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Percutaneous closure of atrial septal defect (ASD)/patent foramen ovale (PFO) can influence systemic hemodynamics. The aim of this research was to evaluate the influence of the closure procedure on morphological and functional characteristics of systemic vascular walls. Fourteen ASD (mean age 40 ± 16 years) and 14 PFO (45 ± 8 years) patients were enrolled in this retrospective study. All underwent percutaneous closure procedure; physical, clinical and biochemical evaluations; echocardiography; carotid evaluation; and brachial artery flow-mediated vasodilatation (FMD). All the evaluations were performed at the time of enrollment, 24 h post-procedure, at 1–6–12-month follow-up. FMD at enrollment was higher in PFO patients as compared to ASD (8.5% [7.6–10.7%] versus 6.5% [5.6–7.6%], p  < 0.0001). FMD values in ASD patients significantly increased during follow-up (enrollment: 6.5% [5.6–7.6%], 12-month follow-up: 8.8% [7.2–10.3%], p  < 0.01). PFO patients showed reduced FMD values 24 h after the procedure (enrollment: 8.5% [7.6–10.7%], 24 h post-procedure: 7% [6.3–9%], p  < 0.001), while recovering endothelial function during follow-up period to baseline values (FMD at 12-month follow-up: 8.2% [7.6–10.5%]). At one-year follow-up, FMD remained inversely related to systolic pulmonary arterial pressure and right and left atrial/ventricle chambers dimensions (RV proximal diameter efflux tract, right atrium [RA] longitudinal diameter, RA transverse diameter, RA area, left ventricle [LV] end-diastolic diameter, left atrium [LA] anteroposterior diameter, LA area; p  < 0.01) in ASD patients. Endothelial function improved after percutaneous closure of ASD, while remaining stable after PFO closure. Therefore, ASD patients seem to improve their cardiovascular risk profile after percutaneous closure of their defect.

This case report highlights an innovative surgical approach in orthotopic heart transplantation (OHT) for a patient with the largest recorded giant left atrium, measuring a biplanar volume of 1906 mL. The patient, a 63‐year‐old man with severe heart failure and a history of mitral and aortic valve replacements, presented with atrial fibrillation, moderate systolic dysfunction, and severe cardiomegaly. Despite optimized medical therapy, his condition warranted heart transplantation. The procedure involved a novel surgical technique utilizing Teflon reinforcement and a bovine pericardial patch to reconstruct the significantly enlarged left atrium. Postoperative outcomes were favorable, with no rejection episodes and resolution of pulmonary symptoms. This report underscores the challenges of atrial size mismatch in OHT and the necessity for tailored surgical strategies to address extreme anatomical variations. The successful outcome exemplifies the potential of customized approaches in complex heart transplant cases.

Left ventricular assist devices are an established therapy for end-stage heart failure. Follow-up of these patients showed complications, such as thrombosis. Our objective was to evaluate the contribution of echocardiography - in association with HeartWare HVAD online logfiles reviews and lactate dehydrogenase titration - for diagnosis and treatment of thrombosis. Seventeen episodes of thrombosis were diagnosed in 8/20 patients with HVAD. Diagnosis was made by trans-thoracic echocardiographic blood flow velocities, logfiles review of power consumption and pump flows, and titration of lactate dehydrogenase. Data were collected at baseline routine control (Group A), during thrombosis (Group B), after thrombolysis (Group C). Thrombolysis was successful in all cases; one patient died of cerebral haemorrhage. Echocardiographic maximal blood flow velocity near the inflow cannula was 598±42 cm/sec (Group B), 379.41±21 cm/sec (Group C), and 378.24±28 cm/sec (Group A) (P<0.00001). In eight (47%) cases, thrombi were visualized in the left ventricle by three-dimensional modality. Logfiles recordings of blood flows were 9.52±0.9 L/min (Group B), 4.02±0.4 L/min (Group C), and 4.04±0.4 L/min (Group A) (P<00001). Power consumption was 5.01±0.7 W (Group B), 3.45±0.2 W (Group C), and 3.46±0.2 W (Group A) (P<0.00001). Lactate dehydrogenase was 756±54 IU (Group B), 234±22 IU (Group A), and 257±36 IU (Group C) (P<0.00001). Echocardiography of increased maximal velocity near the inflow cannula is a sign of HVAD obstruction. Logfile reviews provide a clear picture of HVAD obstruction. Combination of echocardiographic data and review of logfiles detects signs of left ventricular assist devices thrombosis leading to a successful treatment.

