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Lipomas account for about 10% of all cardiac tumors and symptoms are often secondary to the compression of cardiac chambers and the consequent hemodynamic impact. We report the case of a 76–year–old woman with no cardiological history, undergoing oncological follow–up for breast cancer underwent a left radical mastectomy in 2014, not followed by radiotherapy or chemotherapy, who came to our attention due to the identification at the total–body CT scan of a mediastinal mass. A voluminous intrapericardial formation was detected, with a maximum size of 5.4 x 8.6 cm, characterized by adipose attenuation values at baseline. On examination, the patient was asymptomatic and eupneic, in good hemodynamic compensation, in functional class NYHA I. The ECG showed sinus rhythm with regular atrioventricular and intraventricular conduction without significant alterations in repolarization. On the echocardiogram, the left ventricle appeared of normal size and thickness without alterations in the global and segmental systolic function, EF 65%; the right ventricle was regular in size and contractility; a voluminous pericardial mass of about 8 x 4.5 cm was observed in the inferior, posterior and lateral site, homogeneous, not vascularized, not compressing the cardiac cavities and not determining hemodynamic impact. The patient was then submitted to cardiac MRI which confirmed the suspicion of intrapericardial lipoma. Considering the absence of symptoms, the benign nature of the lesion and the absence of compression on the cardiac structures, we decided not to remove the mass and to continue clinical and radiological follow–up, thus monitoring size and symptoms.

We report the case of a 63–year–old obese and hypertensive woman, admitted in hospital with worsening dyspnea for 2 weeks and syncope. A suspected chronic thromboembolism was diagnosed nine months before for a similar clinical picture; hematologic screening excluded thrombophilia and NOACs were prescribed. Two–dimensional transthoracic echocardiography showed enlargement of right chambers, the interventricular septum shifted to the left ventricle, showing “D” sign. Color Doppler flow imaging showed moderate regurgitation in tricuspid valve, with indirect pulmonary pressure estimation 90 mmHg. Left ventricle was normal for dimensions and function. ECG evidenced sinus tachycardia and no specific ST–T alterations. Blood exams evidenced anemia (Hb 9 mg/dl), negative neoplastic markers and absence of occult blood in feces, mildly elevated inflammatory markers, T–Troponin and D–dimer. Naso–pharyngeal swab for SARSCoV2 infection was negative. Chest computed tomography with contrast revealed a large filling defect within bilateral main pulmonary arteries. No lymph nodes or pulmonary pneumonia were detected. Lower extremity venous ultrasound was positive for right popliteal deep vein thrombosis. The global clinical picture suggested an acute pulmonary embolism recurrence, with a severe right ventricle impairment and a concomitant deep vein thrombosis. Some factors were not completely clear: chronic anemia, only mildly increased D–dimer, no specific increase of inflammatory markers. The patient was referred to Cardiac Surgery Unit of IRCCS Foundation Policlinico San Matteo in Pavia, for pulmonary endarterectomy. Unexpectedly the surgical finding was a bilateral pulmonary artery sarcoma, confirmed by histological exam. We thus clarified some uncertain clinical aspects, explainable in the context of a severe neoplastic picture. There were no immediate complications, and a chemotherapy was initiated after a period of cardio–pulmonary rehabilitation. Pulmonary artery intimal sarcoma is a very rare disease, its prevalence is about 0.001–0.003%, it can originate from the left and right pulmonary arteries and intimal layer of pulmonary arteries, forming a tumor growing in the nodular cavity or spreading along the intimal surface. PAS is often misdiagnosed as acute or chronic pulmonary thromboembolism due to its clinical presentation and radiological findings. Thus, early diagnosis is very crucial and may improve patient outcome.

Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations in PKD1 and PKD2 genes, encoding polycystin 1 and 2. We report the case of a 51–year–old woman with arterial hypertension and stage V chronic kidney disease from polycystic kidney disease, without a significant family health history. She was admitted to our Cardiology Ward for worsening dyspnea, dependent oedemas and a 3/6 systolic heart murmur detected. Blood tests showed mild anemia and hyperkalemia, severe renal failure (creatinine 6 mg/dl) and normal both liver and thyroid function. The ECG showed sinus rhythm with normal atrioventricular conduction, low voltage in precordial leads and non–specific repolarization disturbances. Hemodialysis and intravenous decongestion therapy were started. A transthoracic two–dimensional echocardiography was performed and a dilated left ventricle with severe global systolic dysfunction (EF 25%) was documented, with severe secondary mitral regurgitation (MR) with a central jet (EROA 0,5 cm2). A possible bicuspid aortic valve was suggested with moderate aortic regurgitation. CT scans showed small pleural and pericardial effusions, polycystosis affecting both kidneys and liver. Coronary CT showed a subcritical interventricular artery stenosis and confirmed a bicuspid aortic valve. Magnetic resonance angiography was negative for intracranial aneurysms. Finally, genetic testing revealed a heterozygous pathogenic mutation of PKD1 gene (c.9622del G p.Ala3208Hisfs*108 exone 28). Maximum tolerated heart failure therapy was prescribed after discharge, resulting in symptoms reduction but only mild echocardiographic improvement (EF 30% with severe MR). An edge–to–edge transcatheter mitral valve repair was proposed. In literature we learn that PKD1 mutations are linked to various cardiomyopathies: hypertrophic, dilated, left ventricular non compaction. We report the association of ADPKD with a complex dilated cardiomyopathy with severe secondary MR, an aortic congenital defect and an associated subcritical coronary artery stenosis. Further investigations are needed to study the genetic aspect of the ADPKD when associated with different cardiac anomalies.

Objective: This review identified and evaluated apps intended to aid women in conception that were available across major mobile platforms; secondary objectives were to highlight additional criteria and considerations when evaluating conception-related apps. Data Sources: Apple iTunes and Google Play stores were searched using the keywords conception, fertility, and pregnant. Data Selection: Included apps were as follows: contained in the first 50 search results; presented in English; intended for layperson use; updated July 1, 2018, or after; marketed as a conception aid; and used a defined fertility tracking method. Excluded apps were intended for men only, marketed for contraception only, promoted a single fertility service or branded product, or not found in both app stores. Data Extraction: Apps were evaluated using the adapted APPLICATIONS Scoring System. Two additional criteria were assessed: inclusion of a privacy policy and inclusion of a search function, medical terminology glossary, or Frequently Asked Questions section. Data Synthesis: A total of 300 apps were screened; 7 app pairs were analyzed. Scores ranged from 9 to 13 of a possible 15 points (mean = 11; median = 11). No app reported advisement from a health professional during development. Relevance to Patient Care in Clinical Practice: Widely available apps that score highly per the adapted APPLICATIONS Scoring System may be considered for use by and recommended to women seeking apps useful for conception. Conclusion: Evaluation tools should evolve as app features change. Criteria related to privacy and search functions that promote health literacy should be considered for future app evaluation tools.

Several cytogenetic lesions in chromosomes 2, 5, 12, and 16 have been repeatedly coselected with in vitro macrophage differentiation in a clonal murine thymic tumor cell line. Parental-type subclones, which show an extremely immature hemopoietic phenotype, do not carry the aberrations. The frequency of the stable differentiated variants is elevated by 5-azacytidine and bromodeoxyuridine, consistent with chromosome breakage being responsible for the phenotype. The frequency is also raised by dexamethasone. Since variants are 300-3,000-fold more resistant to dexamethasone than parental clones, we interpret this to be largely due to selection. Three of the lesions, on chromosome 2, match those previously described as associated specifically with in vivo-generated murine myeloid tumors, induced by X irradiation and corticosteroid treatment. Several implications follow from these observations. (1) In vitro differentiation in clonal tumor cell lines can be used to select for tumor-associated lesions. This should allow genetic and molecular analysis of the chromosome 2 lesions and of others that may pinpoint genes critical to macrophage differentiation and transformation. (2) Myeloid and lymphoid tumors that occur in response to X irradiation may diverge from a common initiating tumor. (3) The hemopoietic lineage switch phenomenon, previously described by several authors, may be caused by similar or identical chromosome aberrations.