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Background ST‐segment–elevation myocardial infarction complicated with no reflow after primary percutaneous coronary intervention is associated with adverse outcomes. Although several hyperemic drugs have been shown to improve the Thrombolysis in Myocardial Infarction flow, optimal treatment of no reflow remains unsettled. Saline infusion at 20 mL/min via a dedicated microcatheter causes (flow‐mediated) hyperemia. The objective is to compare the efficacy of pharmacologic versus flow‐mediated hyperemia in patients with ST‐segment–elevation myocardial infarction complicated with no reflow. Methods and Results In the RAIN‐FLOW (Treatment of Slow‐Flow After Primary Percutaneous Coronary Intervention With Flow‐Mediated Hyperemia) study, 67 patients with ST‐segment–elevation myocardial infarction and no reflow were randomized to receive either pharmacologic‐mediated hyperemia with intracoronary adenosine or nitroprusside (n=30) versus flow‐mediated hyperemia (n=37). The angiographic corrected Thrombolysis in Myocardial Infarction frame count and the minimal microcirculatory resistance, as assessed with intracoronary pressure‐thermistor wire, dedicated microcatheter, and thermodilution techniques, were compared after study interventions. Both Thrombolysis in Myocardial Infarction frame count(40.2±23.1 versus 39.2±20.7; P=0.858) and minimal microcirculatory resistance (753.6±661.5 versus 993.3±740.8 Wood units; P=0.174) were similar between groups. Thrombolysis in Myocardial Infarction 3 flow was observed in 26.7% versus 27.0% (P=0.899). Flow‐mediated hyperemia showed 2 different thermodilution patterns during saline infusion indicative of the severity of the no reflow phenomenon. In‐hospital death and nonfatal heart failure were observed in 10.4% and 26.9%, respectively. Conclusions Both treatments showed similar (and limited) efficacy restoring coronary flow. Flow‐mediated hyperemia with thermodilution pattern assessment allowed the simultaneous characterization of the no reflow degree and response to hyperemia. No reflow was associated with a high rate of adverse outcomes. Further research is warranted to prevent and to treat no reflow in patients with ST‐segment–elevation myocardial infarction. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT04685941.

IntroductionPatients with diabetes mellitus (DM) have augmented platelet reactivity and diminished responsiveness to clopidogrel. Ticagrelor, a more potent P2Y12 inhibitor, is clinically superior to clopidogrel in acute coronary syndromes, although its role in chronic coronary syndromes (CCS) is still the subject of debate. The aim of this investigation was to compare the pharmacodynamic effectiveness of ticagrelor and clopidogrel in Mediterranean DM patients with CCS.Materials and methodsIn this prospective, randomized, crossover study, patients (n = 20) were randomized (1:1) to receive, on top of aspirin therapy, either ticagrelor 180 mg loading dose (LD)/90 mg maintenance dose (MD) b.i.d. or clopidogrel 600 mg LD/75 mg MD o.d. for 1 week in a crossover fashion with a 2–4 week washout period between regimens. Platelet function measurements were performed at 4 timepoints in each period (baseline, 2 h and 24 h after LD, and 1 week), including light transmission aggregometry (LTA, primary endpoint), VASP assay, Multiplate and VerifyNow P2Y12.ResultsThe ticagrelor LD achieved greater platelet inhibitory effect than clopidogrel LD, assessed with LTA (20 μM ADP as agonist), at 2 h (34.9 ± 3.9% vs. 63.6 ± 3.9%; p < 0.001) and 24 h (39.4 ± 3.5% vs. 52.3 ± 3.8%; p = 0.014). After 1 week of therapy, platelet reactivity was again significantly inferior with ticagrelor compared to clopidogrel (30.7 ± 3.0% vs. 54.3 ± 3.0%; p < 0.001). The results were consistent with the other platelet function assays employed.ConclusionIn Mediterranean patients with DM and CCS, ticagrelor provides a more potent antiplatelet effect than clopidogrel after the LD and during the maintenance phase of therapy.Clinical trial registration[ClinicalTrials.gov], identifier [NCT02457130].

Background Some concerns remain regarding the safety of transcarotid and transsubclavian approaches for transcatheter aortic valve replacement. We aimed to compare the risk of 30‐day complications and death in transcarotid/transsubclavian versus transfemoral transcatheter aortic valve replacement recipients. Methods and Results Data from 20 studies, including 79 426 patients (16 studies) and 3992 patients (4 studies) for the evaluation of the unadjusted and adjusted impact of the arterial approach were sourced, respectively. The use of a transcarotid/transsubclavian approach was associated with an increased risk of stroke when using unadjusted data (risk ratio [RR], 2.28; 95% CI, 1.90–2.72) as well as adjusted data (odds ratio [OR], 1.53; 95% CI, 1.05–2.22). The pooled results deriving from unadjusted data showed an increased risk of 30‐day death (RR, 1.46; 95% CI, 1.22–1.74) and bleeding (RR, 1.53; 95% CI, 1.18–1.97) in patients receiving transcatheter aortic valve replacement through a transcarotid/transsubclavian access (compared with the transfemoral group), but the associations between the arterial access and death (OR, 1.22; 95% CI, 0.89–1.69), bleeding (OR, 1.05; 95% CI, 0.68–1.61) were no longer significant when using adjusted data. No significant effect of the arterial access on vascular complication was observed in unadjusted (RR, 0.84; 95% CI, 0.66–1.06) and adjusted (OR, 0.79; 95% CI, 0.53–1.17) analyses. Conclusions Transcarotid and transsubclavian approaches for transcatheter aortic valve replacement were associated with an increased risk of stroke compared with the transfemoral approach. However, these nonfemoral arterial alternative accesses were not associated with an increased risk of 30‐day death, bleeding, or vascular complication when taking into account the confounding factors.