We explored the significance of the L-Arginine/asymmetric dimethylarginine (L-Arg/ADMA) ratio as a biomarker of endothelial dysfunction in stroke patients. To this aim, we evaluated the correlation, in terms of severity, between the degree of endothelial dysfunction (by L-Arg/ADMA ratio), the methylene tetrahydrofolate reductase (MTHFR) genotype, and the interatrial septum (IAS) phenotype in subject with a history of stroke. Methods and Results: L-Arg, ADMA, and MTHFR genotypes were evaluated; the IAS phenotype was assessed by transesophageal echocardiography. Patients were grouped according to the severity of IAS defects and the residual enzymatic activity of MTHFR-mutated variants, and values of L-Arg/ADMA ratio were measured in each subgroup. Of 57 patients, 10 had a septum integrum (SI), 38 a patent foramen ovale (PFO), and 9 an ostium secundum (OS). The L-Arg/ADMA ratio differed across septum phenotypes (p ≤ 0.01), and was higher in SI than in PFO or OS patients (p ≤ 0.05, p ≤ 0.01, respectively). In the PFO subgroup a negative correlation was found between the L-Arg/ADMA ratio and PFO tunnel length/height ratio (p ≤ 0.05; r = − 0.37; R2 = 0.14). Interestingly, the L-Arg/ADMA ratio varied across MTHFR genotypes (p ≤ 0.0001) and was lower in subgroups carrying the most impaired enzyme with respect to patients carrying the conservative MTHFR (p ≤ 0.0001, p ≤ 0.05, respectively). Consistently, OS patients carried the most dysfunctional MTHFR genotypes, whereas SI patients the least ones. Conclusions: A low L-Arg/ADMA ratio correlates with impaired activity of MTHFR and with the jeopardized IAS phenotype along a severity spectrum encompassing OS, PFO with long/tight tunnel, PFO with short/large tunnel, and SI. This infers that genetic MTHFR defects may underlie endothelial dysfunction-related IAS abnormalities, and predispose to a cryptogenic stroke. Our findings emphasize the role of the L-Arg/ADMA ratio as a reliable marker of stroke susceptibility in carriers of IAS abnormalities, and suggest its potential use both as a diagnostic tool and as a decision aid for therapy.

Takotsubo cardiomyopathy (TTC) is a form of acute left ventricular dysfunction usually reversible and with favorable prognosis. Ventricular septal perforation (VSP) is a very rare life-threatening complication. Percutaneous closure of VSP, despite being challenging, is a possible alternative to surgical repair. We present the first case of an 84-year-old patient with a TTC-related VSP treated by percutaneous approach. The case highlights the need of reconsidering the worldwide accepted consideration of TTC as benignant and allows some speculations on the optimal management of VSP in terms of timing, patient selection and possible alternative interventions.

Nucleophosmin (NPM1) gene mutations rarely occur in non-acute myeloid neoplasms (MNs) with <20% blasts. Among nearly 10,000 patients investigated so far, molecular analyses documented NPM1 mutations in around 2% of myelodysplastic syndrome (MDS) cases, mainly belonging to MDS with excess of blasts, and 3% of myelodysplastic/myeloproliferative neoplasm (MDS/MPN) cases, prevalently classified as chronic myelomonocytic leukemia. These uncommon malignancies are associated with an aggressive clinical course, relatively rapid progression to overt acute myeloid leukemia (AML) and poor survival outcomes, raising controversies on their classification as distinct clinico-pathologic entities. Furthermore, fit patients with NPM1-mutated MNs with <20% blasts could benefit most from upfront intensive chemotherapy for AML rather than from moderate intensity MDS-directed therapies, although no firm conclusion can currently be drawn on best therapeutic approaches, due to the limited available data, obtained from small and mainly retrospective series. Caution is also suggested in definitely diagnosing NPM1-mutated MNs with blast count <20%, since NPM1-mutated AML cases frequently present dysplastic features and multilineage bone marrow cells showing abnormal cytoplasmic NPM1 protein delocalization by immunohistochemical staining, therefore belonging to NPM1-mutated clone regardless of blast morphology. Further prospective studies are warranted to definitely assess whether NPM1 mutations may become sufficient to diagnose AML, irrespective of blast percentage.