A single-sampling strategy of combined ultra-sensitive copeptin and medium-sensitivity cardiac troponin I is noninferior to a 0- and 3-hour serial medium-sensitivity cardiac troponin I sampling in ruling out non-ST-segment elevation myocardial infarction and thus may allow an earlier discharge of patients who are ruled out for non-ST-segment elevation myocardial infarction (ClinicalTrials.gov Identifier NCT01962506).

Experience with angiotensin-receptor neprilysin inhibitors (ARNI) in oncologic patients with heart failure (HF) is limited. We report a case of ARNI started as first-choice therapy in a patient with relapsing hairy cell leukaemia (HCL) and HF with depressed left ventricular ejection fraction (LVEF). A middle-aged male, previously treated with rituximab for HCL, was scheduled for cardiologic screening before starting a new antineoplastic therapy for cancer relapse. The patient had symptomatic HF with reduced LVEF and high NT-proBNP levels. In this patient, early ARNI treatment was well tolerated and produced a rapid and durable improvement of symptoms, LVEF and NT-proBNP levels. Consequently, the oncologic team could start an experimental treatment with obinutuzumab, with complete HCL remission. In conclusion, in this patient with HCL and HF, ARNI therapy was safe and effective, contributing to undelayed cancer treatment.

SARS-CoV-2 infection is associated with an increased risk of venous thromboembolism (VTE), which is common during active illness but unusual in milder cases and after healing. We describe a case of bilateral acute pulmonary embolism occurring 3 months after recovery from a paucisymptomatic SARS-CoV-2 infection. The only VTE risk factor demonstrable was a history of previous SARS-CoV-2 infection, with laboratory signs of residual low-grade inflammation. Clinicians should be aware of VTE as a potential cause of sudden dyspnoea after COVID-19 resolution, especially in the presence of persistent systemic inflammation.

BACKGROUND: in patients hospitalized for heart failure with reduced ejection fraction (HFrEF), randomized controlled trials have demonstrated some advantages in starting sacubitril/valsartan before discharge. However, information about the effects of sacubitril/valsartan use in the acute phase of HfrEF hospitalizations is limited. AIM: To evaluate clinical, biomarker, and echocardiographic effects of starting sacubitril/valsartan in real-world HFrEF patients before discharge. METHODS: retrospective analysis of 124 consecutive patients (58.9% males, 75.6±11.4 years) hospitalized for HFrEF. In 36, sacubitril/valsartan was started before discharge (Group A); in the remaining 88, at the 1-month follow-up visit (Group B). The primary endpoint was time-averaged NT-proBNP level reduction from admission to discharge. RESULTS: Group A showed a worse baseline clinical risk profile (diabetes: 47.2 vs. 20.7%, p=0.007; coronary artery disease: 66.7 vs. 22.7%, p<0.001; systolic blood pressure: 118.0±20.8 vs. 132.9±22.9 mmHg, p=0.001; left ventricular ejection fraction: 28.5±5.5 vs. 32.1±7.6%, p<0.0004). Nevertheless, the time-averaged mean NT-proBNP reduction was significantly higher in group A patients (ratio of change -0.30, 95% CI -0.40 to -0.21, <0.0001 vs. group B). Creatinine and K+ levels did not change significantly during the hospital stay. Multivariate analysis suggested diabetes, coronary artery disease, higher systolic blood pressure, and the need for inotropic support as independent predictors for in-hospital sacubitril/valsartan treatment. CONCLUSIONS: in real-world patients, starting sacubitril/valsartan in-hospital rather than waiting for further stabilization was associated with a more considerable reduction of NT-proBNP levels at discharge, with an excellent safety profile. These data confirm randomized trials results, extending them to higher-risk real-world HFrEF patients.

Introduction Coronary microvascular dysfunction (CMD) is one of the possible manifestation of ischaemic heart disease with signs and symptoms of myocardial ischaemia, but no obstructive coronary artery disease (CAD). CMD is defined by an impaired coronary flow reserve owing to functional and/or structural abnormalities of the microcirculation and it is associated with adverse cardiovascular prognosis. Women are known to be more likely than men to have angina in the absence of obstructive CAD and CMD has been proposed as one of the major reasons for this presentation. However, also in men, CMD should be recognized, in order to give the best treatment to relieve symptoms and improve patient prognosis. Index of microvascular resistance (IMR) and coronary flow reserve (CFR) are needed to diagnose CMD and are now easily obtained with pressure wires measurement. Methods Since the adoption in our Cath Lab of the PressureWire™ X Guidewire with the Coroventis CoroFlow Cardiovascular System (Abbott) we started to study IMR and CFR in patients with no obstructive CAD and typical angina. No acute coronary syndromes have been studied in our Cath Lab so far. In this brief study we report a descriptive analysis of the first patients studied and of the first period of follow-up, focusing on men. Results From January 2022 (date when we received the new software) to April 2022 we studied 24 patients and 8 (33%) were men. Among men, mean age was 58±5 yo and two have been already treated with PCI during the previous 6 months. Mean ejection fraction was 57±2% and mean GFR was 76±20 ml/min/mq. 7 out of 8 patients were affected by dyslipidemia, 5 were smoker, 50% were affected by arterial hypertension and only 1 by diabetes. Mean RFR and FFR in left anterior descending artery were 0.92±0.02 and 0.92±0.03, respectively. In 6/8 (75%) patients IMR derived was &gt;25 and, among them 4 (66%) had CFR&lt;2. After coronary study we tried to optimize medical therapy in all these patients, adding or changing to Zofenopril previous ACE inhibitor therapy, adding or titrating Ranolazine and adding or titrating negative chronotropic therapy (beta blockers or calcium channel blockers). After therapy optimization none of the patients had resumption of symptoms (follow-up from 3 to 7 months). Conclusions Even if historically considered a women's disease, we should remember that CMD also affects men. New widespread technologies should be used systematically to rule out CMD and to define patients’ symptoms mechanisms. This would lead to targeted therapy that could improve patient's lives.