Rupture of a Vulnerable Plaque in a Hazy Angiographic Culprit Lesion During Acute Coronary Syndrome

J INVASIVE CARDIOL 2021;33(6):E487-E488. 

Key words: high risk plaque, plaque rupture, ultra-thin DES, coronary imaging, unstable vulnerable plaque

A 66-year-old man was hospitalized for chest pain with widespread non-specific alterations of the electrocardiogram repolarization, suggestive of acute ischemia in the presence of an intermittent right bundle-branch block. The echocardiogram was within normal limits without showing changes in ventricular kinetics. After an initial benefit from conservative medical therapy, there was a recurrence of anginal symptoms with troponin rise, for which an urgent coronary angiography study was proposed. The right coronary artery (RCA) presented an intermediate degree angiographically (60% at quantitative coronary angiography [QCA]) with the haziness of possible thrombotic significance in the middle tract (Figure 1A). The left coronary artery had diffuse atheromatous lesions and a focal lesion in the middle tract of the anterior descending artery (QCA 40%) with haziness probably secondary to calcification (Figures 1B and 1C).

As it was not possible to establish the culprit lesion from angiography, an optical coherence tomography (OCT) scan (DragonFly catheter; Abbott Cardiovascular) was performed.Intracoronary imaging revealed an eccentric coronary plaque (the reason for angiographic underestimation), subocclusive, and diffuse hypoattenuation of the infrared signal on the mid segment of the RCA. The plaque was classified as fibrolipidic, with a significant necrotic-hemorrhagic core (13 mm²).

Plaque rupture due to hemorrhage within the necrotic core resulted in a narrowing of the vessel and the “squeezing” of its contents out of the vessel with peripheral embolization (Figures 1D-1F). The high-resolution detail shown in Figure 1G highlights several morphologic characteristics of such events; endothelial disruption lining above a thinned fibrous cap measuring <65 microns and cavitation crater are clearly visible. A small thrombus remnant is also evident, attached to one end of the disrupted endothelial layer.

The treatment strategy for this culprit lesion was not easy to determine due to the presence of cavitation (with the risk of poor apposition of struts) in a soft plaque (and related to the risk of further rupture and embolization) with the presence of both thrombotic material and a large sidebranch. Respective wiring of the lesion and sidebranch was performed, and after a mild predilation with a 2.5 mm non-compliant balloon, an Evermine 3.5 x 19 mm stent (Merit Life Sciences) was implanted. We deliberately chose a stent with an ultra-thin platform with an ultralight 50 µm-thick strut coated with a biodegradable release polymer that releases everolimus. These latest-generation drug-eluting stents have the potential benefit of reduced flow disturbance and probably better endothelialization and faster arterial healing.

Further optimization of the stent implant was performed with an OCT scan and postdilation with a 3.5 x 8 mm non-compliant balloon without plaque shift, embolization, malapposition, and residual dissection. A good final angiographic result was obtained with a final Thrombolysis in Myocardial Infarction 3 flow.

In the presence of an equivocal culprit lesion in the context of an acute coronary syndrome, the OCT scan defines the severity and composition of the plaque, elucidating (as in this pathognomonic case) the mechanism related to plaque rupture. Furthermore, OCT analysis allowed stent implantation with adequate sizing and length, and subsequent final optimization of the result (Figures 1H and 1I). In the presence of non-unequivocal lesions, in the context of acute coronary syndrome, the use of OCT imaging defined the etiology and mechanism of plaque instability, reducing cardiovascular events. 

In this clinical scenario, it is necessary to have a low threshold for the use of intracoronary imaging methods. In a challenging scenario, resorting to intracoronary imaging when possible can reduce the risk of procedural and postprocedural complications. 

From the ¹Cardiovascular Department, ASST Santi Paolo e Carlo, Milan, Italy; ²Interventional Cardiology Unit, GVM Care & Research Maria Cecilia Hospital, Cotignola, Italy; ³Department of Biomedicine and Prevention II, University of Tor Vergata, Rome, Italy; ⁴Invasive Cardiology Unit, Humanitas Clinical and Research Center, IRCCS, Rozzano, Milan, Italy; and ⁵Department of Biomedical Sciences, Humanitas University, Pieve Emanuele, Milan, Italy.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.

Manuscript accepted December 4, 2020. 

The authors report that patient consent was provided for publication of the images used herein.

Address for correspondence: Alberto Cereda, MD, Cardiovascular Department, ASST Santi Paolo e Carlo, Milano, Italy. Email: tskcer@hotmail.it