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Aims: The Non-adherence Academic Research Consortium (NARC) has recently developed a consensus-based standardized classification for medication non-adherence in cardiovascular clinical trials. We aimed to assess the prevalence of NARC-defined self-reported non-adherence to P2Y12 inhibitors and its impact on clinical outcomes in patients undergoing percutaneous coronary intervention (PCI). Methods and results: Using a standardized questionnaire administered at 1 year after PCI, we assessed the 4 NARC-defined non-adherence levels including type, decision-maker, reasons, and timing within the Bern PCI registry. The primary endpoint was the patient-oriented composite endpoint (POCE) defined as a composite of death, myocardial infarction, stroke, and any revascularization at 1 year. The recommended P2Y12 inhibitor duration was 12 months. Among 3,896 patients, P2Y12 inhibitor non-adherence was observed in 647 (17%) patients. Discontinuation was permanent in the majority of patients (84%). The decision was mainly driven by a physician (94%), and rarely by patients (6%). The most frequent reason was risk profile change (43%), followed by unlisted reasons (25%), surgery (17%), and adverse events (14%). Non-adherence occurred early (<30 days) in 21%, late (30–180 days) in 45%, and very late (>180 days) in 33%. The majority of POCE events (n = 421/502, 84%) occurred during adherence to the prescribed P2Y12 inhibitor. Permanent discontinuation, doctor-driven non-adherence, and risk profile change emerged as independent predictors for POCE. Conclusions: In real-world PCI population treated with 1-year DAPT, non-adherence was observed in nearly one-fifth of patients. Non-adherence to P2Y12 inhibitors was associated with worse clinical outcomes, while the risk was related to underlying contexts. ClinicalTrials.gov identifier: NCT02241291. [ABSTRACT FROM AUTHOR]

Aims To validate the set of clinical and biochemical criteria proposed by consensus by the Academic Research Consortium (ARC) for High Bleeding Risk (HBR) for the identification of HBR patients. These criteria were categorized into major and minor , if expected to carry in isolation, respectively, ≥4% and <4% Bleeding Academic Research Consortium (BARC) 3 or 5 bleeding risk within 1-year after percutaneous coronary intervention (PCI). High bleeding risk patients are those meeting at least 1 major or 2 minor criteria. Methods and results All patients undergoing PCI at Bern University Hospital, between February 2009 and September 2018 were prospectively entered into the Bern PCI Registry (NCT02241291). Age, haemoglobin, platelet count, creatinine, and use of oral anticoagulation were prospectively collected, while the remaining HBR criteria except for planned surgery were retrospectively adjudicated. A total of 16 580 participants with complete ARC-HBR criteria were included. After assigning 1 point to each major and 0.5 point to each minor criterion, we observed for every 0.5 score increase a step-wise augmentation of BARC 3 or 5 bleeding rates at 1 year ranging from 1.90% among patients fulfilling no criterion, through 4.01%, 5.98%, 7.42%, 8.60%, 12.21%, 12.29%, and 17.64%. All major and five out of six minor criteria, conferred in isolation a risk for BARC 3 or 5 bleeding at 1 year exceeding 4% at the upper limit of the 95% confidence intervals. Conclusion All major and the majority of minor ARC-HBR criteria identify in isolation patients at HBR. Open in new tab Download slide Open in new tab Download slide [ABSTRACT FROM AUTHOR]

