Editing Vulnerable plaque (section)

==Detection==
While a single ruptured plaque can be identified during autopsy as the cause of a coronary event, there is currently no way to identify a culprit lesion before it ruptures.<ref>Heart Disease and Stroke Statistics – 2006 update, American Heart Association.</ref>

Because artery walls typically enlarge in response to enlarging plaques, these plaques do not usually produce much [[stenosis]] of the artery lumen. Therefore, they are not detected by [[cardiac stress tests]] or [[angiography]], the tests most commonly performed clinically with the goal of predicting susceptibility to future heart attack. In contrast to conventional angiography, cardiac CT angiography does enable visualization of the vessel wall as well as plaque composition. Some of the CT derived plaque characteristics can help predict for acute coronary syndrome.<ref>{{cite journal | author = Versteylen MO | display-authors = etal | year = 2013 | title = Additive value of semi-automated quantification of coronary artery disease using cardiac CT-angiography to predict for future acute coronary syndrome | journal = J Am Coll Cardiol | volume =  61| issue = 22| pages =  2296–2305| doi = 10.1016/j.jacc.2013.02.065 | pmid = 23562925 | doi-access = free }}</ref> In addition, because these lesions do not produce significant stenoses, they are typically not considered "critical" and/or interventionable by interventional cardiologists, even though research indicates that they are the more important lesions for producing heart attacks.

The tests most commonly performed clinically with the goal of testing susceptibility to future heart attack include several medical research efforts, starting in the early to mid-1990s, using [[intravascular ultrasound]] (IVUS), [[thermography]], near-infrared spectroscopy, careful clinical follow-up, and other methods, to predict these lesions and the individuals most prone to future heart attacks. These efforts remain largely research with no useful clinical methods to date (2006). Furthermore, the usefulness of detecting individual vulnerable plaques by invasive methods has been questioned because many "vulnerable" plaques rupture without any associated symptoms and it remains unclear if the risk of invasive detection methods is outweighed by clinical benefit.<ref>{{Cite journal |last1=Arbab-Zadeh|first1=A.|last2=Fuster|first2=V. |year=2015 |title=The myth of the "vulnerable plaque": transitioning from a focus on individual lesions to atherosclerotic disease burden for coronary artery disease risk assessment.|journal=Journal of the American College of Cardiology |volume=65 |issue=8 |pages=846–855 |doi= 10.1016/j.jacc.2014.11.041|pmc=4344871 |pmid=25601032}}</ref><ref>{{Cite journal |last1=Libby|first1=P.|last2=Pasterkamp|first2=G. |year=2015 |title=Requiem for the 'vulnerable plaque'.|journal=European Heart Journal |volume=36 |issue=43 |pages=2984–2987 |doi= 10.1093/eurheartj/ehv349|pmid=26206212|url=https://dash.harvard.edu/bitstream/handle/1/23031209/Requiem_Fig1.pdf?sequence=2|doi-access=free}}</ref>

Another approach to detecting and understanding plaque behavior, used in research and by a few clinicians, is to use ultrasound to non-invasively measure [[Intima-media thickness|wall thickness]] (usually abbreviated [[Intima-media thickness|IMT]]) in portions of larger arteries closest to the skin, such as the carotid or femoral arteries. While stability vs. vulnerability cannot be readily distinguished in this way, quantitative baseline measurements of the thickest portions of the arterial wall (locations with the most plaque accumulation). Documenting the IMT, location of each measurement and plaque size, a basis for tracking and partially verifying the effects of medical treatments on the progression, stability, or potential regression of plaque, within a given individual over time, may be achieved.