Persistent pulmonary hypertension of the newborn (PPHN) is one of the main causes of neonatal morbidity and mortality. It is characterized by sustained elevation of pulmonary vascular resistance (PVR), preventing an increase in pulmonary blood flow after birth. The affected neonates fail to establish blood oxygenation, precipitating severe respiratory distress, hypoxemia, and eventually death. Inhaled nitric oxide (iNO), the only approved pulmonary vasodilator for PPHN, constitutes, alongside supportive therapy, the basis of its treatment. However, nearly 40% of infants are iNO resistant. The cornerstones of increased PVR in PPHN are pulmonary vasoconstriction and vascular remodeling. A better understanding of PPHN pathophysiology may enlighten targeted and more effective therapies. Sildenafil, prostaglandins, milrinone, and bosentan, acting as vasodilators, besides glucocorticoids, playing a role on reducing inflammation, have all shown potential beneficial effects on newborns with PPHN. Furthermore, experimental evidence in PPHN animal models supports prospective use of emergent therapies, such as soluble guanylyl cyclase (sGC) activators/stimulators, l-citrulline, Rho-kinase inhibitors, peroxisome proliferator-activated receptor-γ (PPAR-γ) agonists, recombinant superoxide dismutase (rhSOD), tetrahydrobiopterin (BH4) analogs, ω-3 long-chain polyunsaturated fatty acids (LC-PUFAs), 5-HT2A receptor antagonists, and recombinant human vascular endothelial growth factor (rhVEGF). This review focuses on current knowledge on alternative and novel pathways involved in PPHN pathogenesis, as well as recent progress regarding experimental and clinical evidence on potential therapeutic approaches for PPHN.

With advances in scanner technology, postprocessing techniques, and the development of novel positron emission tomography (PET) tracers, the applications of PET for the study of coronary heart disease have been gaining momentum in the last few years. Depending on the tracer and acquisition protocol, cardiac PET can be used to evaluate the atherosclerotic lesion (plaque imaging) and to assess its potential consequences—ischemic versus nonischemic (perfusion imaging) and viable versus scarred (viability imaging) myocardium. The scope of this review is to summarize the role of PET in coronary heart disease.

Background Covid-19 is associated with an increased risk of pulmonary embolism (PE) therefore, should the cut off d-dimer value be adjusted for these patients? Material and methods Retrospective and observational study to understand if there is a d-dimer cut-off that could guide clinics to perform a thoracic computed tomography angiography (CTA) in patients with covid-19. The population was covid-19 patients admitted to covid-19 dedicated wards of a University Hospital Centre for one year. Results and conclusions 725 (52%) patients with covid-19 had a d-dimer value dosed during the first 5 days of the disease. Those, 63 (9%) did a CTA with a diagnosis of 16 (25%) PE. Gender was equally represented, median age was 70 years (ID = 3.49) and the majority (94%) survived. Thirteen (81%) patients with PE had a d-dimer value above 2500 ng/mL (OR = 9.244, 95% CI 2.248–9.837), with 7 (54%) with values over 10000 ng/mL, but in 3 (9%) it was under 1500 ng/mL. Seventy-three (63%) of patients with a d-dimer over 1500 ng/mL did not had a thoracic CTA performed. In our population PE was not a frequent outcome. The results are influenced by the low number of thoracic CTA performed because, even tough the cut-off d-dimer value used at our hospital to perform a thoracic CTA to exclude PE is 1500 ng/mL, most patients with that d-dimer value did not take the exam and so PE could not be excluded. Although in most PE cases the d-dimer value was above 2500 ng/mL, the results of our study cannot verify if that is a better cut-off value.

Background:In elderly patients, single chamber pacing may be considered. For sinus rhythm patients, VDD pacemaker (PM), by preserving atrial sensing, is a more physiological mode than VVI devices. This study aims to evaluate the long-term performance of VDD PM in elderly patients with atrioventricular block (AVB). Methods: We conducted a retrospective, observational study of 200 elderly patients (≥75 years) with AVB and normal sinus rhythm who consecutively implanted VDD PM between 2016 and 2018. Baseline clinical characteristics were analyzed, complications related to pacemaker implantation were assessed and a 3-years follow-up (FUP) was made. Results: Mean age was 84 ± 5 years. After 3-years FUP, 90.5% (n = 181) of the patients preserved their original VDD mode. Only 19 patients (9.5%) switched to VVIR mode, 5.5% (n = 11) due to P-wave undersensing and 4% (n = 8) due to permanent AF. Those patients had a less amplitude of sensed P wave at baseline [median value of 1.30 (IQR 0.99-2.0) versus 0.97 (IQR 0.38-1.68), p = 0.04]. One third of the patients died dur-ing the FUP, 89% (n = 58) from non-cardiovascular causes. All-cause, CV, and non-CV mortality did not relate with atrial sensing loss during FUP (p = 0.58, p = 0.38 and p = 0.80, respectively). However, atrial sensing loss during FUP was associated with de novo atrial fibrillation (12.7% vs. 31.6%, p = 0.038). Conclusion:VDD pacing is a reliable pacing modality in elderly patients even in longterm. The majority of VDD-paced elderly patients maintained their original VDD mode program, with good atrial sensing.

No abstract