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BACKGROUND High-flow (non-ischemic) priapism is a rare urological condition usually related to blind trauma to the penis or perineum causing an arterial-lacunar fistula. It can be treated conservatively, but in some cases when conservative treatment fails, the interventional approach is indicated. In the past, only surgical treatment was available, which was associated with a significant risk of complications. Endovascular techniques use a novel approach and offer clinical benefits for the patient. CASE REPORT A 51-year-old man was admitted to the hospital after referral from the urology department with high-flow priapism related to blunt trauma. Angio-computed tomography showed extravasation of contrast medium to the corpus cavernosum, and angiography revealed a fistula between the distal segment of the left internal pudendal artery and corpora cavernosa. A successful endovascular microembolization of the arterial-lacunar fistula with the use of microcoils was performed. The postprocedural period was uneventful and the patient was discharged. Despite incomplete angiographic follow-up at 6 months, the initial symptoms were fully resolved with the absence of any erectile dysfunction and no recurrence of priapism occurred. CONCLUSIONS Post-traumatic high-flow priapism can be safely and effectively treated by endovascular means. Microembolization has proven to be successful and beneficial to preserve sexual functions.

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Vasopressin (AVP) is a key neurohormone involved in the regulation of body functions. Due to its urine-concentrating effect in the kidneys, it is often referred to as antidiuretic hormone. Besides its antidiuretic renal effects, AVP is a potent neurohormone involved in the regulation of arterial blood pressure, sympathetic activity, baroreflex sensitivity, glucose homeostasis, release of glucocorticoids and catecholamines, stress response, anxiety, memory, and behavior. Vasopressin is synthesized in the paraventricular (PVN) and supraoptic nuclei (SON) of the hypothalamus and released into the circulation from the posterior lobe of the pituitary gland together with a C-terminal fragment of pro-vasopressin, known as copeptin. Additionally, vasopressinergic neurons project from the hypothalamus to the brainstem nuclei. Increased release of AVP into the circulation and elevated levels of its surrogate marker copeptin are found in pulmonary diseases, arterial hypertension, heart failure, obstructive sleep apnoea, severe infections, COVID-19 due to SARS-CoV-2 infection, and brain injuries. All these conditions are usually accompanied by respiratory disturbances. The main stimuli that trigger AVP release include hyperosmolality, hypovolemia, hypotension, hypoxia, hypoglycemia, strenuous exercise, and angiotensin II (Ang II) and the same stimuli are known to affect pulmonary ventilation. In this light, we hypothesize that increased AVP release and changes in ventilation are not coincidental, but that the neurohormone contributes to the regulation of the respiratory system by fine-tuning of breathing in order to restore homeostasis. We discuss evidence in support of this presumption. Specifically, vasopressinergic neurons innervate the brainstem nuclei involved in the control of respiration. Moreover, vasopressin V1a receptors (V1aRs) are expressed on neurons in the respiratory centers of the brainstem, in the circumventricular organs (CVOs) that lack a blood-brain barrier, and on the chemosensitive type I cells in the carotid bodies. Finally, peripheral and central administrations of AVP or antagonists of V1aRs increase/decrease phrenic nerve activity and pulmonary ventilation in a site-specific manner. Altogether, the findings discussed in this review strongly argue for the hypothesis that vasopressin affects ventilation both as a blood-borne neurohormone and as a neurotransmitter within the central nervous system.

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After transcatheter aortic valve implantation (TAVI) there is consistently identified decrease in platelets accompanied by a leucocyte (white blood cell, WBC) increase. We aimed to analyze the prognostic value of early platelet and WBC count changes (thromboinflammatory response) after successful TAVI. Among 432 consecutive patients [median 83.0 years of age, 63.4% women], platelets and WBCs were measured before and for 7 days post-TAVI. Follow-up was 36.9 (21.4 to 48.0) months. Platelet decrease (∆%Platelet-max) and parallel WBC increase (∆%WBC-max) were seen at days 1 to 3. Both ∆%Platelet-max ≤-37.6% and ∆%WBC-max >72.5% predicted mortality (area under the curve = 0.569 and area under the curve = 0.626). The 30-day and 1-year mortality (13.1% and 26.2%) were highest among 28% patients with a greater decrease in platelets and a greater increase in WBCs; intermediate (0.9% and 12.3%) among 52.5% patients with either a greater decrease in platelets or a greater increase in WBCs, but not both; and lowest (0% and 6.6%) among 19.5% patients with a lesser decrease in platelets and a lesser increase in WBCs (p <0.001). Estimated 4-year mortality rates were 53.7% versus 36.2% versus 24.5%, respectively, p <0.001. Bleeding, surgical wounds, acute kidney, and brain injury predicted a more intense thromboinflammatory response, whereas use of the newer generations had the opposite effect. In conclusion, substantial thromboinflammatory response identified after successful TAVI predicts a higher long-term mortality.

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The use of Left Ventricular Assist Devices (LVADs) has substantially increased in recent years, being a valid therapeutic option for a growing population of patients with advanced heart failure. A 54 year old male had had the HeartMate 3™ implanted in a prepericardiac location due to end-stage congestive heart failure. We present the angiographic data of our patient.

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