Interpreting Myocardial Infarction Analyses in ISCHEMIA

Separating Facts From Fallacy

Raffaele De Caterina; David L. Brown


Eur Heart J. 2021;42(31):2986-2989. 

In This Article

Reduction of Future Myocardial Infarction by an Invasive Strategy—Biologically Plausible?

Pathological observations over the past 40 years have consistently demonstrated that culprit plaques responsible for most spontaneous MIs share common histological characteristics,[6] including inflammation, a thin fibrous cap, positive remodelling, and a large necrotic core, often found together in the so-called thin-capped fibroatheromas. These adverse plaque characteristics are demonstrable prospectively by advanced imaging techniques, including intravascular ultrasound with virtual histology, optical coherence tomography, or coronary computed tomography (CT) angiography. Even with advanced techniques, however, these imaging-based plaque characteristics have remarkably poor positive predictive value for clinical events. In the PROSPECT trial, 596 thin-cap fibroatheromas were identified using intravascular ultrasound, but only 6 patients had an MI within 3.4 years.[7] In the SCOT-HEART trial, 1376 plaques with adverse characteristics were identified on CT, yet across the entire cohort only 41 patients had an MI after 4.7 years.[8] Similarly, in the PROMISE trial, 1019 coronary plaques with adverse characteristics were observed on CT, yet only 24 subsequent non-fatal MIs occurred.[9] It strains credulity that less sophisticated angiographic selection of a lesion based simply on the degree of stenosis or physiologic lesion selection for PCI based on an inducible trans-stenotic pressure gradient would outperform advanced imaging techniques, identify plaques at the risk of rupture, and by intervening on them, avert downstream MIs. More likely, stenosis reduction by PCI ameliorates the trans-stenotic gradient, thus preventing the development of Type 2 MIs that are easily confused with Type 1 MIs based on clinical and angiographic criteria. Conversely, CABG may prevent future Type 1 MIs because bypass grafts to the mid-coronary arteries not only treat culprit lesions (even anatomically complex ones) but also provide prophylaxis against new proximal lesions, whereas stents treat only identified stenotic segments with no effect on remote native coronary artery disease (CAD) progression.[10]