This study examined the value of endothelial shear stress (ESS) estimated in 3-dimensional quantitative coronary angiography (3D-QCA) models in detecting plaques that are likely to progress and cause events. Cumulative evidence has shown that plaque characteristics and ESS derived from intravascular ultrasound (IVUS)−based reconstructions enable prediction of lesions that will cause cardiovascular events. However, the prognostic value of ESS estimated by 3D-QCA in nonflow limiting lesions is yet unclear. This study analyzed baseline virtual histology (VH)-IVUS and angiographic data from 28 lipid-rich lesions (i.e., fibroatheromas) that caused major adverse cardiovascular events or required revascularization (MACE-R) at 5-year follow-up and 119 lipid-rich plaques from a control group that remained quiescent. The segments studied by VH-IVUS at baseline were reconstructed using 3D-QCA software. In the obtained geometries, blood flow simulation was performed, and the pressure gradient across the lipid-rich plaque and the mean ESS values in 3-mm segments were estimated. The additive value of these hemodynamic indexes in predicting MACE-R beyond plaque characteristics was examined. MACE-R lesions were longer, had smaller minimum lumen area, increased plaque burden (PB), were exposed to higher ESS, and exhibited a higher pressure gradient. In multivariable analysis, PB (hazard ratio: 1.08; p = 0.004) and the maximum 3-mm ESS value (hazard ratio: 1.11; p = 0.001) were independent predictors of MACE-R. Lesions exposed to high ESS (>4.95 Pa) with a high-risk anatomy (minimal lumen area <4 mm2 and PB >70%) had a higher MACE-R rate (53.8%) than those with a low-risk anatomy exposed to high ESS (31.6%) or those exposed to low ESS who had high- (20.0%) or low-risk anatomy (7.1%; p < 0.001). In the present study, 3D-QCA-derived local hemodynamic variables provided useful prognostic information, and, in combination with lesion anatomy, enabled more accurate identification of MACE-R lesions. [ABSTRACT FROM AUTHOR]

This study sought to examine the utility of multimodality intravascular imaging and of the endothelial shear stress (ESS) distribution to predict atherosclerotic evolution. There is robust evidence that intravascular ultrasound (IVUS)-derived plaque characteristics and ESS distribution can predict, with however limited accuracy, atherosclerotic evolution; nevertheless, it is yet unclear whether multimodality imaging and ESS mapping enable more accurate prediction of coronary plaque progression. A total of 44 patients admitted with a myocardial infarction that had successful revascularization and 3-vessel IVUS and optical coherence tomography (OCT) imaging at baseline and 13-month follow-up were included in the study. The IVUS data acquired at baseline in the nonculprit vessels were fused with x-ray angiography to reconstruct coronary anatomy and in the obtained models blood flow simulation was performed and the ESS was estimated. The baseline plaque characteristics and ESS distribution were used to identify predictors of disease progression: defined as a lumen reduction and an increase in plaque burden at follow-up. Seventy-three vessels were included in the final analysis. Baseline ESS and the IVUS-derived but not the OCT-derived plaque characteristics were independently associated with a decrease in lumen area and an increase in plaque burden. Low ESS (odds ratio: 0.45; 95% confidence interval: 0.28 to 0.71; p < 0.001) and plaque burden (odds ratio: 0.73; 95% confidence interval: 0.54 to 0.97; p = 0.030) were the only independent predictors of disease progression at follow-up. The accuracy of the IVUS-derived plaque characteristics in predicting disease progression did not improve when ESS (AUC: 0.824 vs. 0.847; p = 0.127) or when OCT variables and ESS (AUC: 0.842; p = 0.611) were added into the model. ESS and OCT-derived variables did not improve the efficacy of IVUS in predicting disease progression. Further research is required to investigate whether multimodality imaging combined with ESS mapping will allow more reliable vulnerable plaque detection. (Comparison of Biomatrix Versus Gazelle in ST-Elevation Myocardial Infarction [STEMI] [COMFORTABLE]; NCT00962416) [ABSTRACT FROM AUTHOR]

