We reported a case of 46–year–old women without cardiovascular risk factors, with a diagnosis of relapsed metastatic melanoma undergoing treatment with immune check–point inhibitors (ICI), ipilimumab and nivolumab. A transthoracic echocardiogram was performed before starting the treatment that showing normal indices of biventricular function and a normal value of global longitudinal strain (GLS). After the third immunotherapy cycle, she presented to the hospital for diplopia and blurred vision; in the suspicion of ICI–related toxicity, muscle–specific enzymes and troponin I high sensitivity (TnI hs) were assayed and were found elevated (TnI hs 712 ng/L). Brain natriuretic peptide (BNP), electrocardiogram (ECG) and echocardiogram were within the limits. Given the positivity of cardiac markers in an asymptomatic patient, it was concluded for grade I ICI–related toxicity. Immunotherapy was discontinued and the patient was admitted to the cardiology intensive care unit. She underwent telemetry monitoring and a cardiac magnetic resonance (CMR) were performed showing a thin stria of sub–epicardial oedema along anterior wall without late gadolinium enhancement or altered kinetics. During hospitalization, patient was treated with methylprednisolone 1g i.v. for the first days with benefit and she was discharged with oral prednisolone, reducing the dose by 10 mg/week under clinical, ECG and TnI surveillance. I.v. immunoglobulins were started due to myopathy involvement. The tapering of corticosteroids after 15 days caused a flare–up of troponin levels, which resolved after increasing the steroid dosage. After a thorough discussion between experts, it was decided to resume ICI treatment. Myocarditis is a severe complication of ICI that occurs in 0.27–1.14% of patients and develops early. Surveillance should be done by biomarker assay, as major cardiac events occur in up to 40% of patients with normal ejection fraction. The clinical diagnosis includes the cTn elevation with 1 major criterion (CMR positive for Lake Louis criteria) or 2 minor criteria. The treatment strategy consists of interruption of ICI therapy, immunosuppressive agents and cardiac monitoring. Current guidelines recommend permanently ending ICI therapy when patients develop grade 3 or 4 toxicities; conversely, it may be considered again in case of grade 1 (asymptomatic biomarker elevation) or 2 (biomarker elevation and mild symptoms) toxicity.

Background Pericardial agenesis (1) is a congenital developmental disorder of the pleuro–pericardial membranes that is usually asymptomatic. A pericardial cyst (2) is a congenital cyst composed of mesothelial cells originating most often from the right pericardium. Hypoplasia of the posterior mitral leaflet (3) is congenital and it is very rarely diagnosed in adulthood. These alterations are usually sporadic and not associated. Case presentation A 53–year–old woman with obesity and bronchial asthma was referred to the emergency department for left hemiparesis and concomitant dyspnoea in new–onset atrial fibrillation. A right frontal ischemic stroke was diagnosed. During the hospitalization transthoracic echocardiography was performed showing a large prolapsed anterior mitral leaflet (AML) with an eccentric and significant regurgitation. Transesophageal echocardiography was performed. It confirmed the severity of mitral regurgitation, due to a large AML prolapse, but also showed a severely hypoplastic posterior leaflet (PML). Swinging motion was also reported in the absence of pericardial effusion. In the past the patient was surgically treated for an anterior pericardial cyst that was excised. Old CT images were reviewed and showed the absence of pericardial sheets along posterior and lateral left ventricle walls, which were not contiguous to the cyst (that was anterior). The patient was finally candidated to surgery for mitral valve replacement. Discussion The case report shows a unique case of association between partial pericardial agenesis, pericardial cyst, severe PML hypoplasia with AML prolapse and severe mitral regurgitation. The association of these three anomalies has never been described before. This could indicate a common pathogenetic denominator and therefore the need to look for this combination of structural abnormalities in carriers of even just one of them. Bibliography 1. Lopez D. et al, doi: 10.1016/j.pcad.2016.12.002 2. Khayata M. et al, doi: 10.1007/s11886–019–1153–5 3. Parato VM. et al, doi: 10.4103/jcecho.jcecho_73_17

Background Procalcitonin (PCT) is an acute phase protein which plasma levels raise also in sterile inflammation. For this reason, its role in the acute coronary syndrome (ACS) setting would be twofold: as a marker of infection and also as a prognosticator of generic inflammation. High PCT values have been related to worse prognosis in patients with cardiogenic shock. If PCT values may predict the risk of bacterial infections and long–term outcome in patients with acute coronary syndromes has been less investigated. Methods Consecutive patients with a diagnosis of ACS with PCT level assessed during the first 24 hours of hospitalization were enrolled. The primary outcome was the occurrence of bacterial infection defined by the occurrence of fever and of at least one positive blood or urinary culture with clinical signs of infection. The secondary outcome was the 1–year occurrence of the composite outcome all–cause mortality, stroke and myocardial infarction. Results Overall 569 patients have been enrolled (mean age 69.37±14 years, 30% females): 44 (8%) of them met criteria for bacterial infection. Age, female sex, smoking habit, heart rate, systolic blood pressure (SBP), heart failure after admission, coronary angiography, hemoglobin, creatinine clearance and PCT above the cut–off value were predictors of the outcome. After multivariate analysis, PCT and SBP resulted as independent predictors of bacterial infections (OR for PCT above the cut–off 2.67, 95%CI 1.09–6.53, p = 0.032; OR for SBP 0.98, 95%CI 0.97–0.99, p = 0.043). At 1–year, the composite outcome of all–cause death, MI and stroke occurred in 104 patients (18%). PCT did not result as an independent predictor of the composite outcome. Conclusions In patients with ACS PCT levels at hospital admission are predictor of bacterial infection but not of the composite lomg–term outcome of all–cause mortality, stroke and myocardial infarction.