A 34-year-old man who experienced a 30-minute episode of chest pain at rest was admitted to the coronary care unit after becoming symptom free. His ECG was normal. A few hours later, he suffered a 5-minute period of recurrent chest pain with transient ST-segment elevation (Figure 1). The level of creatine phosphokinase reached its peak at 800 IU (upper limit=199 IU), and the maximum troponin T level was 1.85 μg/L. Noninvasive coronary imaging with a 16-slice spiral computed tomography scanner (MSCT) (Sensation 16, Siemens AG; Forchheim, Germany) suggested a nonobstructive lesion in the mid-left anterior descending artery (LAD) (Figure 2), which was confirmed with coronary angiography. Coronary spasm was excluded by methergin provocation test, which only showed general vasoconstriction (31% reduction of reference diameter) but no focal spasm. Intravascular ultrasound (IVUS) (CVIS Atlantis 40-MHz 3F catheter, Boston Scientific, TOMTEC ECG-gated acquisition system) demonstrated a local plaque with vessel remodeling in the mid-LAD. The plaque was covered by a thin layer of speckling, which was different from the plaque and blood speckles, suggesting clot formation (Figure 3B). A small rupture was visible at the proximal shoulder of the plaque (Figure 3A), which was better delineated with a 4D reconstruction image (Movie I). Coronary flow reserve was 4.3, indicating a non–flow-limiting plaque. IVUS palpography demonstrated a strain pattern, which strongly suggested the presence of a vulnerable plaque (Figure 4A and 4B; Movie II). Given the clinical presentation and ultrasound findings, and despite the non–flow-limiting obstruction, we decided after considerable deliberation to implant a drug-eluting stent in the diseased part of the mid-LAD. The procedure and recovery after stent implantation were uneventful.
Figure 1. ECG. Normal sinus heart rhythm. A, Early repolarization in leads II, III, aVF, V5, and V6. B, Transient ST elevation in leads I, aVL, and V2 through V6 associated with 5 minutes of chest pain. C, ECG changes restored when patient was free of pain.
Figure 2. Multislice spiral CT coronary angiogram. A, Volume-rendered reconstruction demonstrates nonsignificant stenosis of the mid-LAD (arrowhead). Maximum plaque diameter was 2.8 mm; minimal lumen area, 5 mm2 (2.6×1.8 mm); and reference lumen area, 8 to 9 mm2 (3.4×2.7 mm). Longitudinal plaque size is 13 mm. The multiplanar, cross-sectional images show slight narrowing of the LAD (B). The attenuation value of the plaque was measured as 80 Hounsfield units, suggesting a mixed plaque composition without calcification (C and D, arrowheads). The entire segment can be shown in a single plane by means of vessel tracking (E, arrowhead). The great cardiac vein can be differentiated from the plaque by the higher and homogeneous attenuation of the venous lumen (v). RCA indicates right coronary artery; LCX, left circumflex artery.
Figure 3. IVUS system: Boston Scientific Galaxy. IVUS catheter: Boston Scientific Atlantis 3F 40 MHz. Motorized pullback 0.5 mm/s. Images digitally stored. Top panel shows a longitudinal reconstruction from the IVUS acquisition in the mid-LAD. The lowercase characters a through d indicate the locations of the cross sections A through D. At b and c in the longitudinal view, a soft plaque with different densities is visible. Cross section D shows a normal 3-layered aspect of the LAD distal from the lesion. Cross sections B and C show an eccentric soft plaque between the 6 o’clock and 2 o’clock positions, with thrombus present at the 12 o’clock position. Cross section A shows a small eccentric plaque from the 12 o’clock to the 4 o’clock position, with a “broken” cap (arrow) indicating a former plaque rupture.
Figure 4. Palpograms were calculated using Jomed InVision Gold, a Jomed 20-MHz Avanar catheter, and a dedicated workstation for radio-frequency analysis. Palpography delivers strain information for the plaque surface. The right side of panel B represents the longitudinal view of the palpogram (top: distal LAD; bottom: proximal LAD). In the middle of panel B, a scale ranging from 0% (blue) to 2% (yellow) characterizes the strain pattern. The strain images are color coded; blue indicates stiff (low-strain) material, and red indicates softer (higher-strain) material. In the cross section shown on the left side of panel B, which is in a position identical to that in the IVUS image in panel A (40 MHz), an eccentric soft plaque is visible with shoulders of high strain (arrows) on either side of the otherwise stable cap. Between the 10 o’clock and 12 o’clock positions, the palpogram appears to show an area of high strain; however, this is caused by the nearby cardiac vein (AIV). The white line indicates the position of the cross section across the longitudinal map. Adjacent cross sections show the continuity of the soft caps forming a halo.
Footnotes
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Movies I and II are available in the online-only Data Supplement at http://www.circulationaha.org.
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The editor of Images in Cardiovascular Medicine is Hugh A. McAllister, Jr, MD, Chief, Department of Pathology, St Luke’s Episcopal Hospital and Texas Heart Institute, and Clinical Professor of Pathology, University of Texas Medical School and Baylor College of Medicine.
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Circulation encourages readers to submit cardiovascular images to the Circulation Editorial Office, St Luke’s Episcopal Hospital/Texas Heart Institute, 6720 Bertner Ave, MC1-267, Houston, TX 77030.
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- Detection of a Vulnerable Coronary Plaque
