[2.218-11.550]; P < .001), hospitalization for HT .508]; P = .001), and for HF ]; P = .008). These effects remained statistically significant event after corrections for confounding factors including age, BMI, gender, smoking, dyslipidaemia, diabetes, and presence of antihypertensive therapies.

Aims  The aim of this study is to analyse the prognostic implications of right ventricular (RV) dysfunction as detected by strain analysis in patients with severe tricuspid regurgitation (TR). The evaluation of RV systolic function in presence of severe TR is of paramount importance for operative risk stratification; however, it remains challenging, as conventional echocardiographic indexes usually lead to overestimation. Methods and results We enrolled 250 consecutive patients with severe TR referred to our centre. Baseline clinical and echocardiographic data and follow-up outcomes were collected. Patients were predominantly female, with multiple cardiovascular risk factors and comorbidities, history of heart failure, and atrial fibrillation. Most of them had presented with clinical signs of RV heart failure (RVHF) and advanced New York Heart Association class. The RV strain analysis [both RV free wall longitudinal strain (RVFWLS) and RV global longitudinal strain (RVGLS)] reclassified ∼42–56% of patients with normal RV systolic function according to conventional parameters in patients with impaired RV systolic function. RVFWLS ≤17% (absolute values, AUC: 0.66, P = 0.002) predicted the presence of RVHF [odds ratio (OR) 0.93, P = 0.01]. At follow-up, patients with RVFWLS &gt;14% (absolute values, AUC: 0.70, P = 0.001, sensitivity 72%, specificity 54%) showed a better survival (P = 0.01). Conclusion Different ranges of RVFWLS have different implications in patients with severe TR, allowing to identify a preclinical and a clinical window, with correlations to RVHF and survival.

Cardiac conduction and/or rhythm abnormalities (CCRA) are the most frequent and life-threatening complications in DM1. In order to determine prevalence, incidence, characteristics, age of onset and predictors of CCRA, CCRA progression and sudden cardiac death (SCD) in DM1, we collected ECG/24hECG-Holter data from a yearly updated 34-year database of a cohort of 103 DM1 patients without cardiac abnormalities at baseline, followed for at least 1 year. Fifty-five patients developed CCRA [39 developed conduction abnormalities (CCA) and 16 rhythm abnormalities (CRA)], which progressed in 22. Nine had SCD. Risk and incidence of CCRA amounted to 53.4 and 6.83% person-years (CCA: 37.9 and 4.8%; CRA 15.5 and 2%), respectively; risk and incidence of SCD amounted to 8.74 and 0.67% person-years, respectively. CTG expansion represented a predictor of CCRA incidence (HR 1.10, p = 0.04), CCRA progression (HR 1.28, p = 0.001) and SCD (HR 1.39, p = 0.002). MIRS progression during follow-up was associated with CCRA prevalence (OR 5.82, p = 0.004); older age and larger CTG expansion to SCD prevalence (OR 2.67, p = 0.012; OR 1.54, p = 0.005). Age of CCRA onset and CCRA progression was significantly lower in patients with larger CTG expansion and in those with MIRS progression. Age when SCD occurred was significantly lower in patients with larger CTG expansion. Amongst recorded cardiac abnormalities, both atrial flutter (OR 8.70; p = 0.031) and paroxysmal supraventricular tachycardia (OR 8.67; p = 0.040) were associated with SCD. Although all DM1patients may develop cardiac abnormalities at any time in their life, patients older than 30 years with larger CTG expansion and MIRS progression in particular should be carefully monitored via periodical ECG.

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