Science / Technology - Lecture/Discussion - WPI Only
Monday, November 5, 2012
4:00 PM-5:00 PM
Despite tremendous advances in the recognition and management of risk factors for atheromatous disease as well as the treatment of acute events, it remains responsible for substantial morbidity and mortality in the Western world and is an increasing problem in China and the Far East. This involves multiple vascular beds including the coronary, carotid, intracranial, aortic or peripheral territories.
Focusing on the prevention of stroke, until recently the risk of carotid disease in symptomatic patients was determined by simple luminal measurements based conventional angiography, all on more subjective changes in Doppler ultrasound measurements which would establish whether a patient should undergo carotid endarterectomy or optimal medical therapy. Developments in MR and CT over the past decade have given us alternative tools to measure luminal stenosis which have reduced risks when compared with conventional X ray angiography. The relentless progression of faster, more robust sequences and contrast agents have only recently allowed us to assess plaque itself, rather than its effect on the degree of stenosis. We are now able to image individual plaque components including the fibrous cap, lipid core and haemorrhage.
The current goal is to be better able to characterise plaque risk, whether it is in the carotid, coronary or peripheral vasculature. MR imaging of the carotid is feasible due to its size and superficial position, equivalent reproducible imaging of the coronary arteries being considerably more challenging. Although the carotid artery may be viewed as a surrogate for disease in the coronaries, this is probably an oversimplification. Nevertheless it remains an important and practical target.
Our understanding of the natural history of atheroma development continues to grow. Whilst the assessment of risk is aided by the quantification of individual morphological components in plaque viewed with MR, it has been difficult to image true plaque function. We can use MR to assess the contribution of local flow dynamics and the individual components of plaque to produce maps of stress in a specific patient. In addition, enticing studies of plaque activity demonstrated by FDG PET have shown that it is possible to image inflammatory activity in man. We now have MR contrast agents that are taken up by macrophages and are visible with high-resolution MR. We are also able to image not only individual plaque structure, but also function allowing an improved understanding of why two patients will identical degrees of luminal stenosis may have completely different degrees of vulnerability; why one patient should be symptomatic and the other asymptomatic. Indeed the interactions between biomechanical stresses and inflammation are probably extremely complex as it is not yet possible to define the initiating process and their interactions.
Biomedical engineering presents tremendous opportunities for the identification of vulnerable plaques. Whilst there has been a major focus on plaque stress, other biomechanical properties such as fatigue may also play a part in determining risk.
There have been tremendous advances in our ability to access plaque vulnerability using MR over the last few years. The challenge is to validate these techniques in the carotid and to take them into the coronary as the relentless progress of technology continues.
Suggested Audiences: Adult, College
Last Modified: September 12, 2012 at 9:05 AM