This study assessed changes in optical coherence tomography (OCT)-defined plaque composition in patients with ST-elevation myocardial infarction (STEMI) receiving high-intensity statin treatment. OCT is a high-resolution modality capable of measuring plaque characteristics including fibrous cap thickness (FCT) and macrophage infiltration. There is limited in vivo evidence regarding the effects of statins on OCT-defined coronary atheroma composition and no evidence in the context of STEMI. In the IBIS-4 (Integrated Biomarker Imaging Study-4), 103 patients underwent intravascular ultrasonography and OCT of 2 noninfarct-related coronary arteries in the acute phase of STEMI. Patients were treated with high-dose rosuvastatin for 13 months. Serial OCT imaging was available in 153 arteries from 83 patients. We measured FCT by using a semi-automated method. Co-primary endpoints consisted of the change in minimum FCT (measured in fibroatheromas) and change in macrophage line arc. At 13 months, median low-density lipoprotein cholesterol had decreased from 128 mg/dl to 73.6 mg/dl. Minimum FCT, measured in 31 lesions from 27 patients, increased from 64.9 ± 19.9 μm to 87.9 ± 38.1 μm (p = 0.008). Macrophage line arc decreased from 9.6° ± 12.8° to 6.4° ± 9.6° (p < 0.0001). The secondary endpoint, mean lipid arc, decreased from 55.9° ± 37° to 43.5° ± 33.5°. In lesion-level analyses (n = 191), 9 of 13 thin-cap fibroatheromata (TCFAs) at baseline (69.2%) regressed to non-TCFA morphology, whereas 2 of 178 non-TCFA lesions (1.1%) progressed to TCFAs. In this observational study, we found significant increase in minimum FCT, reduction in macrophage accumulation, and frequent regression of TCFAs to other plaque phenotypes in nonculprit lesions of patients with STEMI treated with high-intensity statin therapy. [ABSTRACT FROM AUTHOR]

Aims To examine the efficacy of angiography derived endothelial shear stress (ESS) in predicting atherosclerotic disease progression. Methods and results Thirty-five patients admitted with ST-elevation myocardial infarction that had three-vessel intravascular ultrasound (IVUS) immediately after revascularization and at 13 months follow-up were included. Three dimensional (3D) reconstruction of the non-culprit vessels were performed using (i) quantitative coronary angiography (QCA) and (ii) methodology involving fusion of IVUS and biplane angiography. In both models, blood flow simulation was performed and the minimum predominant ESS was estimated in 3 mm segments. Baseline plaque characteristics and ESS were used to identify predictors of atherosclerotic disease progression defied as plaque area increase and lumen reduction at follow-up. Fifty-four vessels were included in the final analysis. A moderate correlation was noted between ESS estimated in the 3D QCA and the IVUS-derived models (r  = 0.588, P  < 0.001); 3D QCA accurately identified segments exposed to low (<1 Pa) ESS in the IVUS-based reconstructions (AUC: 0.793, P  < 0.001). Low 3D QCA-derived ESS (<1.75 Pa) was associated with an increase in plaque area, burden, and necrotic core at follow-up. In multivariate analysis, low ESS estimated either in 3D QCA [odds ratio (OR): 2.07, 95% confidence interval (CI): 1.17–3.67; P  = 0.012) or in IVUS (<1 Pa; OR: 2.23, 95% CI: 1.23–4.03; P  = 0.008) models, and plaque burden were independent predictors of atherosclerotic disease progression; 3D QCA and IVUS-derived models had a similar accuracy in predicting disease progression (AUC: 0.826 vs. 0.827, P  = 0.907). Conclusions 3D QCA-derived ESS can predict disease progression. Further research is required to examine its value in detecting vulnerable plaques. [ABSTRACT FROM AUTHOR]

Background: The study aims to assess characteristics and outcomes of patients suffering a mechanical complication (MC) after ST-segment elevation myocardial infarction (STEMI) in a contemporary cohort of patients in the percutaneous coronary intervention era. Methods and results: This retrospective single-center cohort study encompasses 2508 patients admitted with STEMI between March 9, 2009 and June 30, 2014. A total of 26 patients (1.1%) suffered a mechanical complication: ventricular septal rupture (VSR) in 17, ventricular free wall rupture (VFWR) in 2, a combination of VSD and VFWR in 2, and papillary muscle rupture (PMR) in 5 patients. Older age (74.5 ± 10.4 years versus 63.9 ± 13.1 years, p < 0.001), female sex (42.3% versus 23.3%, p = 0.034), and a longer latency period between symptom onset and angiography (> 24h: 42.3% versus 16.2%, p = 0.002) were more frequent among patients with MC as compared to patients without MC. The majority of MC patients had multivessel disease (77%) and presented in cardiogenic shock (Killip class IV: 73.1%). Nine patients (7 VSR, 2 VFWR & VSR) were treated conservatively and died. Out of the remaining 10 VSR patients, four underwent surgery, three underwent implantation of an occluder device, and another three patients had surgical repair following occluder device implantation. All patients with isolated VFWR and PMR underwent emergency surgery. At 30 days, mortality for VSR, VFWR, VFWR & VSR and PMR amounted to 71%, 50%, 100% and 0%, respectively. Conclusions: Despite advances in the management of STEMI patients, mortality of mechanical complications stays considerable in this contemporary cohort. Older age, female sex, and a prolonged latency period between symptom onset and angiography are associated with the occurrence of these complications. [ABSTRACT FROM AUTHOR]

