Background: A multidisciplinary approach might be pivotal for the management of patients with valvular heart disease (VHD), but clinical outcome data are lacking. Methods and Results: At our institution, since 2014, internal guidelines recommended heart team consultations for patients with VHD. The clinical/echocardiographic characteristics, treatment recommendations, performed treatment, and early clinical outcomes of consecutive, hospitalized patients with VHD undergoing heart team evaluation were collected. Surgical risk was prospectively assessed by the EuroSCORE II and STS‐PROM. The primary end point of the study was early mortality. A total of 1004 patients with VHD with high clinical complexity (mean age, 75 years; mean EuroSCORE II, 9.4%; mean STS‐PROM, 5.6%; 48% ischemic heart disease; 29% chronic kidney disease, 9% oncologic/hematologic diseases) were enrolled. The heart team recommended an interventional treatment for 807 (80%) patients and conservative management for 197 (20%) patients. Management crossovers occurred in only 5% of patients. The recommended intervention was cardiac surgery for 230 (23%) patients, percutaneous treatment in 516 (51%) patients, and hybrid treatment in 61 (6%) patients. Early mortality occurred in 24 patients (2.4%) and was independently predicted by aortic stenosis, left ventricular ejection fraction, pulmonary artery systolic pressure, and conservative management recommendation. In patients referred to treatment, observed early mortality (1.7%) was significantly lower ( P <0.001) than expected on the bases of both the STS‐PROM (5.2%) and EuroSCORE II (9.7%). Conclusions: Within the limitations of its single‐center and observational design, the present study suggests that heart team–based management of patients with complex VHD is feasible and allows referral to a wide spectrum of interventions with promising early clinical results.

Background: the RIGENERA trial assessed the efficacy of granulocyte-colony stimulating factor (G-CSF) in the improvement of clinical outcomes in patients with severe acute myocardial infarction. However, there is no evidence available regarding the long-term safety and efficacy of this treatment. Methods: in order to evaluate the long-term effects on the incidence of major adverse events, on the symptom burden, on the quality of life and the mean life expectancy and on the left ventricular (LV) function, we performed a clinical and echocardiographic evaluation together with an assessment using the Minnesota Living with Heart Failure Questionnaire (MLHFQ) and the Seattle Heart Failure Model (SHFM) at 10-years follow-up, in the patients cohorts enrolled in the RIGENERA trial. Results: thirty-two patients were eligible for the prospective clinical and echocardiography analyses. A significant reduction in adverse LV remodeling was observed in G-CSF group compared to controls, 9% vs. 48% (p = 0.030). The New York Heart Association (NYHA) functional class was lower in G-CSF group vs. controls (p = 0.040), with lower burden of symptoms and higher quality of life (p = 0.049). The mean life expectancy was significantly higher in G-CSF group compared to controls (15 ± 4 years vs. 12 ± 4 years, p = 0.046. No difference was found in the incidence of major adverse events. Conclusions: this longest available follow-up on G-CSF treatment in patients with severe acute myocardial infarction (AMI) showed that this treatment was safe and associated with a reduction of adverse LV remodeling and higher quality of life, in comparison with standard-of-care treatment.

Background: In ST-segment elevation myocardial infarction (STEMI), predictors of subclinical dysfunction of remote myocardium are unknown. We prospectively aimed at identifying clinical and biochemical correlates of remote subclinical dysfunction and its impact on left ventricular ejection fraction (LVEF).Methods: One-hundred thirty-three patients (63.9 ± 12.1 years, 68% male) with first successfully treated (54% anterior, 46% non-anterior, p = 0.19) STEMI underwent echocardiography at 5 ± 2 days after onset and at 8 ± 2-month follow-up, and were compared to 13 age and sex-matched (63.3 ± 11.4) healthy controls. All 16 left ventricular (LV) segments were grouped into ischemic, border, and remote myocardium: mean value of longitudinal strain (LS) within grouped segments were expressed as iLS, bLS, rLS, respectively. LV end-diastolic (EDV), end-systolic (ESV) volumes indexed for body surface area (EDVi, ESVi, respectively), LVEF and global LS (GLS) were determined. Creatinine, glomerular filtration rate, admission level of NT-pro-brain-natriuretic peptide (NT-proBNP) and troponin peaks were considered for the analysis.Results: At baseline, rLS (15.5 ± 4.4) was better than iLS (12.9 ± 4.8, p < 0.001), but lower than that in controls (19.1 ± 2.7, p < 0.001) and similar to bLS (15 ± 5.4, p = ns), and did not differ between patients with single or multivessel coronary artery disease (CAD). At multivariate regression analysis, only admission NT-proBNP levels but not peak Tn levels independently predicted rLS (β = −0.58, p = 0.001), as well as iLS (β = −0.52, p = 0.001). Both at baseline and at follow-up, rLS correlated to LVEF similarly to iLS and bLS (p < 0.001 for all). Median value of rLS at baseline was 15%: compared to patients with rLS ≥ 15% at baseline, patients with rLS < 15% showed lower LVEF (52.3 ± 9.4 vs. 58.6 ± 7.6, p < 0.001) and GLS (16.3 ± 3.9 vs. 19.9 ± 3.2), and higher EDVi (62.3 ± 19.9 vs. 54 ± 12, p = 0.009) and ESVi (30.6 ± 15.5 vs. 22.3 ± 7.6, p < 0.001) at follow-up.Conclusion: In optimally treated STEMI, dysfunction of remote myocardium assessed by LS: (1) is predicted by elevated NT-proBNP; (2) could be independent of CAD extent and infarct size; (3) is associated to worse LV morphological and functional indexes at follow-up.

Background: Non-ST-elevation myocardial infarction (NSTEMI) and unstable angina (UA) are caused often by destabilization of non-flow limiting inflamed coronary artery plaques. ¹⁸F-fluorodeoxyglucose (FDG) uptake with positron emission tomography/computed tomography (PET/CT) reveals plaque inflammation, while intracoronary optical coherence tomography (OCT) reliably identifies morphological features of coronary instability, such as plaque rupture or erosion. We aimed to prospectively compare these two innovative biotechnologies in the characterization of coronary artery inflammation, which has never been attempted before. Methods: OCT and FDG PET/CT were performed in 18 patients with single vessel coronary artery disease, treated by percutaneous coronary intervention (PCI) with stent implantation, divided into 2 groups: NSTEMI/UA (n = 10) and stable angina (n = 8) patients. Results: Plaque rupture/erosion recurred more frequently [100% vs 25%, p = 0.001] and FDG uptake was greater [TBR median 1.50 vs 0.87, p = 0.004] in NSTEMI/UA than stable angina patients. FDG uptake resulted greater in patients with than without plaque rupture/erosion [1.2 (0.86–1.96) vs 0.87 (0.66–1.07), p = 0.013]. Among NSTEMI/UA patients, no significant difference in FDG uptake was found between ruptured and eroded plaques. The highest FDG uptake values were found in ruptured plaques, belonging to patients with NSTEMI/UA. OCT and PET/CT agreed in 72% of patients [p = 0.018]: 100% of patients with plaque rupture/erosion and increased FDG uptake had NSTEMI/UA. Conclusion: For the first time, we demonstrated that the correspondence between increased FDG uptake with PET/CT and morphology of coronary plaque instability at OCT is high.