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Purpose: The risk of sudden cardiac death (SCD) is increased during endurance competitive sports. Coronary artery disease (CAD) is the most common cause of SCD in master athletes ≥ 35 years old (MAs). To reduce the risk of SCD self-assessment of symptoms by questionnaire, and evaluation of cardiovascular risk-score, are recommended as pre-participation cardiovascular evaluation (PCVE). We aimed to examine whether PCVE predicts CVD in MAs with or without increased risk as measured by validated score instruments. Methods: We performed a single-site observational cohort study of healthy MAs based on findings at PCVE. They were allocated in two different groups: those MAs with reported symptoms on the questionnaire and/or with elevated cardiovascular risk score were allocated to a symptom group (SG), while MAs with no symptoms, nor raised risk score were defined as control group (CG). Thereafter, all were examined with extended examinations: resting-ECG, cardiorespiratory exercise testing and echocardiography. Results: Total, 81 (18 women) MAs participated in the study. There were no differences at baseline between SG (n = 39) and CG (n = 42); sex (p = 0.11), age (55.0 ± 9.8 vs. 51.9 ± 11.1 years; p = 0.18), maximal oxygen uptake (49.8 ± 7.6 vs. 51.6 ± 7.0 ml/kg/min; p = 0.26), resting heart rate (61.4 ± 12.8 vs. 60.2 ± 11.0/min; p = 0.66), training hours/week (7.0 ± 3.2 vs. 7.1 ± 3.1; p = 0.88). After further examination, sixteen (20%) MAs were found with CVD: 12 in SG, 4 in CG (p = 0.024). The negative predictive value and specificity of the PCVE were 90% and 58%, respectively. Conclusion: Negative findings on PCVE by questionnaire and cardiovascular risk-score may be a strategy to exclude subjects from preparticipation screening, thus saving resources. [ABSTRACT FROM AUTHOR]

Aims Permanent pacemaker (PM) implantation is common after transcatheter aortic valve implantation (TAVI). Left ventricular mechanical dispersion (MeDi) by speckle tracking echocardiography is a marker of fibrosis that causes alterations in the conduction system. We hypothesized that MeDi can be a predictor of the need for PM implantation after TAVI. Methods and results Consecutively, 200 TAVI patients were enrolled. Transthoracic echocardiography and electrocardiography examinations were recorded before TAVI to evaluate global longitudinal strain (GLS), MeDi, and conduction disturbances. PM implantation information was obtained 3 months after TAVI. Patients were stratified into PM or no PM group. Mean age was 80 + 7 years (44% women). Twenty-nine patients (16%) received PM. MeDi, QRS duration, existence of right bundle branch abnormality (RBBB), and first-degree atrioventricular (AV) block were significantly different between groups. MeDi was 57 ± 15 ms and 48 ± 12 ms in PM and no PM groups, respectively (P < 0.001). In multivariate analysis, MeDi predicted the need for PM after TAVI independently of GLS, QRS duration, RBBB, and first-degree AV block [odds ratio (OR): 1.73, 95% confidence interval (CI): 1.22–2.45] with an area under the curve (AUC) of 0.68 in receiver operating characteristic (ROC) curves. Moreover, RBBB was an independent predictor of PM need after TAVI (OR: 8.98, 95% CI: 1.78–45.03). When added to RBBB, MeDi had an incremental predictive value with an AUC of 0.73 in ROC curves (P = 0.01). Conclusion MeDi may be used as an echocardiographic functional predictor of the need for PM after TAVI. [ABSTRACT FROM AUTHOR]

Clinical differentiation between athletes' hearts and those with hypertrophic cardiomyopathy (HCM) can be challenging. We aimed to explore the role of speckle tracking echocardiography (STE) and cardiac magnetic resonance imaging (CMR) in the differentiation between athletes' hearts and those with mild HCM. We compared 30 competitive endurance elite athletes (7% female, age 41 ± 9 years) and 20 mild phenotypic mutation-positive HCM carriers (15% female, age 51 ± 12 years) with left ventricular wall thickness 13 ± 1 mm. Mechanical dispersion (MD) was assessed by means of STE. Native T1-time and extracellular volume (ECV) were assessed by means of CMR. MD was higher in HCM mutation carriers than in athletes (54 ± 16 ms vs. 40 ± 11 ms, p = 0.001). Athletes had a lower native T1-time (1204 (IQR 1191, 1234) ms vs. 1265 (IQR 1255, 1312) ms, p < 0.001) and lower ECV (22.7 ± 3.2% vs. 25.6 ± 4.1%, p = 0.01). MD > 44 ms optimally discriminated between athletes and HCM mutation carriers (AUC 0.78, 95% CI 0.65–0.91). Among the CMR parameters, the native T1-time had the best discriminatory ability, identifying all HCM mutation carriers (100% sensitivity) with a specificity of 75% (AUC 0.83, 95% CI 0.71–0.96) using a native T1-time > 1230 ms as the cutoff. STE and CMR tissue characterization may be tools that can differentiate athletes' hearts from those with mild HCM. [ABSTRACT FROM AUTHOR]