Background: The purpose of the present study was to assess the short- and long-term progression of cardiac allograft vasculopathy (CAV) using serial 3-vessel quantitative coronary angiography (QCA). Methods: CAV progression was assessed using serial 3-vessel QCA analysis at baseline, 1-year and long-term angiographic follow-up (8.5±3.7 years) after heart transplantation. The change in minimal lumen diameter (MLD) and percent diameter stenosis (%DS) was serially assessed within matched segments. Patients were graded according to the ISHLT-CAV classification and grouped as ISHLT-CAV0 and ISHLT-CAV1-3. The primary endpoint was mean change in MLD and %DS. Results: A total of 41 patients and 520 matched segments were available for serial 3-vessel QCA. Overall, MLD decreased non-significantly from baseline to 1-year follow-up and significantly from 1-year to the long-term angiographic follow-up (Δ-0.08mm/year [95%CI -0.11 to -0.05], P<0.001). %DS increased significantly from baseline to 1-year (Δ+0.96%/year [95%CI 0.04 to 1.88], P = 0.041) and from 1-year to long-term angiographic follow-up (Δ+0.61%/year [95%CI 0.33 to 0.88], P<0.001). ISHLT-CAV1-3 at 1 year and at long-term angiographic follow-up was observed in 22% and 61%, respectively. Between baseline and long-term angiographic follow-up, a significant reduction in MLD was observed within both groups without a significant difference in the reduction between the two groups (ISHLT-CAV0: median -0.49mm [IQR -0.54 to -0.43] vs. ISHLT-CAV1-3: median -0.40mm [IQR -0.44 to -0.35], P = 0.4). Conclusion: The current data suggest that QCA can’t predict CAV beyond 1 year, but, QCA affirmed that CAV progresses to a similar extent in patients who do not develop visual CAV during long-term follow-up. [ABSTRACT FROM AUTHOR]

Background--Low endothelial shear stress (ESS) is associated with plaque progression and vulnerability. To date, changes in plaque phenotype over time in relation to ESS have not been studied in humans. The aim of this study was to investigate whether local ESS can predict subsequent changes to plaque phenotype using optical coherence tomography. Methods and Results--A total of 25 coronary arteries from 20 patients who underwent baseline and 6-month follow-up optical coherence tomography were included. Arteries were divided into serial 3-mm segments, and plaque characteristics were evaluated in each segment. A total of 145 segments were divided into low-ESS group (ESS <1 Pa) and higher- ESS group (ESS =1 Pa) based on baseline computational flow dynamics analyses. At baseline, low-ESS segments had significantly thinner fibrous cap thickness compared with higher-ESS segments (128.2±12.3 versus 165.0±12.0 µm; P=0.03), although lipid arc was similar. At follow-up, fibrous cap thickness remained thin in low-ESS segments, whereas it significantly increased in higher-ESS segments (165.0±12.0 to 182.2±14.1 µm; P=0.04). Lipid arc widened only in plaques with low ESS (126.4±15.2° to 141.1±14.0°; P=0.01). After adjustment, baseline ESS was associated with fibrous cap thickness (ß, 9.089; 95% confidence interval, 2.539-15.640; P=0.007) and lipid arc (β, -4.381; 95% confidence interval, -6.946 to -1.815; P=0.001) at follow-up. Conclusions--Low ESS is significantly associated with baseline high-risk plaque phenotype and progression to higher-risk phenotype at 6 months. [ABSTRACT FROM AUTHOR]