Transcatheter tricuspid valve intervention (TTVI) has recently emerged as an alternative for the treatment of severe tricuspid regurgitation (TR). Multiple percutaneous devices have been developed in the last decade with promising early results. Among them, the coaptation devices are designed to reduce TR severity by valve leaflet plication or occupying the regurgitant orifice with a spacer. To date, the MitraClip/TriClip devices (Abbott, Santa Clara, CA, USA), the PASCAL system (Edwards Lifesciencies, Irvine, CA, USA), and the FORMA device (Edwards Lifesciencies, Irvine, CA, USA) have been used as coaptation devices for treating severe TR. The present document aimed to review the clinical evidence on coaptation devices in the field of TTVI, describing its design characteristics, main procedural steps, and early and mid-term outcomes.

Paciente de 64 años con infarto agudo de miocardio con elevación del segmento ST por oclusión de la descendente anterior al que se implantó un armazón vascular bioabsorbible (AVB) directo de 3 × 18 mm (figura 1A-C). Posteriormente tuvo buena evolución bajo tratamiento con ácido acetilsalicílico y atorvastatina. A los 52 meses presentó reinfarto anterior por oclusión del mismo segmento de la descendente anterior. Se realizó tromboaspiración con recuperación del flujo (figura 1D-E), y por tomografía de coherencia óptica se visualizaron remanentes de struts, aunque prácticamente indiscernibles en el segmento del AVB. La trombosis se atribuyó a rotura de placa lipídica neoateroesclerótica (figura 1H-I, vídeo del material adicional). En la figura 1G-L se señalan los marcadores del AVB (almohadilla) y la presencia de la neoplaca lipídica rota (asterisco y flecha, respectivamente). Se implantó un stent metálico liberador de fármaco en el interior del stent (figura 1F). Figura 1. El objetivo principal de los AVB es eliminar el riesgo de trombosis muy tardía una vez que el dispositivo ha desaparecido. En diversas series de trombosis muy tardías en stents metálicos liberadores de fármaco, una de las causas principales visualizadas por tomografía de coherencia óptica es la rotura de una placa neoateroesclerótica lipídica...

Sixty-four year-old male patient with ST-segment elevation acute myocardial infarction due to occlusion of his anterior descending artery who received one 3 × 18 mm direct bioresorbable vascular scaffold (BVS) (figure 1A-C). Then he received acetylsalicylic acid and atorvastatin. Fifty-two months later he experienced an anterior reinfarction due to the occlusion of the same segment of the anterior descending artery. Thrombo-aspiration with flow recovery (figure 1D-E) was conducted and the optical coherence tomography showed strut remnants almost indistinguishable in the BVS segment. Thrombosis was attributed to a tear in the neoatherosclerotic lipid plaque (figura 1H-I, video of the supplementary data). Figures figura 1G-L show the BVS markers (pound sign) and the presence of the aforementioned torn lipid plaque (asterisk and arrow, respectively). One drug-eluting metallic stent was implanted inside the stent (figura 1F). Figure 1. The primary goal of BVSs is to eliminate the risk of very late thrombosis once the device is gone. In several series of very late thromboses in drug-eluting metallic stents, one of the main causes seen in the optical coherence tomography is the tear of the neoatherosclerotic lipid-laden plaque (26% to 31%). Therefore, we should expect a significant drop in...

Abstract Background In patients undergoing left atrial appendage (LAA) closure, an accurate sizing of the LAA is key to optimize device sizing, procedural success and reduce complications. Previous studies have shown that intraprocedural volume loading increases LAA dimensions and improves device sizing. However, the safety and effects on LAA and device sizing of administering a fluid bolus during pre-procedural transesophageal echocardiography (TEE) are unknown. The aim of this study was to determine the safety and impact on LAA dimensions and device sizing of an intravenous (IV) fluid bolus administered during TEE in the setting of the pre-procedural work-up for LAA closure. Methods The study included a total of 72 patients who underwent TEE to assess suitability for LAAC and received a 500 ml IV bolus of normal saline. The LAA landing zone (LZ) and depth were measured by TEE before and after volume loading, and these measurements were used to predict the device size implanted during a subsequent percutaneous LAAC procedure. Results There were no complications associated with volume loading. The baseline mean LZ was 19.6 ± 3.6 mm at 90o, and 20.2 ± 4.1 mm at 135o. Following fluid bolus, the maximum diameter increased 1.5 ± 1.0 mm at 90o (p