Aims The Italian Society of Interventional Cardiology (GIse) registry Of Transcatheter treatment of mitral valve regurgitaTiOn (GIOTTO) was conceived in order to assess the safety and efficacy of MitraClip therapy in Italy. The aim of this study was to assess procedural and mid‐term outcomes, and clinical and echocardiographic predictors of mid‐term mortality after MitraClip therapy, stratifying the results according to the diagnosis of functional and degenerative mitral regurgitation (FMR vs. DMR). Methods and results Between January 2016 and March 2020, 1659 patients were prospectively included in the GIOTTO registry (FMR 59.4% vs. DMR 40.6%). Acute Mitral Valve Academic Research Consortium (MVARC) technical success was achieved in 97.2% of patients, without differences between FMR and DMR and with sustained results at 30 days. In the study population, all‐cause mortality was 4.0%, 17.5% and 34.6% at 30 days, 1 year and 2 years, respectively. Cardiovascular death was the most frequent cause of mortality. Overall hospitalization rates were 6.3%, 23.4% and 31.7% at 30 days, 1 year and 2 years, respectively. The most frequent cause of hospitalization was heart failure, particularly in the first 30 days. FMR and MVARC structural and functional failure were strongly associated with 1‐year mortality. Residual mitral regurgitation 1+ (rMR) was independently related to a reduced risk of 1‐year mortality (hazard ratio 0.62; P = 0.005). Coherently, at 2‐year follow up, FMR was associated with worse outcomes than DMR, and Kaplan–Meier all‐cause mortality was related to rMR. Conclusions Functional mitral regurgitation aetiology affects 1‐year mortality after MitraClip implantation, and differences in mortality and hospitalization rates between FMR and DMR can be observed within 2 years. Optimal rMR 1+ was correlated to a more favourable mid‐term outcome, particularly in FMR.

Objectives To analyze left ventricular (LV) myocardial deformation and contractile reserve (CR) in asymptomatic patients with severe aortic regurgitation (AR) at rest and during exercise, and their correlation with functional capacity. Background The natural history of chronic AR is characterized by a prolonged silent phase before onset of symptoms and overt LV dysfunction. Assessment of LV systolic function and contractile reserve has an important role in the decision‐making of AR asymptomatic patients. Methods Standard echo, lung ultrasound, and LV 2D speckle tracking strain were performed at rest and during exercise in asymptomatic patients with severe AR and in age‐ and sex‐comparable healthy controls. Results 115 AR patients (male sex 58.2%; 52.3 ± 18.3 years) and 55 controls were enrolled. Baseline LV ejection fraction was comparable between the groups. Resting LV global longitudinal strain (GLS) and myocardial work efficiency (MWE) were significantly reduced in AR (GLS‐15.8 ± 2.8 vs −21.4 ± 4.4; P < .001). Patients with AR and CR− showed reduced resting LV GLS and MWE and increased B‐lines. MWE was closely related to peak effort watts, VO2, LV E/e′, and B‐lines, at a multivariable analysis. Both GLS and MWE were strong independent predictors of CR. A resting LV GLS cutoff of −12% differentiated CR+ and CR− (78% sensitivity and 84% specificity). Conclusions The lower resting values of LV GLS and MWE in severe AR asymptomatic patients suggest an early subclinical myocardial damage that seems to be closely associated with lower exercise capacity, greater pulmonary congestion, and blunted LV contractile reserve during stress.

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Summary:Methanol intoxication produces a well recognized clinical picture characterized by gastrointestinal, ocular and nervous system symptoms. The effect of poisoning on the cardiovascular system has not been well documented.We report the case of a 55 year old man whose acute methanol intoxication caused severe reversible cardiac failure. This represents the first description of an association between methanol toxicity and acute cardiac dysfunction in man.

Background Procedural success after transcatheter edge‐to‐edge mitral valve repair (TEER) is defined as a reduction of mitral regurgitation (MR) degree to