Aims Compared with bare metal stents, first-generation drug-eluting stents (DES) are associated with an increased risk of late restenosis and stent thrombosis (ST). Whether this risk continues or attenuates during long-term follow-up remains unknown. Methods and results We extended the follow-up of 1012 patients [sirolimus-eluting stent (SES): N = 503 and paclitaxel-eluting stent (PES): N = 509] included in the all-comers, randomized Sirolimus-Eluting vs. Paclitaxel-Eluting Stents for Coronary Revascularization (SIRTAX) trial to 10 years. Follow-up was complete in 895 patients (88.4%) at 10 years. At 1, 5, and 10 years of follow-up, rates of ischaemia-driven target lesion revascularization (ID-TLR) were 8.1%, 14.6% and 17.7%, respectively, and rates of ST were 1.9%, 4.5% and 5.6%, respectively. The annual risks of ID-TLR and definite ST were significantly higher between 1 and 5 years as compared with the 5- to 10-year period [ID-TLR: 1.8% vs. 0.7%/year, hazard ratio (HR) 0.36, 95% confidence intervals (95% CI) 0.21–0.62, P < 0.001; definite ST: 0.67% vs. 0.23%/year, HR 0.31, 95% CI 0.13–0.75, P = 0.01]. The attenuation of the risk of ID-TLR and ST beyond 5 years was independent of age. Major adverse events (cardiac death, myocardial infarction, and ID-TLR) occurred in 33.7% of SES-and 33.8% of PES-treated patients (P = 0.72). Conclusions During long-term follow-up through 10 years, the annual risks of ID-TLR and definite ST significantly decreased beyond 5 years after first-generation DES implantation. These findings may have important implications for secondary prevention after percutaneous coronary intervention with first-generation DES including long-term antiplatelet therapy. [ABSTRACT FROM AUTHOR]

Background--Cardiac troponin detected by new-generation, highly sensitive assays predicts clinical outcomes among patients with stable coronary artery disease (SCAD) treated medically. The prognostic value of baseline high-sensitivity cardiac troponin T (hs-cTnT) elevation in SCAD patients undergoing elective percutaneous coronary interventions is not well established. This study assessed the association of preprocedural levels of hs-cTnT with 1-year clinical outcomes among SCAD patients undergoing percutaneous coronary intervention. Methods and Results--Between 2010 and 2014, 6974 consecutive patients were prospectively enrolled in the Bern Percutaneous Coronary Interventions Registry. Among patients with SCAD (n=2029), 527 (26%) had elevated preprocedural hs-cTnT above the upper reference limit of 14 ng/L. The primary end point, mortality within 1 year, occurred in 20 patients (1.4%) with normal hs-cTnT versus 39 patients (7.7%) with elevated baseline hs-cTnT (P<0.001). Patients with elevated hscTnT had increased risks of all-cause (hazard ratio 5.73; 95% confidence intervals 3.34-9.83; P<0.001) and cardiac mortality (hazard ratio 4.68; 95% confidence interval 2.12-10.31; P<0.001). Preprocedural hs-TnT elevation remained an independent predictor of 1-year mortality after adjustment for relevant risk factors, including age, sex, and renal failure (adjusted hazard ratio 2.08; 95% confidence interval 1.10-3.92; P=0.024). A graded mortality risk was observed across higher tertiles of elevated preprocedural hs-cTnT, but not among patients with hs-cTnT below the upper reference limit. Conclusions--Preprocedural elevation of hs-cTnT is observed in one fourth of SCAD patients undergoing elective percutaneous coronary intervention. Increased levels of preprocedural hs-cTnT are proportionally related to the risk of death and emerged as independent predictors of all-cause mortality within 1 year. [ABSTRACT FROM AUTHOR]

