T he advent of coronary stents in conjunction with potent adjunctive medical treatment has resulted in substantial improvements in the efficacy and safety of percutaneous coronary interventions (PCIs).1 Although infrequent, stent thrombosis remains an important concern because of its sequelae, including myocardial infarction and death in up to 80%. 2,3 Early stent thrombosis is largely independent of stent type and mainly related to procedural variables, including major edge dissections and stent underexpansion. 4 Conversely, the mechanisms underlying very late stent thrombosis (VLST), occurring beyond 1 year after drug-eluting stent (DES) implantation, remain poorly defined, and the translation of mechanistic insights into therapeutic approaches is unsatisfactory. Despite an attenuation of the risk for VLST with the use of newer-generation DES, which is similar to that of bare metal stents, the accumulated long-term risk is still notable. Clinical Perspective on p 660Because of its high resolution (10-20 μm), optical coherence tomography (OCT) has become the imaging modality of choice for the in vivo assessment of stent failures, including VLST. 5 As a result of the infrequent encounter of this Background-The pathomechanisms underlying very late stent thrombosis (VLST) after implantation of drug-eluting stents (DES) are incompletely understood. Using optical coherence tomography, we investigated potential causes of this adverse event. Methods and Results-Between August 2010 and December 2014, 64 patients were investigated at the time point of VLST as part of an international optical coherence tomography registry. Optical coherence tomography pullbacks were performed after restoration of flow and analyzed at 0.4 mm. A total of 38 early-and 20 newer-generation drug-eluting stents were suitable for analysis. VLST occurred at a median of 4.7 years (interquartile range, 3.1-7.5 years). An underlying putative cause by optical coherence tomography was identified in 98% of cases. The most frequent findings were strut malapposition (34.5%), neoatherosclerosis (27.6%), uncovered struts (12.1%), and stent underexpansion (6.9%). Uncovered and malapposed struts were more frequent in thrombosed compared with nonthrombosed regions (ratio of percentages, 8.26; 95% confidence interval, 6.82-10.04; P<0.001 and 13.03; 95% confidence interval, 10. 13-16.93; P<0.001, respectively). The maximal length of malapposed or uncovered struts (3.40 mm; 95% confidence interval, 2.55-4.25; versus 1.29 mm; 95% confidence interval, 0.81-1.77; P<0.001), but not the maximal or average axial malapposition distance, was greater in thrombosed compared with nonthrombosed segments. The associations of both uncovered and malapposed struts with thrombus were consistent among early-and newer-generation drug-eluting stents. Conclusions-The leading associated findings in VLST patients in descending order were malapposition, neoatherosclerosis, uncovered struts, and stent underexpansion without differences between patients treated with early-and new...
P ulmonary hypertension (PH) frequently coexists with severe aortic stenosis (AS) and confers a worse prognosis.1,2 Transcatheter aortic valve implantation (TAVI) is an alternative therapeutic modality to surgical aortic valve replacement (SAVR) for patients with symptomatic severe AS who are either inoperable or high risk for conventional SAVR.3-5 Patient selection for TAVI relies on clinical and anatomic factors, and risk assessment is a critical component of the procedural planning. 6 Previous studies have shown PH to be a predictor of mortality after TAVI. [7][8][9][10][11] However, studies to date have focused mainly on PH severity rather than hemodynamic presentation and used noninvasive measurements of pulmonary artery systolic pressure (PASP), which correlate only modestly with invasive measurements.12 According toBackground-Pulmonary hypertension (PH) frequently coexists with severe aortic stenosis, and PH severity has been shown to predict outcomes after transcatheter aortic valve implantation (TAVI). The effect of PH hemodynamic presentation on clinical outcomes after TAVI is unknown. Methods and Results-Of 606 consecutive patients undergoing TAVI, 433 (71.4%) patients with severe aortic stenosis and a preprocedural right heart catheterization were assessed. Patients were dichotomized according to whether PH was present (mean pulmonary artery pressure, ≥25 mm Hg; n=325) or not (n=108). Patients with PH were further dichotomized by left ventricular end-diastolic pressure into postcapillary (left ventricular end-diastolic pressure, >15 mm Hg; n=269) and precapillary groups (left ventricular end-diastolic pressure, ≤15 mm Hg; n=56). Finally, patients with postcapillary PH were divided into isolated (n=220) and combined (n=49) subgroups according to whether the diastolic pressure difference (diastolic pulmonary artery pressure−left ventricular end-diastolic pressure) was normal (<7 mm Hg) or elevated (≥7 mm Hg). Primary end point was mortality at 1 year. PH was present in 325 of 433 (75%) patients and was predominantly postcapillary (n=269/325; 82%
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