated through the release of nitric oxide. Endothelial dysfunction is associated with atherosclerosis and its risk factors. It is independently correlated to adverse cardiovascular events, including myocardial infarction, coronary death, and the need for revascularization. 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) protect against cardiovascular death, myocardial ischemia, myocardial infarction, and stroke. Although cholesterol reduction accounts for some of these benefits, others appear to be independent of cholesterol lowering. The endothelium mediates many of these "lipid-dependent" and "lipid-independent" actions of statins. This chapter reviews the effects of statins on endothelial dysfunction. To do so, a brief outline of the biology of the endothelium is a prerequisite. This will be followed by a summary of the advances in vascular research on cholesterol-dependent and cholesterol-independent effects of statins, with a focus on the endothelium. Ultimately, clinical relevance of observations derived from basic biology will be discussed.

Arteriosclerosis↗
PubMed2003

Use of ACE Inhibitors for Secondary Prevention.

The role of the renin-angiotensin system as a regulator of blood pressure, body fluids, electrolytes, and neurohormonal activation has been established for more than two decades. The dramatic benefits of angiotensin-converting enzyme (ACE) inhibition on overall mortality, progression to heart failure, and major cardiovascular events were first demonstrated in patients with congestive heart failure (CHF) or left ventricular dysfunction. ACE inhibitors should be prescribed for all patients with symptomatic CHF and for all asymptomatic patients with a left ventricular ejection fraction less than 35% to 40%, unless contraindicated or not tolerated, and therapy should be continued indefinitely. Data have shown that ACE inhibition improves oxidative stress, endothelial and ventricular function, and reduces ventricular remodeling as well as progression of carotid intimal and medial thickening. Current evidence suggests that ACE inhibitors should be prescribed as early as possible for all patients with acute myocardial infarction, unless contraindicated or not tolerated, and that they should be continued for at least 6 weeks; moreover, because these patients automatically qualify as high-risk individuals, indefinite therapy should be considered. Likewise, individuals at increased risk for major cardiovascular events (diabetic patients with additional risk factors and patients with known vascular disease) should be prescribed ACE inhibitors, unless contraindicated or not tolerated, and therapy should be continued indefinitely. There is not sufficient evidence at present to recommend the use of ACE inhibitors after coronary revascularization for the specific goal of preventing restenosis or graft disease, in the absence of decreased ejection fraction, CHF, or a new myocardial infarction.

Journal Article↗