Aims The purpose of the present study was to investigate the relationship between in-stent neoatherosclerosis (NA) and native atherosclerosis progression of untreated coronary segments. Methods and results In-stent NA was assessed by optical coherence tomography (OCT) among patients included in the SIRTAX-LATE OCT study 5 years after drug-eluting stent (DES) (sirolimus-eluting and paclitaxel-eluting stents) implantation. Neoatherosclerosis was defined as the presence of fibroatheroma or fibrocalcific plaque within the neointima of stented segments with a longitudinal extension >1.0 mm. Atherosclerosis progression in untreated native coronary segments was evaluated by serial quantitative coronary angiography (QCA). The change in minimal lumen diameter (MLD) was serially assessed within matched segments at baseline and 5-year angiographic follow-up. The key clinical endpoint was non-target lesion (non-TL) revascularization throughout 5 years. A total of 88 patients with 88 lesions were available for OCT analysis 5 years after DES implantation. In-stent NA was observed in 16% of lesions with the majority of plaques being fibroatheromas (11.4%) followed by fibrocalcific plaques (5.7%). A total of 704 non-TL segments were serially evaluated by QCA. Between baseline and 5-year follow-up, the reduction in MLD was significantly more pronounced in patients with NA (-0.25 mm, 95% CI -0.36 to -0.17 mm) when compared with patients without NA (-0.13 mm, 95% CI -0.17 to -0.10 mm, P = 0.002). Similarly, non-TL revascularization was more frequent in patients with NA (78.6%) when compared with patients without NA (44.6%, P = 0.028) throughout 5 years. Conclusions In-stent NA is more common among patients with angiographic and clinical evidence of native atherosclerosis progression suggesting similar pathophysiological mechanisms. [ABSTRACT FROM AUTHOR]

Background--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%). Compared with baseline, systolic pulmonary artery pressure immediately improved after TAVI in patients with postcapillary combined (57.8±14.1 versus 50.4±17.3 mm Hg; P=0.015) but not in those with precapillary (49.0±12.6 versus 51.6±14.3; P=0.36). When compared with no PH, a higher 1-year mortality rate was observed in both precapillary (hazard ratio, 2.30; 95% confidence interval, 1.02-5.22; P=0.046) and combined (hazard ratio, 3.15; 95% confidence interval, 1.43-6.93; P=0.004) but not isolated PH patients (P=0.11). After adjustment, combined PH remained a strong predictor of 1-year mortality after TAVI (hazard ratio, 3.28; P=0.005). Conclusions--Invasive stratification of PH according to hemodynamic presentation predicts acute response to treatment and 1-year mortality after TAVI. [ABSTRACT FROM AUTHOR]

Introduction: Anemia and renal impairment are important co-morbidities among patients with coronary artery disease undergoing Percutaneous Coronary Intervention (PCI). Disease progression to eventual death can be understood as the combined effect of baseline characteristics and intermediate outcomes. Methods: Using data from a prospective cohort study, we investigated clinical pathways reflecting the transitions from PCI through intermediate ischemic or hemorrhagic events to all-cause mortality in a multi-state analysis as a function of anemia (hemoglobin concentration <120 g/l and <130 g/l, for women and men, respectively) and renal impairment (creatinine clearance <60 ml/min) at baseline. Results: Among 6029 patients undergoing PCI, anemia and renal impairment were observed isolated or in combination in 990 (16.4%), 384 (6.4%), and 309 (5.1%) patients, respectively. The most frequent transition was from PCI to death (6.7%, 95% CI 6.1–7.3), followed by ischemic events (4.8%, 95 CI 4.3–5.4) and bleeding (3.4%, 95% CI 3.0–3.9). Among patients with both anemia and renal impairment, the risk of death was increased 4-fold as compared to the reference group (HR 3.9, 95% CI 2.9–5.4) and roughly doubled as compared to patients with either anemia (HR 1.7, 95% CI 1.3–2.2) or renal impairment (HR 2.1, 95% CI 1.5–2.9) alone. Hazard ratios indicated an increased risk of bleeding in all three groups compared to patients with neither anemia nor renal impairment. Conclusions: Applying a multi-state model we found evidence for a gradient of risk for the composite of bleeding, ischemic events, or death as a function of hemoglobin value and estimated glomerular filtration rate at baseline. [ABSTRACT FROM AUTHOR]

