Teaching has employed more and more digital and online tools, especially nowadays with the COVID-19 pandemic. IoT has been notoriously troublesome for teaching due to its multidisciplinary nature, involving fields such as computing, electrical engineering, business, humanities studies, and others. Several methodologies have been developed to teach IoT and create solutions, including the Three Phase Methodology (TpM). This paper presents the development of an Integrated Digital Learning Environment (IDLE-IoT), for distance teaching of IoT, based on TpM and Bloom's Taxonomy, integrated with a hardware platform.

The Internet of Things (IoT) is a multidisciplinary field involving different areas of knowledge. The development of IoT solutions depends on the integration and collaborative work between professionals from all of these areas. This has led to the development of methodologies to teach IoT, such as the three‐phase methodology (TpM). This study presents a collaborative system that operationalizes the use of the TpM, aiding in the process of teaching IoT. This system guides and integrates teams developing IoT solutions while providing easy and structured access to information about the project. The system has been used in short and graduation courses. The results have demonstrated its efficiency in assisting students to develop solutions while applying the TpM.

Background Despite recent advances in treatment, heart failure (HF) continues to be associated with high mortality rates. In this setting, 123iodine-meta-iodobenzylguanidine (123I-MIBG) scintigraphy emerges as a promising tool for the prediction of clinical outcomes in HF due to its ability to assess cardiac sympathetic innervation. However, 123I-MIBG scintigraphy's correlation with myocardial remodeling and cardiopulmonary exercise capacity has not yet been fully elucidated. Objectives To evaluate cardiac sympathetic activity through 123I-MIBG scintigraphy, and to analyze its correlation with myocardial remodeling and exercise capacity in HF patients. Methods Symptomatic HF patients (NYHA class II–III) stratified by LVEF as HFpEF (LVEF 45%) and HFrE'F (LVEF <45%) and healthy controls were enrolled. HF patients were euvolemic under optimized treatment at the time of enrollment. All individuals underwent CMR with morphology/function and extracellular volume fraction (ECV) assessment, global longitudinal strain (GLS) by echocardiogram, cardiopulmonary exercise testing (CPET), cardiac sympathetic imaging 123I-MIBG scintigraphy (mIBG), and NT-proBNP. Results Eighty individuals were recruited allocated into the following groups: HFpEF (n=33, 59.42±12.63 years, LVEF: 59.82±9.87, NT-proBNP: 409.40±693.37, H2FPEF-score: 5±2), HFrEF (n=28, 53.93±11.40 years; LVEF: 29.81±8.67, NT-proBNP: 1662,34±2016,73) and healthy controls (42.65±13.96 years, LVEF: 65.27±4.73, NT-proBNP: 44,43±33,28) were enrolled. While ECV was elevated in HF groups (HFpEF: 0.32±0.05%, HFrEF: 0.31±0.41% and controls: 0.26±0.03, p<0.05), adjusted maximum oxygen consumption (VO2max) was markedly reduced vs. controls (HFpEF: 18.58±6.29mL/kg/min, HFrEF: 17.60±3.89mL/kg/min, controls: 29.73±9.98mL/kg/min, p<0.001). The MIBG heart-to-mediastinum ratio at 4 hours (H/M) was significantly lower in HF compared with controls (HFpEF: 1.59±0.25, HFrEF: 1.45±0.15 and controls: 1.92±0.25, p<0.001). Interestingly, the H/M ratio was more impaired with HFrEF compared to HFpEF (Fig. 1A). As a result, the mean myocardial washout rate was increased in HF patients (HFrEF 36.38±14.35, HFpEF 29.92±18.33 vs. controls 8.0±27.01, p<0.001). In addition, considering all HF patients, H/M was inversely associated with ECV (R: −0.45, p<0.001, Fig. 1B), NT-proBNP (R: −0.55, p<0.001) and VO2max (R: −0.27, p: <0.024, Fig. 1C). GLS was inversely associated with H/M in HFrEF but not HFpEF (HFrEF: R: −0.535, p<0.001 and HFpEF: R: −0.036, p=NS, Fig. 1D). Conclusion Cardiac sympathetic activity assessed by 123I-MIBG was abnormal in patients with HF with reduced and preserved EF as compared to controls. H/M, a validated marker for cardiac sympathetic activity, showed a strong correlation with markers of functional capacity and myocardial remodeling. Sympathetic innervation appears to be a limiting factor for global longitudinal strain in HFrEF, while in HFpEF longitudinal strain is independent of sympathetic activity Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): The São Paulo Research Foundation

