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• Recurrent cerebral ischemia after PFO closure is not rare (0.92/100 patients/year). • Obesity, ROPE score < 7 and migraine were predictors of recurrent stroke/TIA. • Future studies are required to refine prevention of recurrent stroke after PFO closure. Transcatheter patent foramen ovale closure lowers recurrent stroke in patients with cryptogenic stroke or transient ischemic attack with an indication for closure. However, the incidence of recurrent stroke is not negligible and underlying pathophysiology remains largely unknown. We sought to evaluate the prevalence of recurrent ischemic neurological events and to assess its predictors after transcatheter patent foramen ovale closure. We enrolled consecutive patients who underwent patent foramen ovale closure for secondary prevention of neurological ischemic events at the University Hospital of Parma between 2006 and 2021. Clinical and procedure-related features were collected for each patient. The incidence of recurrent ischemic neurological events was assessed at follow-up. We enrolled a total of 169 patients with mean Risk of Paradoxical Embolism score at hospital admission of 6.4 ± 1.5. The primary indication was previous cryptogenic stroke (94 [55.6 %] subjects), followed by transient ischemic attack (75 [44.4 %]). Among patients with complete outcome data (n= 154), after a median follow-up of 112 months, recurrent cerebral ischemia occurred in 13 [8.4 %], with an annualized rate of 0.92/100 patients. The presence of obesity [OR 5.268, p = 0.018], Risk of Paradoxical Embolism score < 7 [OR 5.991, p = 0.035] and migraine [OR = 5.932 p = 0.012] were independent positive predictors of recurrent stroke/ transient ischemic attack after patent foramen ovale closure. The presence of obesity, Risk of Paradoxical Embolism score < 7 and migraine were independent positive predictors of recurrent ischemic neurological events after patent foramen ovale closure. [ABSTRACT FROM AUTHOR]

Sudden cardiac death (SCD) is the unexpected death of an individual not attributable to an extracardiac cause, usually within 1 h of symptom onset (or within 24 h of last being seen in good health if the death is unwitnessed). SCD causes can be divided into structural, with coronary heart disease (CHD) as main player, and inherited arrhythmia syndromes, that account 1-- 2% of SCD in Western countries [[1]]. In conclusion, this study provides a relevant contribution in understanding SCD pathophysiological mechanisms, underlying the role of hypertension and inflammation. [Extracted from the article]

Abstract Takotsubo syndrome (TS) is a condition of transient regional ventricular systolic dysfunction, usually presenting with acute chest pain and/or dyspnea, that is increasingly recognized especially in post-menopausal women following a psychological or physical stress. Initially considered as a benign condition with an isolated and self-limiting episode, it is now recognized that it is associated with a significant risk of in-hospital mortality and of recurrence. We herein describe a case of a 61-year-old female with left ventricular non-compaction cardiomyopathy (LVNC) who experienced a recurrence of TS, highlighting the potential pathophysiological role for LVNC in predisposing this syndrome and its recurrence. Moreover, we underscored possible therapeutic implications deriving from this case. Highlights • Takotsubo syndrome (TS) is an acute form of neurocardiogenic stunning. • Altered autonomic-limbic processing supports brain-heart axis in TS. • Sympathetic activation with catecholamine release, causes myocardial toxicity and/or coronary microvascular dysfunction. • Left ventricular non-compaction cardiomyopathy (LVNC) is a rare disease characterized by a subverted myocardial architecture. • LVNC may predispose to TS because associated with coronary microvascular and autonomic dysfunction. [ABSTRACT FROM AUTHOR]