Introducing the vulnerable plaque concept, Professor Erling Falk, a cardiovascular pathologist from the University of Aarhus, Denmark, will explain that most heart attacks occur in people with average levels of risk factors who would not be considered eligible for preventive treatment. “In fact," he says, "if you reviewed MI patients the day before their event, only 25% would have been identified as high risk."
A recent Swedish study showed that only 1% of an over-50% decrease CHD mortality between 1986 and 2002 could be attributed to local treatment of stenotic lesions by PCI or CABG surgery.
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Angiographic detail visualised by optical
coherence tomography
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The explanation is simple, says Falk: “Atherosclerosis is a multifocal disease, there's never one single plaque, and the symptomatic plaques that do get treated today don't tend to be the dangerous ones.”
It is the stenotic plaques with their fibrotic lesions which give rise to the symptoms of stable angina (by narrowing the lumen); the vulnerable plaques prone to rupture tend to expand outside the vessel wall, thereby avoiding symptoms. Conventional angiography, adds Falk, only detects lesions that block the lumen, creating a need to develop alternatives for diagnosing the nonobstructive but dangerous vulnerable plaques.
In this respect Dr Francesco Prati, from San Giovanni-Addolorata Hospital in Rome, will propose that optical coherence tomography (OCT) - a novel intravascular imaging modality based on infrared light emissions - represents the most promising technology for identifying them. “The technique allows high-resolution arterial-wall imaging in the range of 10-20 microns, allowing penetrance into the arterial wall and visualisation of specific components of the atherosclerotic plaques, including calcification, fibrotic tissue, necrotic lipid pools and thrombotic components,” says Prati, who is planning a prospective registry study to review outcomes of patients screened with OCT.
Dr Nilesh Samani from the University of Leicester, UK, will review progress on identifying inflammatory markers - such as C-reactive protein, interleukins 6 and 18, glutathione peroxidase and myeloperoxidase - which might help predict events.
“For markers to become a usable concept we need to show they increase predictive power over known risk factors,” says Samani, adding that, since no one marker is coming through “particularly strongly”, the latest concept is to explore panels of markers.
But the circumstances, he cautions, are not simple: “Just because a plaque ruptures doesn't necessarily mean it will result in clinical complications. For the holistic picture we need also to think of the vulnerable blood and vulnerable patient.”
Falk also questions whether there is really a need to go high-tech. Ankle brachial blood pressure indexes (ABI), coronary artery calcium scores by CT and carotid artery screening by ultrasound all represent non-invasive simple tests that can be used to identify people with atherosclerosis. “While such tests don't distinguish between malignant and benign atherosclerosis," he says, "they do reveal the extent of the disease process and thus identify vulnerable people. The more disease patients have, the higher their likelihood of having a vulnerable plaque, and the need for systemic preventive treatment.”
Vulnerable plaque: still a black hole for the cardiologist, Tuesday 1 September 11:00-12:30, Cairo - Zone 6, FPN 3716-3719