Biomedical subjects

John R Davies

Publications and source records attributed to John R Davies.

6 recordsLinked to original sources

PubMed2006

Radionuclide imaging for the detection of inflammation in vulnerable plaques.

Imaging of atheromatous plaques has traditionally centered on assessing the degree of luminal stenosis. More recently it has become clear that the vulnerable atherosclerotic plaques responsible for the majority of life-threatening syndromes are characterized by high numbers of inflammatory cells and proteins. This has highlighted the urgent need for suitable imaging techniques that can identify and quantify levels of inflammation within atheromatous lesions. Positron emission tomography and single-photon emission computed tomography imaging hold promise in this regard. Tracer compounds capable of assessing macrophage recruitment, foam cell generation, matrix metalloproteinase production, macrophage apoptosis, and macrophage metabolism have been developed and tested in the carotid and peripheral circulation. The identification of inflamed lesions within the coronary circulation, however, remains elusive owing to small plaque size, cardiac and respiratory motion, and lack of a suitable specific nuclear tracer.

Animals↗

PubMed2005

Identification of culprit lesions after transient ischemic attack by combined 18F fluorodeoxyglucose positron-emission tomography and high-resolution magnetic resonance imaging.

BACKGROUND AND PURPOSE: Carotid endarterectomy is currently guided by angiographic appearance on the assumption that the most stenotic lesion visible at angiography is likely to be the lesion from which future embolic events will arise. However, risk of plaque rupture, the most common cause of atherosclerosis-related thromboembolism, is dictated by the composition of the plaque, in particular the degree of inflammation. Angiography may, therefore, be an unreliable method of identifying vulnerable plaques. In this study, plaque inflammation was quantified before endarterectomy using the combination of 18F fluorodeoxyglucose positron (FDG)-emission tomography (PET) and high-resolution MRI (HRMRI). METHODS: Twelve patients, all of whom had suffered a recent transient ischemic attack, had a severe stenosis in the ipsilateral carotid artery, and were awaiting carotid endarterectomy underwent FDG-PET and HRMRI scanning. A semiquantitative estimate of plaque inflammation was calculated for all of the lesions identified on HRMRI. RESULTS: In 7 of 12 patients (58%), high FDG uptake was seen in the lesion targeted for endarterectomy. In the remaining 5 patients, FDG uptake in the targeted lesion was low. In these 5 patients, 3 had nonstenotic lesions identified on HRMRI that exhibited a high level of FDG uptake. All 3 of the highly inflamed nonstenotic lesions were located in a vascular territory compatible with the patients' presenting symptoms. CONCLUSIONS: Our data suggest that angiography may not always identify the culprit lesion. Combined FDG-PET and HRMRI can assess the degree of inflammation in stenotic and nonstenotic plaques and could potentially be used to identify lesions responsible for embolic events.

Aged↗

PubMed2005

Imaging the vertebral artery.

Although conventional intraarterial digital subtraction angiography remains the gold standard method for imaging the vertebral artery, noninvasive modalities such as ultrasound, multislice computed tomographic angiography and magnetic resonance angiography are constantly improving and are playing an increasingly important role in diagnosing vertebral artery pathology in clinical practice. This paper reviews the current state of vertebral artery imaging from an evidence-based perspective. Normal anatomy, normal variants and a number of pathological entities such as vertebral atherosclerosis, arterial dissection, arteriovenous fistula, subclavian steal syndrome and vertebrobasilar dolichoectasia are discussed.

Angiography, Digital Subtraction↗

PubMed2005

Imaging of atherosclerosis -- can we predict plaque rupture?

Rupture of so-called vulnerable or unstable atherosclerotic lesions is responsible for a significant proportion of myocardial infarcts and strokes. However, timely identification of such plaques, in order to allow for aggressive local and systemic therapy, remains problematic. In order to address this problem, there is a need to develop techniques that can image the cellular, biochemical, and molecular components that typify the vulnerable plaque. In this article, both techniques that are in current clinical use and those being evaluated in clinical trials are reviewed with regard to their ability to identify unstable lesions at risk of rupture.

Coronary Angiography↗

PubMed2004

Molecular and metabolic imaging of atherosclerosis.

Atherosclerosis is a systemic disease that affects most major arteries of the body and is the most common cause of premature death in the western world. It develops slowly and often asymptomatically, so that for many patients its first manifestation is sudden cardiac death, stroke, or myocardial infarction. The current gold standard for imaging atherosclerosis is x-ray angiography. However, recent advances in understanding of the pathobiology of atherosclerosis have highlighted the inadequacies of this technique and the need for better imaging approaches. The purpose of this article is to briefly outline the biology of atherosclerosis and to review the techniques available to image it, concentrating specifically on those that detect metabolic or inflammatory changes within the atherosclerotic plaque.

Arteriosclerosis↗

PubMedDate not supplied

Targeting the vulnerable plaque: the evolving role of nuclear imaging.

The majority of acute ischemic events relating to atherosclerosis are caused by plaque rupture and ensuing thrombosis. The risk of plaque rupture is dictated in part by plaque morphology, which in turn is influenced by pathophysiologic mechanisms at the cellular and molecular level. Anatomic imaging modalities such as intravascular ultrasound, high-resolution magnetic resonance imaging, and multislice computed tomography can identify morphologic features of the vulnerable plaque, such as a large lipid core and thin fibrous cap, but give little or no information regarding molecular and cellular mechanisms, such as endothelial function, macrophage activation, lipid transport and metabolism, and cell death. Recent studies suggest that nuclear imaging may be able to provide images of sufficient quality to identify and quantify some of these molecular and cellular pathophysiologic processes. In the future this could allow for the early identification and noninvasive monitoring of vulnerable plaque.

Animals↗