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Background Erectile dysfunction (ED) is a prevalent health problem that seriously impacts men's quality of life. The potential treatment of ED by percutaneous approach has emerged with valid angiographic results and a significant improvement in symptoms and quality of life. In addition, cell-based regenerative therapies aiming at enhancing neovascularization have been successfully performed with peripheral blood mononuclear cells (PBMNCs) in diabetic patients affected by critical limb ischaemia. Case summary We report a case of a young insulin dependent (ID) diabetic patients who suffered of severe vasculogenic erectile dysfunction associated with a poor response for more than 1 year to oral phosphodiesterase-5 inhibitors (PDE5i) and intracavernous (IC) phosphodiesterase type 1 (PDE1) therapy. At selective angiography of the pelvic district, a severe atherosclerotic disease of the internal iliac and pudendal artery was evident with absence of distal vascularization of the cavernous bodies. The patient was treated by mechanical revascularization with drug-coated balloon and drug-eluting stent placement associated with IC injection of autologous PBMNCs. Immediate and 1-year clinical and angiographic follow-up are described. Discussion Percutaneous revascularization with drug-coated balloon and drug-eluting stent associated with IC autologous PBMNCs cells injection is a safe and effective procedure to restore normal erectile function in diabetic patients affected by severe vasculogenic ED not responding to conventional oral drug therapies.

According to the European and American guidelines, surgery represents the treatment of choice for mitral valve (MV) disease. However, a number of patients are deemed unsuitable for surgery due to a prohibitive/high operative risk. In such cases, transcatheter therapies aiming at MV repair have been proven to be a valuable alternative and have been recently introduced in the latest American guidelines on valvular heart disease. Indeed, percutaneous repair techniques, particularly transcatheter edge-to-edge, have gained a broad experience and demonstrated to be safe and effective. However, given the complexity and heterogeneity of MV anatomy and pathology, transcatheter MV implantation (TMVI) has grown as a possible alternative to percutaneous MV repair. Current data about TMVI are still limited and come from different settings: valve-in-native MV, valve-in-valve (ViV), valve-in-ring (ViR), and valve-in-mitral annular calcification. Preliminary data are promising although several open issues still need to be addressed. This paper provides a comprehensive review of the available devices in the different clinical settings, to discuss potentialities, limitations, and future directions for TMVI.

Introduction Vasovagal syncope is traditionally considered a benign condition due to parasympathetic nervous system activation. Here is a case of reflex syncopal episodes that triggered recurrent Takotsubo Syndrome (TS) with life–threatening presentation. Report of a Case A 71-year-old female presented to the Emergency Department (ED) complaining with dyspnoea and chest pain developed half an hour after a vasovagal syncope. Her past medical history was consistent with arterial hypertension, dyslipidaemia, and well-tolerated reflex syncopal episodes since she was a child. At hospital admission, a 12-leads ECG showed T-wave inversion in anterior leads while transthoracic echocardiogram (TTE) showed hypokinesia of the mid-apical segments, reduced left ventricular ejection fraction (LVEF) [40%], and severe mitral regurgitation (MR). Blood tests revealed increased hs-troponin I values [peak value: 1500 ng/L]. A coronary angiography (CA) was thus performed in the suspect of NSTEMI, showing non obstructive coronary disease. A diagnosis of TS was eventually made with ECG normalisation and resolution of echocardiographic abnormalities at 6 month follow-up. Five years later, the patients presented to the ED because of a new syncopal episode followed by severe pulmonary oedema. Since the presence of electrocardiographic T-wave inversion, apical segments akinesia and elevated hs-troponin I were consistent with NSTEMI, a CA was performed revealing (again!) normal coronary vessels. A suspect of TS relapse was thus made. Three months after discharge, ECG and echocardiogram were normal and a syncope diagnostic work–up was suggested. A 24/h ambulatory blood pressure monitoring demonstrated normal pressure values and a tilt test confirmed the well-established history of reflex syncope showing a remarkable cardioinhibitory response. A pacemaker implant was thus indicated. Discussion TS is a heart syndrome characterized by transient contractile dysfunction historically related to catecholamine activation of alpha and beta receptors. While sympathetic system involvement in the development of TS is clearly established, new evidence is emerging about the vagal role in the etiopathogenesis of the disease. Although syncopal episodes could be related to TS, because of LVOT obstruction or major arrhythmias, according to our experience, TS may be triggered by vagal hypertonus [i.e., after vasovagal syncopal episodes]. In similar situation, the implantation of a pace-maker could be considered to prevent future dangerous complications related to recurrent reflex syncope even if well tolerated by the patients. Conclusion In our experience, recurrent episodes of TS appeared triggered by reflex syncope. A condition traditionally considered benign may instead have life-threatening consequences. Moreover, the role of parasympathetic and vagal tone in the development of TS needs further investigation that may lead to the design of new strategies of clinical diagnosis and management.