Objective: The advantage of beta-blockers has been postulated in patients with Takotsubo syndrome (TTS) given the pathophysiological role of catecholamines. We hypothesised that beta-blocker treatment after discharge may improve the long-term clinical outcome in this patient population.Methods: This was an observational, multicentre study including consecutive patients with TTS diagnosis prospectively enrolled in the Takotsubo Italian Network (TIN) register from January 2007 to December 2018. TTS was diagnosed according to the TIN, Heart Failure Association and InterTAK Diagnostic Criteria. The primary study outcome was the occurrence of all-cause death at the longest available follow-up; secondary outcomes were TTS recurrence, cardiac and non-cardiac death.Results: The study population included 825 patients (median age: 72.0 (63.0–78.0) years; 91.9 % female): 488 (59.2%) were discharged on beta-blockers and 337 (40.8%) without beta-blockers. The median follow-up was 24.0 months. The adjusted Cox regression analysis showed a significantly lower risk for all-cause death (adjusted HR: 0.563; 95% CI: 0.356 to 0.889) and non-cardiac death (adjusted HR: 0.525; 95% CI: 0.309 to 0.893) in patients receiving versus those not receiving beta-blockers, but no significant differences in terms of TTS recurrence (adjusted HR: 0.607; 95% CI: 0.311 to 1.187) and cardiac death (adjusted HR: 0.699; 95% CI: 0.284 to 1.722). The positive survival effect of beta-blockers was higher in patients with hypertension than in those without (p_interaction=0.014), and in patients who developed cardiogenic shock during the acute phase than in those who did not (p_interaction=0.047).Conclusions: In this real-world register population, beta-blockers were associated with a significantly higher long-term survival, particularly in patients with hypertension and in those who developed cardiogenic shock during the acute phase.

Objectives: Recently, echo-tracking-derived measures of arterial stiffness have been introduced in clinical practice for the assessment of one-point pulse wave velocity. The purpose of this study was to find a relation between carotid–femoral pulse wave velocity and one-point carotid pulse wave velocity, and to find a value of one-point carotid pulse wave velocity that predicts carotid–femoral pulse wave velocity higher than 12 m/s. Methods: A total of 160 consecutive subjects (112 male/48 female, mean age = 51.5 ± 14.1 years; 96 healthy, 44 hypertensives, 13 with aortic valve disease, and 7 with left ventricular dysfunction) were studied. Carotid–femoral pulse wave velocity was measured with the SphygmoCor system and one-point carotid pulse wave velocity with high-definition echo-tracking system (ProSound Alpha10; Aloka, Tokyo, Japan). Results: Both carotid–femoral pulse wave velocity and one-point carotid pulse wave velocity correlated significantly with each other (r = 0.539, p < 0.001) and with age (one-point carotid pulse wave velocity r = 0.618, carotid–femoral pulse wave velocity r = 0.617, p < 0.0001 for both). Median value of carotid–femoral pulse wave velocity (7.2 m/s, 95% confidence interval = 6.2–8.9) was systematically higher than that of one-point carotid pulse wave velocity (5.8 m/s, 95% confidence interval = 5–6.6). The area under the receiver operating characteristic curve was 0.85, identifying the cutoff for one-point pulse wave velocity of 6.65 m/s as the best predictor of carotid–femoral pulse wave velocity more than 12 m/s (sensitivity = 0.818, specificity = 0.819). Conclusions: One-point carotid pulse wave velocity correlates with carotid–femoral pulse wave velocity, and the cutoff of 6.65 m/s was the best predictor of carotid–femoral pulse wave velocity over 12 m/s.

Mitral valve prolapse (MVP) is the most common valvular disease with a prevalence of 2%. It has generally a benign course; however, recent findings suggested an association between MVP and complex arrhythmias and eventually cardiac arrest and for this reason, it is also called arrhythmogenic MVP. Subjects who experience this complication are in general young women, with thickened mitral leaflets or bileaflet prolapse not necessarily associated with severe mitral regurgitation (MR). The nature of the relation between MVP and cardiac arrest is not clearly understood. Actually, the challenging task is to find the cluster of prognostic factors including T-wave inversion, polymorphic premature ventricular contractions, bileaflet prolapse, MR severity, but most importantly, those parameters of hypercontractility, mitral annulus disjunction (MAD), and myocardial fibrosis using a multimodality approach. Transthoracic echocardiography is the first-line imaging modality for the diagnosis of MVP, but also for detecting MAD and hypercontractility, followed by cardiac magnetic resonance for tissue characterization and detection of myocardial and papillary muscle fibrosis, using either late gadolinium enhancement (at the basal segment of the inferolateral wall and papillary muscles) (macro-fibrosis), or diffuse fibrosis by T1 mapping (native and post contrast T1). Moreover, there are also preliminary data on positron emission tomography utilizing ¹⁸F-fluorodeoxyglucose as a tool for providing evidence of early myocardial inflammation. The objective of this review article is to provide the clinician with an overview and a practical clinical approach to MVP for risk stratification and treatment guidance.

Background: Tricuspid regurgitation velocity (TRV) is the most widely used parameter by transthoracic echocardiography (TTE) in the evaluation of patients with suspected pulmonary hypertension (PH). Objectives: To explore the physiologic range of TRV in healthy adults and to investigate its clinical determinants. Methods: In the first part of the study, 614 healthy individuals (age 45.7± 14.7 years, 60.26% women) were prospectively assessed by TTE. In the second part, a pooled meta-analysis of 16 already published studies with TRV values in healthy subjects (n = 981) was performed. Statistical analysis included the calculation of 95% quantiles for defining reference ranges. Results: In the prospectively enrolled cohort, mean TRV was 2.01 ± 0.29 m/s (5–95% CI 1.987–2.033 m/s). It was significantly but weakly positively correlated with age, body mass index, systolic blood pressure, diastolic blood pressure, left atrial volume and negative with mitral inflow E/A ratio. No significant differences were found between males and females. The prospectively enrolled data revealed similar values to the literature-based datasets resulting in a mean TRV of 1.96 m/s (95% CI 1.91–2.02 m/s) and a 95% quantile of 2.55 m/s. Conclusions: To the best of our knowledge, this is the largest dataset to describe reference ranges of TRV and their clinical determinants in healthy adults years. The determined cut-off value of 2.55 m/s of this study has to be confirmed in specific pathologies such as patients at risk of PH.