Читать книгу Interventional Cardiology - Группа авторов - Страница 45

With the concept of “vulnerable” plaque not nearly as straightforward as once thought, there are challenges to creating a therapeutic strategy for assessing the risk of rupture of vulnerable plaques in asymptomatic patients.

First, there must be an ability to identify the vulnerable plaque with non‐invasive or invasive techniques. It has been demonstrated that coronary plaque composition can be studied with invasive and non‐invasive imaging techniques, allowing real‐time analysis and in‐vivo plaque characterization including the identification of TCFA, however the severity of the inflammatory infiltration of the cap, which certainly plays a major role in plaque disruption, cannot be accurately evaluated even with the most advanced in‐vivo imaging techniques. Moreover, dynamic plaque changes, such as abrupt intra‐plaque haemorrhages from vasa‐vasorum which may be fundamental in predicting the potentiality of a plaque to rupture, will be extremely difficult to identify with real‐time imaging techniques.

A second challenge is that a lesion‐specific approach requires that the number of vulnerable plaques in each patient needs to be known and the number of such lesions need to be limited. That is not the case, however. Several pathological studies indicate the presence of multiple “lipid‐rich” vulnerable plaques in patients dying after ACS or with sudden coronary death [84, 87]. Further complicating the issue: coronary occlusion and myocardial infarction usually evolve from mild to moderate stenosis – 68% of the time, according to an analysis of data from different studies.

The third and fourth challenge is that the natural history of the vulnerable plaque (with respect to incidence of acute events) has to be documented in patients treated with patient‐specific systemic therapy; and the approach has to be proven to significantly reduce the incidence of future events relative to its natural history. At this time, neither is documented nor proved.

Fifth, we believe that at the current stage it is not possible to know which vulnerable plaques will never rupture. Although we suspect it is the vast majority of them, we may have to shift to a more appropriate therapeutic target. In addition, targeting not only the vulnerable plaque but also the vulnerable blood (prone to thrombosis) and/or vulnerable myocardium (prone to life‐threatening arrhythmia) may be also important to reduce the risk of fatal events.