Aims Our aim was to evaluate the invasive haemodynamic indices of high-risk symptomatic patients presenting with ‘paradoxical’ low-flow, low-gradient, severe aortic stenosis (AS) (PLF-LG) and low-flow, low-gradient severe AS (LEF-LG) and to compare clinical outcomes following transcatheter aortic valve implantation (TAVI) among these challenging AS subgroups. Methods and results Of 534 symptomatic patients undergoing TAVI, 385 had a full pre-procedural right and left heart catheterization. A total of 208 patients had high-gradient severe AS [HGAS; mean gradient (MG) ≥40 mmHg], 85 had PLF-LG [MG ≤ 40 mmHg, indexed aortic valve area [iAVA] ≤0.6 cm2 m−2, stroke volume index ≤35 mL/m2, ejection fraction (EF) ≥50%], and 61 had LEF-LG (MG ≤ 40 mmHg, iAVA ≤0.6 cm2 m−2, EF ≤40%). Compared with HGAS, PLF-LG and LEF-LG had higher systemic vascular resistances (HGAS: 1912 ± 654 vs. PLF-LG: 2006 ± 586 vs. LEF-LG: 2216 ± 765 dyne s m−5, P = 0.007) but lower valvulo-arterial impedances (HGAS: 7.8 ± 2.7 vs. PLF-LG: 6.9 ± 1.9 vs. LEF-LG: 7.7 ± 2.5 mmHg mL−1 m−2, P = 0.027). At 30 days, no differences in cardiac death (6.5 vs. 4.9 vs. 6.6%, P = 0.90) or death (8.4 vs. 6.1 vs. 6.6%, P = 0.88) were observed among HGAS, PLF-LG, and LEF-LG groups, respectively. At 1 year, New York Heart Association functional improvement occurred in most surviving patients (HGAS: 69.2% vs. PLF-LG: 71.7% vs. LEF-LG: 89.3%, P = 0.09) and no significant differences in overall mortality were observed (17.6 vs. 20.5 vs. 24.5%, P = 0.67). Compared with HGAS, LEF-LG had a higher 1 year cardiac mortality (adjusted hazard ratio 2.45, 95% confidence interval 1.04–5.75, P = 0.04). Conclusion TAVI in PLF-LG or LEF-LG patients is associated with overall mortality rates comparable with HGAS patients and all groups profit symptomatically to a similar extent. [ABSTRACT FROM PUBLISHER]

Supplemental Digital Content is available in the text. Background—: Although ticagrelor has improved clinical outcomes among patients with acute coronary syndrome compared with clopidogrel, adherence to this new antiplatelet agent in real-world practice has not been fully investigated. Methods and Results—: Between November 2011 and June 2014, 1278 of 4831 consecutive patients (26.5%) undergoing percutaneous coronary intervention at a tertiary care center were treated with ticagrelor. Premature ticagrelor cessation was categorized into (1) change, when ticagrelor was replaced by prasugrel; (2) de-escalation, when ticagrelor was replaced by clopidogrel; and (3) premature discontinuation, when ticagrelor was discontinued without P2Y12 inhibitor replacement. Of 1278 patients treated with ticagrelor, premature treatment cessation occurred in 212 patients (17%). De-escalation to clopidogrel was the most frequent scenario (57%; n=120), followed by premature discontinuation (28%; n=60) and change to prasugrel (15%; n=32). Reasons for ticagrelor cessation included adverse effects (49%), initiation of oral anticoagulation (19%), and unspecified general practitioner preference (10%). Most frequent adverse effects leading to premature ticagrelor cessation were bleeding (41%), dyspnea (29%), and gastrointestinal symptoms (18%). Premature ticagrelor cessation was not associated with an increased risk of cardiac death, myocardial infarction, or stroke (hazard ratio, 0.73; 95% confidence interval: 0.40–1.32; P=0.29). Conclusions—: Premature ticagrelor cessation in routine clinical practice occurred in 1 of 6 patients and was primarily related to adverse effects among which bleeding and dyspnea were the most frequent. Although premature ticagrelor cessation was not associated with adverse cardiovascular outcomes, this finding requires careful interpretation in view of the modest sample size. Clinical Trial Registration—: URL: https://www.clinicaltrials.gov. Unique identifier: NCT02241291. [ABSTRACT FROM AUTHOR]

