The battle has been going on for several years: which technology will be the first to reliably depict the components of the diseased arterial wall and more specifically to identify the presence of vulnerable plaques?
Erling Falk in his opening talk defined the anatomic targets to be identified by imaging. Three main pieces of information are needed:
1. plaque burden,
2. plaque activity
3. plaque vulnerability.
Whereas CT, MRI and IVUS are able to measure plaque burden, plaque activity is much more difficult to characterise. The macrophage ist the prime target for imaging of plaque activity. However, in contrast to wideheld opinion, an increased number of macrophages is only found in the endangered fibrous cap and that may be difficult to identify by current imaging techniques. There is also the issue of neovascularisation of the plaque, the amount of which is indicative of plaque activity. The vulnerable plaque is characterised by increased plaque size and an increased size of the necrotic core. However, there is a hugh overlap between vulnerable and stable plaques. This indicates the difficulty of differentiating between these two entities with the aim of instituting a targeted therapy towards the most vulnerable plaques only. Vulnerable plaques unfortunately have less calcium than stable plaques. Their fibrous cap is thinner than that of stable plaques and there is an increased number of macrophages and possibly also thrombus.
Gerard Helft pointed to the fact that calcium scoring by multislice CT could not solve the problem of identifying the vulnerable plaque, although it is probably the most practical way of defining coronary plaque burden. However, calcific spots on CT images do not identify areas with subsequent coronary occlusions. Even with the current improvements in technology, it remains difficult to differentiate between fibrous and fatty components of the plaque by using CT. An important shortcoming of CT in detecting vulnerable plaques is the limited spatial resolution. Vulnerable plaques have fibrous caps which are thinner than 70µm. However, the spatial resolution of CT is in the order of 400µm with current leading edge technology.
Valentin Fuster said that imaging was the cornerstone of understanding the pathophysiology of atherosclerosis both in animal models and in humans. He presented his view of the atherosclerotic process and showed how imaging including CT, MRI and PET were helpful to demonstrate that some of the theoretical assumptions indeed were operative in the living body. With MRI, a correlation between the presence of fat in the intima and the number of vasa vasorum could be demonstrated. Moreover, microvessels were increased in areas with ruptured plaques. MRI can also show that lipid lowering leads to plaque regression. The features of the vulnerable plaques cannot yet be demonstrated in the coronaries by MRI due to limited spatial resolution. However, progress has been made in the carotid arteries. Using fusion imaging by PET and MRI lesions responsible for cerebrovascular events could retrospectively be identified. However, the real goal of prospective identification of lesion prone to rupture in the near future is still not in immediate reach.
Steve Nissen was the last speaker and he addressed the role of IVUS. The main advantage of IVUS over the other techniques is the unique spatial resolution which currently is in the order of 75µm. This enables IVUS to identify the presence and extent of atherosclerosis early in the disease process. In donor hearts of US adults aged 30 years IVUS identified substantial amounts of atheromatosis in >50%! In several important trials IVUS showed a linear correlation between the amount of LDL cholesterol lowering and the amount of regression of the atheromatous coronary burden. However, for practical reasons the prospective identification of vulnerable plaques by this highly invasive technique cannot be routinely performed. Moreover, identification of macrophages in fibrous caps cannot be achieved even by this high resolution technique.