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High-intensity rosuvastatin therapy over 13 months is associated with regression of coronary atherosclerosis in non-infarct-related arteries without changes in RF-IVUS defined necrotic core or plaque phenotype among STEMI patients.

Aims Due to bioprosthetic valve degeneration, aortic valve-in-valve (ViV) procedures are increasingly performed. There are no data on long-term outcomes after aortic ViV. Our aim was to perform a large-scale assessment of long-term survival and reintervention after aortic ViV. Methods and results A total of 1006 aortic ViV procedures performed more than 5 years ago [mean age 77.7 ± 9.7 years; 58.8% male; median STS-PROM score 7.3% (4.2–12.0)] were included in the analysis. Patients were treated with Medtronic self-expandable valves (CoreValve/Evolut, Medtronic Inc., Minneapolis, MN, USA) (n = 523, 52.0%), Edwards balloon-expandable valves (EBEV, SAPIEN/SAPIEN XT/SAPIEN 3, Edwards Lifesciences, Irvine, CA, USA) (n = 435, 43.2%), and other devices (n = 48, 4.8%). Survival was lower at 8 years in patients with small-failed bioprostheses [internal diameter (ID) ≤ 20 mm] compared with those with large-failed bioprostheses (ID > 20 mm) (33.2% vs. 40.5%, P = 0.01). Independent correlates for mortality included smaller-failed bioprosthetic valves [hazard ratio (HR) 1.07 (95% confidence interval (CI) 1.02–1.13)], age [HR 1.21 (95% CI 1.01–1.45)], and non-transfemoral access [HR 1.43 (95% CI 1.11–1.84)]. There were 40 reinterventions after ViV. Independent correlates for all-cause reintervention included pre-existing severe prosthesis–patient mismatch [subhazard ratio (SHR) 4.34 (95% CI 1.31–14.39)], device malposition [SHR 3.75 (95% CI 1.36–10.35)], EBEV [SHR 3.34 (95% CI 1.26–8.85)], and age [SHR 0.59 (95% CI 0.44–0.78)]. Conclusions The size of the original failed valve may influence long-term mortality, and the type of the transcatheter valve may influence the need for reintervention after aortic ViV.

Background: Platypnea-orthodeoxia syndrome (POS) is a rare clinical phenomenon, associating normal oxygen saturation in a supine position and arterial hypoxemia in an upright position. This pathology can be secondary to an intracardiac shunt, a pulmonary vascular shunt or a ventilation-perfusion mismatch. Cardiac POS occurs in the presence of a right-to-left cardiac shunt, most commonly through a patent foramen ovale (PFO). Methods and results: From our single-center prospective database of percutaneous PFO closure we identified five patients (4 females, mean age: 77 ± 11 years) out of 224 (2.2%) patients with a PFO who presented with a POS of cardiac origin. Transthoracic and transoesophageal echocardiographic examinations revealed the underlying mechanisms of POS and the diagnosis was confirmed by right-and-left cardiac catheterization (RLC) and by measuring serial blood oxygen saturation in the pulmonary veins and left atrium in supine and upright positions. PFO was associated with atrial septal aneurysm and a persistent prominent Eustachian valve in 3 patients. All patients underwent a successful percutaneous PFO closure without any immediate or subsequent complications (mean follow-up of 24 ± 18 months). Immediately after the procedure, mean arterial oxygen saturation improved from 83% ± 3 to 93% ± 2 in an upright position and symptoms disappeared. Conclusion: POS is a rare and under-diagnosed pathology that must be actively investigated in the presence of position-dependent hypoxemia. The diagnostic work-up must exclude other causes of hypoxemia and confirm the intracardiac shunt using either contrast echocardiography or RLC. For cardiac POS, percutaneous PFO closure is a safe and effective technique that immediately relieves orthodeoxia and patient symptoms.

Background— Pulmonary arterial hypertension (PAH) may develop in patients with atrial septal defects (ASD); however, little is known about associated risk factors and its evolution after transcatheter ASD closure. Methods and Results— We conducted a cohort study on 215 adults with attempted transcatheter ASD closure from 1999 to 2006. Patients were classified according to baseline systolic pulmonary artery pressures as having no (I, <40 mm Hg), mild (II, 40 to 49 mm Hg), moderate (III, 50 to 59 mm Hg), or severe (IV, ≥60 mm Hg) PAH. Independent predictors of moderate or severe PAH were older age (odds ratio [OR], 1.10 per year; P <0.0001), larger ASD (OR, 1.13 per millimeter; P =0.0052), female sex (OR, 3.9; P =0.0313), and at least moderate tricuspid regurgitation (OR, 3.6; P =0.0043). At 15 (interquartile range, 8 to 43) months post–ASD closure, patients with higher baseline pressures were more likely to experience a ≥5-mm Hg decrease (33.7%, 73.9%, 79.2%, and 100.0% in groups I to IV, P <0.0001), with a larger magnitude of reduction (0, 8, 17, and 22 mm Hg; P <0.0001). However, normalization of pressures (<40 mm Hg) occurred less frequently in patients with more advanced PAH (90.2%, 71.7%, 66.7%, and 23.5%, P <0.0001). Among patients with moderate or severe PAH, independent predictors of normalization were lower baseline pressures (OR, 0.91 per mm Hg; P =0.0418) and no more than mild tricuspid regurgitation (OR, 0.14; P =0.0420). Conclusion— In adults with ASDs, severity of PAH is modulated by age, sex, defect size, and degree of tricuspid regurgitation. Patients with moderate or severe PAH may benefit from substantial reductions in pulmonary artery pressures after transcatheter ASD closure, although the PAH values remain elevated in a sizeable proportion.