Background An abnormal increase of cardiomyocyte mass of the left ventricle is observed in physiological and pathological phenotypes of hypertrophy. Aims To apply CMR tissue characterization using native T1/T2 and post-contrast T1 mapping and identify tissue phenotypes corresponding to physiological and pathological hypertrophy, in athletes and heart failure (HF), respectively. Methods/Results 187 individuals were prospectively enrolled, in 4 groups: Athletes (n=56, 32±13 years), HF with and without preserved ejection fraction (HFpEF: n=49, 62±12 years; HFrEF: n=49, 54±16 years, H2FpEF-score: 4.8 [3–9]), and healthy controls (n=33, 41±13.7 years). All participants underwent cardiopulmonary exercise testing and a multiparametric CMR study to assess morphology/function, T2, native T1, extracellular volume fraction (ECV), and intracellular lifetime of water (a marker of cardiomyocyte diameter). As expected, LVEF varied significantly among groups (Athletes: 64.7±6.1%, HFpEF: 59.3±10.7%, HFrEF: 29.4±8.5%, and controls: 65.4±4.3%, p<0.001) and was markedly reduced in HFrEF. Both LV mass index (Athletes: 64.1±15.8 g/m2, HFpEF: 62.3±24 g/m2, HFrEF: 79.5±36.7 g/m2, and controls: 42±9.2 g/m2, p<0.001) and cardiomyocyte mass index (calculated as (1 − ECV) x LV mass/BSA) (Athletes: 47.9±13.1 g/m2, HFpEF: 42.2±17.2 g/m2, HFrEF: 55.69±24.70 g/m2, and controls: 30.7±6.9 g/m2, p<0.001, Fig. 1A) were elevated in athletes and HF, compared to controls. Athletes and HFpEF patients showed concentric LV remodeling, while the eccentric LV remodeling was observed in HFrEF (Fig. 1B). In the HF groups NT-proBNP was elevated (Athletes: 34.6±16.8 ng/dL, HFpEF: 473.2±700.1 ng/dL, HFrEF: 1,365.3±1,772 ng/dL, and controls: 34.3±29 ng/dL, p<0.005), and adjusted maximum oxygen consumption was markedly reduced (Athletes: 49.4±9.3 mL/kg/min, HFpEF: 18.3±5.5 mL/kg/min, HFrEF: 17.1±4.2 mL/kg/min, and controls: 30.3±10.2 mL/kg/min, p<0.005). ECV was larger in both HF groups (athletes: 0.27±0.04, HFpEF: 0.31±0.05, HFrEF: 0.32±0.04, and controls: 0.26±0.02, p<0.001). The intracellular lifetime of water was longer among athletes compared to controls and shorter in HFrEF compared to HFpEF (Athletes: 0.17±0.07, HFpEF: 0.15±0.05, HFrEF: 0.13±0.05, and controls: 0.14±0.05, p<0.001). Native T1 was reduced in athletes compared to controls and elevated in the HF groups (Athletes: 1,173.4±63.2 ms, HFpEF: 1,262.8±62.4 ms, HFrEF: 1,275.1±59.9 ms, and controls: 1,212.78±76.01 ms, p<0.001). Lastly, the an increased T2 was indicative of edema in HF patients (Fig. 2). Conclusions In a prospective observational study with CMR T1/T2 mapping, physiological hypertrophy is characterized by increased cardiomyocyte diameter, normal ECV, and a decrease in native T1, due to the larger cardiomyocyte volume. In contrast, with pathological hypertrophy in HF, is associated with an increased and an above-normal native T1. Cardiomyocyte diameter appears reduced in HFrEF compared to HFpEF, reflecting the transition to an eccentric LV shape. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): The São Paulo Research Foundation

Background ATTR-related Familial Amyloid Polyneuropathy (FAP) is a hereditary disease that primarily affects peripheral nerve function. Few studies have investigated cardiac involvement and myocardial tissue remodeling in FAP. Aim To investigate subclinical myocardial tissue remodeling in FAP patients without cardiomyopathy using a multiparametric CMR protocol. Results Thirty-one FAP patients (46.9±16.1 years, 57% female, 60% Val30Met mutation) and 33 healthy controls (41.3±13.7 years, 58% female) were enrolled, undergoing a multiparametric CMR protocol for assessment of ventricular morphology and function, native myocardial T1, extracellular volume fraction (ECV) and intracellular lifetime of water). Cardiopulmonary exercise capacity was evaluated with a cycle ergometer. Cardiac high-sensitive troponin T (cTnT) and NT-proBNP were measured to assess for cardiac injury. The majority of ATTR-PN patients were in stage 1 (70%) with mild symptoms of sensory, motor and autonomic neuropathy. Adjusted maximum oxygen consumption was reduced among FAP patients compared to healthy controls (FAP: 22.2±8.2 mL/kg/min vs. controls: 30.3±10.2 mL/kg/min, p<0.001). Although none of FAP patients reported heart failure symptoms, NT-proBNP (FAP: 251.240±624.446 ng/dL, vs. controls: 34.3±29 ng/dL, p<0.005) and cTnT (FAP: 13.2 [3.0, 19.0] ng/dL, vs. controls: 3.6 [3.0, 6.0] ng/dL, p<0.005) were elevated, and both correlated with ECV (cTnT: R=0.81, P<0.001; NT-proBNP: R=0.61, P=0.001, Fig. 1). While LVEF was preserved among FAP patients (FAP: 67.9±8.2% vs. controls: 65.4±4.3%, p=NS), LVmass index was increased compared to control subjects (FAP: 58.5±18.8 vs. and controls: 42±9.2 g/m2, p<0.005). Both native T1 (FAP: 1,303.924±120.152, vs. controls: 1,212.78±76.01 ms, p<0.05) and ECV (FAP: 0.36±0.1, vs. controls: 0.26±0.02, p<0.001) were markedly elevated among FAP patients. In contrast the intracellular lifetime of water, a validated marker of cardiomyocyte size was reduced in the FAP group (FAP: 0.082±0.04 vs. controls: 0.14±0.05, p<0.001). There was a trend for ECV to increase linearly with FAP stage, and native T1 trended higher in stage 1 and 2 patients compared to stage 0. Both ECV (R=0.89, p<0.001) and native T1 (R=0.62, p<0.001) were correlated with LVmass index (Fig 2). Conclusion In FAP without clinical signs of cardiac involvement, significant extracellular matrix expansion was present. The increase of LV mass in these patients is associated with expansion of the extracellular matrix, possibly as a result of diffuse replacement fibrosis, and below-normal cardiomyocyte diameter. These findings from serum biomarkers and CMR tissue phenotyping provide evidence of sub-clinical cardiac involvement through adverse myocardial tissue remodeling in FAP patients presenting with mostly mild symptoms of peripheral neuropathy. Funding Acknowledgement Type of funding sources: Private company. Main funding source(s): Pfizer