Fractional flow reserve (FFR) is regarded as the gold standard for the physiological assessment of intermediate coronary artery stenoses. However, FFR does not allow assessment of plaque morphology and lesion geometry. Intracoronary imaging techniques such as intravascular ultrasound (IVUS) and optical coherence tomography (OCT) can help treatment planning by optimising stent implantation, which can improve patient outcomes. The aim of this meta-analysis is to compare the efficacy of IVUS and OCT-derived metrics in detecting flow limiting stenoses in non-left main stem lesions. A systematic review of PubMed, Medline, and Cochrane databases was performed and identified studies examining the diagnostic accuracy of IVUS and OCT in detecting significant stenoses when compared to FFR. A total of 33 (7537 lesions) studies (24 IVUS, 7 OCT and 2 IVUS & OCT studies) were included in the meta-analysis. Pooled analysis showed that IVUS- and OCT-derived minimum lumen area (MLA) had a similar sensitivity in predicting haemodynamically significant lesions (IVUS-MLA: 0.747 vs OCT-MLA 0.732, p = 0.519). However, OCT-MLA had a higher specificity (0.763 vs 0.665, p < 0.001) and diagnostic accuracy in detecting flow-limiting stenoses than IVUS-MLA (AUC 0.810 vs 0.754, p = 0.045). Sub-analysis of the studies with the clinically significant FFR cut-off value of 0.80 yielded similar results demonstrating that OCT-MLA has a better accuracy than IVUS-MLA in detecting haemodynamically significant stenoses (AUC 0.809 vs 0.750, p = 0.034). OCT with its superior image resolution appears to be the preferable intravascular imaging modality for the detection of haemodynamically significant stenoses in non-left main stem lesions. • FFR allows accurate physiological assessment of intermediate coronary stenosis. • IVUS and OCT allow accurate assessment of vessel geometry and plaque morphology. • IVUS and OCT-derived MLA have similar sensitivity to detect flow limiting lesions. • OCT-derived MLA has the best diagnostic accuracy to identify significant stenosis. • The superiority of OCT-derived MLA is not affected by vessel size. [ABSTRACT FROM AUTHOR]

The prevalence of acute coronary syndromes (ACS) among young individuals is increasing, but the phenotypic characteristics, causes and clinical outcomes in this group have not been well described. Between 2009 and 2017, 8712 ACS patients underwent percutaneous coronary intervention (PCI) and were prospectively enrolled. We defined a young patient as female <50 years and male <45 years. The causes of ACS were defined by an adjudication committee. The primary endpoint was the patient-oriented composite endpoint (POCE) of all-cause mortality, myocardial infarction or any revascularization at 12 months. Among 8712 ACS patients, 472 (5.4%) patients were young (26% female). The main cause of ACS in young patients was atherosclerosis (86.5%), followed by coronary artery embolism (9%), and spontaneous coronary artery dissection (SCAD) (4.5%). POCE occurred less frequently in young compared to old patients (8.5% vs. 16.7%, hazard ratio 0.48 (95% confidence interval 0.35–0.66), p < 0.001). The rates of the individual components of the POCE were lower in young including all-cause mortality (3.2% versus 9.5%, 0.32 (0.19–0.54), p < 0.001), myocardial infarction (1.9% versus 3.7%, 0.49 (0.25–0.95), p = 0.035) and any revascularization (5.1% versus 7.4%, 0.65 (0.43–0.97), p = 0.037). Young patients with SCAD had a higher rate of death as compared to those with atherosclerosis, mainly attributed to cardiac deaths. One out of 20 ACS patients undergoing PCI was young and the principal cause was atherosclerosis. Young carry a lower risk for future events compared to older ACS patients. The underlying cause leading to ACS should be considered in appropriate risk stratification of young patients. Clinical Trial Registration: Clinicaltrials.gov. NCT02241291 • Approximately one out of 20 ACS patients undergoing PCI for ACS was young (female <50 years, male <45 years). • The principal mechanism of ACS in young patients was atherosclerosis (86.5%), followed by coronary artery embolism (CAE) (9%), and spontaneous coronary artery dissection (SCAD) (4.5%). • As compared to older patients, young patients had a lower risk for the primary endpoint POCE and for its individual components at 12 months. [ABSTRACT FROM AUTHOR]