Aims: Cardiac disease progression prior to first ventricular arrhythmia (VA) in LMNA genotype-positive patients is not described.Methods and Results: We performed a primary prevention cohort study, including consecutive LMNA genotype-positive patients from our centre. Patients underwent repeated clinical, electrocardiographic, and echocardiographic examinations. Electrocardiographic and echocardiographic disease progression as a predictor of first-time VA was evaluated by generalized estimation equation analyses. Threshold values at transition to an arrhythmic phenotype were assessed by threshold regression analyses. We included 94 LMNA genotype-positive patients without previous VA (age 38 ± 15 years, 32% probands, 53% females). Nineteen (20%) patients experienced VA during 4.6 (interquartile range 2.1-7.3) years follow up, at mean age 50 ± 11 years. We analysed 536 echocardiographic and 261 electrocardiogram examinations. Individual patient disease progression was associated with VA [left ventricular ejection fraction (LVEF) odds ratio (OR) 1.4, 95% confidence interval (CI) 1.2-1.6 per 5% reduction, left ventricular end-diastolic volume index (LVEDVi) OR 1.2 (95% CI 1.1-1.3) per 5 mL/m2 increase, PR interval OR 1.2 (95% CI 1.1-1.4) per 10 ms increase]. Threshold values for transition to an arrhythmic phenotype were LVEF 44%, LVEDVi 77 mL/m2, and PR interval 280 ms.Conclusions: Incidence of first-time VA was 20% during 4.6 years follow up in LMNA genotype-positive patients. Individual patient disease progression by ECG and echocardiography were strong predictors of VA, indicating that disease progression rate may have additional value to absolute measurements when considering primary preventive ICD. Threshold values of LVEF <44%, LVEDVi >77 mL/m2, and PR interval >280 ms indicated transition to a more arrhythmogenic phenotype. [ABSTRACT FROM AUTHOR]

Aims Arrhythmic mitral valve syndrome is linked to life-threatening ventricular arrhythmias. The incidence, morphology and methods for risk stratification are not well known. This prospective study aimed to describe the incidence and the morphology of ventricular arrhythmia and propose risk stratification in patients with arrhythmic mitral valve syndrome. Methods Arrhythmic mitral valve syndrome patients were monitored for ventricular tachyarrhythmias by implantable loop recorders (ILR) and secondary preventive implantable cardioverter-defibrillators (ICD). Severe ventricular arrhythmias included ventricular fibrillation, appropriate or aborted ICD therapy, sustained ventricular tachycardia and non-sustained ventricular tachycardia with symptoms of hemodynamic instability. Results During 3.1 years of follow-up, severe ventricular arrhythmia was recorded in seven (12%) of 60 patients implanted with ILR [first event incidence rate 4% per person-year, 95% confidence interval (CI) 2–9] and in four (20%) of 20 patients with ICD (re-event incidence rate 8% per person-year, 95% CI 3–21). In the ILR group, severe ventricular arrhythmia was associated with frequent premature ventricular complexes, more non-sustained ventricular tachycardias, greater left ventricular diameter and greater posterolateral mitral annular disjunction distance (all P < 0.02). Conclusions The yearly incidence of ventricular arrhythmia was high in arrhythmic mitral valve syndrome patients without previous severe arrhythmias using continuous heart rhythm monitoring. The incidence was even higher in patients with secondary preventive ICD. Frequent premature ventricular complexes, non-sustained ventricular tachycardias, greater left ventricular diameter and greater posterolateral mitral annular disjunction distance were predictors of first severe arrhythmic event. [ABSTRACT FROM AUTHOR]