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The much-hyped hypothesis that operators can stop heart attacks before they happen -- by prospectively identifying the lesions inside coronary arteries that will rupture, giving rise to acute coronary syndromes -- is real, according to , director of cardiovascular research and education for Columbia University Medical Center/New York-Presbyterian Hospital and co-director of medical research and education at the Cardiovascular Research Foundation.

"Now we're really working on fine-tuning what the best modality is to identify those plaques, and whether those patients should be treated primarily with systemic therapies or, perhaps, even focal treatments," Stone says in this exclusive video from 番茄社区app, reviewing the state of the search for the "holy grail" of cardiology.

A transcript of his comments follows:

The Vulnerable Plaque Hypothesis refers to us being able to identify the types of lesions inside coronary arteries that cause acute coronary syndromes, myocardial infarctions, and sudden coronary death. And, we've known for many years that pathologically these lesions are of a certain subtype. They're most likely called thin-cap fibroatheromas, or what we call TCFAs. But sometimes, they are also lesions that are prone to erosion or sometimes large, calcified nodules.

Now, we're actually able to identify those lesions in patients. First of all, we have noninvasive imaging, and then invasive imaging. Noninvasive imaging modalities, and particularly CT angiography, can identify lipid-rich plaques that are most likely thin-cap fibroatheromas that are large, positively, remodeled plaques with low amounts of calcium, low Hounsfield Units (HU). And those seem to place patients at risk for future events.

In addition, we can use the increased signal to noise ratio from invasive catheter technology, having the catheter right up against the plaque. And, we've done a pretty good job of being able to validate the vulnerable plaque hypothesis using radio frequency, intravascular ultrasound, or VH-IVUS, in the PROSPECT study, and subsequently in several other studies, we were able to identify thin-cap fibroatheromas by VH, which then subsequently went on to have rapid lesion progression, and caused acute coronary syndrome type of events.

We're now looking at other modalities such as optimal coherence tomography and near-infrared spectroscopy to look for lipid-rich plaques or thin-cap fibroatheromas, and that will help us identify high-risk patients and plaques who can most benefit from potent systemic therapies, and perhaps even one day focal or regional vulnerable plaque treatments, such as bioresorbable scaffolds.

What we've learned is that the development of vulnerable plaque comes from systemic inflammation. And that kind of underlies the drive for plaques to progress, which is a 20 to 50-year process. And there is a first steadied progression in which plaques become developed in the coronary arteries and then remodel, lay down lipid, and then suddenly transform into more severe phenotypes. And we know that plaques rupture and heal all the time; that's often a silent process. But when you get to a severe enough lesion stenosis severity or severe enough amount of plaque burden, then another plaque rupture, or another thrombotic event on top of the plaque, can cause either sudden death or massive myocardial infarction, or unstable angina.

So, vulnerable plaque is a real phenomenon. We can identify plaques, prospectively, which place patients at risk for future cardiac events. And now we're really working on fine-tuning what the best modality is to identify those plaques, and whether those patients should be treated primarily with systemic therapies or, perhaps, even focal treatments.

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