Focused broadband miniature polyvinylidene fluoride-trifluoroethylene (PVDF TrFE) ultrasonic transducers were investigated for intravascular (IVUS) second-harmonic imaging. Modeling and experimental studies demonstrated that focused transducers, unlike conventional flat transducers, build up second harmonic peak pressures faster and stronger, leading to an increased SNR of second harmonic content within the coronary geometry. Experimental results demonstrated that focused second harmonic pressures could be controlled to occur at specific depths by controlling the f-number of the transducer. The experimental results were in good agreement with the modeled results. Experiments were conducted using three imaging modalities: fundamental 20 MHz (F20), second harmonic 40 MHz (H40), and fundamental 40 MHz (F40). The lateral resolutions for a 1-mm transducer (f-number 3.2) at F20, F40, and H40 were experimentally measured to be 162, 123, and 124 microm, respectively, which agreed well with the theoretical calculations with <<8% error. Lateral resolution was further characterized in the three modes, using a micromachined phantom consisting of fixed bars and spaces with widths ranging from 20 to 160 microm. H40 exhibited better lateral resolution, clearly displaying 40- and 60-microm bars with about 4 dB and 7 dB greater signal strength compared with F20. Ex vivo human aorta images were obtained in the second-harmonic imaging mode to show the feasibility of high resolution second-harmonic IVUS using focused transducers.

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Thin-cap fibroatheromas (TCFA) are prone to plaque rupture and thrombosis. Intravascular ultrasound (IVUS) virtual histology (VH) assesses plaque composition and lesion morphology in vivo. Methods & Results: We used serial (baseline and follow-up @11 mos) VH-IVUS to study non-culprit plaque morphology in 221 lesions (plaque burden >40%) in 106 pts. Lesions were classified into 4 types based on plaque composition; pathological intimal thickening (PIT), thin-capped fibroatheroma (TCFA), thick-capped fibroatheroma (ThCFA), fibrotic/fibrocalcific. At baseline, 21 lesions were TCFAs (confluent necrotic core contacting to the lumen). Overall during follow-up (Figure ), 16/21 (76%) TCFAs healed: 13 became ThCFAs, 2 TCFAs became PIT, 1 TCFA became fibrotic, and 5 TCFAs (24%) remains unchanged although the location of the necrotic core in contact with the lumen shifted axially. Compared to TCFAs that healed, TCFAs that remained TCFAs were more often proximal in location (distance from coronary ostium to the lesion of 19±6 vs. 41±22mm, respectively, p=0.037) and had larger lumen area (9.9±3.1 vs. 6.9±1.8 mm2, p=0.013), vessel area (22.8±6.4 vs. 15.3±2.6 mm2, p=0.001), plaque area (12.9±4.9 vs. 8.4±1.7 mm2, p=0.005), calcium area (1.3±0.6 vs. 0.6±0.3 mm2, p=0.014), and necrotic core area (2.6±1.0 vs. 1.6±0.7 mm2, p=0.015). In addition, 6 new TCFAs developed; these 6 late-developing TCFAs had the appearance of PIT at baseline (Figure ). Conclusion: Although most TCFAs seem to stabilize or heal during 12 mos follow-up, proximal TCFAs in larger vessels with more plaque and calcium and a larger necrotic core appear to heal less often and new TCFAs can develop.

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