Endurance exercise in seniors: Tonic, toxin or neither?

INTRODUCTION: Cardiac adaptation to sustained exercise in the athletes is established. However, exercise-associated effect on the cardiac function of the elderly has to be elucidated. The aim of this study was to analyse left (LV) and right ventricular (RV) characteristics at different levels of chronic exercise in the senior heart. MATERIALS AND METHODS: We studied 178 participants in the World Senior Games (mean age 68 ± 8 years, 86 were men; 48%). Three groups were defined based on the type and intensity of sports: low-, moderate- and high-intensity level. Exclusion criteria were coronary artery disease, atrial fibrillation, valvular heart disease or uncontrolled hypertension. LV and RV size and function were evaluated with an echocardiogram. RESULTS: LV trans-mitral inflow deceleration time decreased in parallel to the intensity of chronic exercise: 242 ± 54 ms in low-, 221 ± 52 ms in moderate- and 215 ± 58 ms in high-intensity level, p = .03. Left atrial volume index (LAVI) was larger in high-intensity group, p = .001. The LAVI remained significantly larger when adjusting for age, gender, heart rate, hypertension and diabetes (p = .002). LV and RV sizes were larger in the high-intensity group. LV ejection fraction and RV systolic function evaluated by tissue Doppler velocity, atrioventricular plane displacement and strain did not differ between groups. CONCLUSION: Left ventricular diastolic filling is not only preserved, but may also be enhanced in long-term, top-level senior athletes. Moreover, LV and RV systolic function remain unchanged at different levels of exercise. This supports the beneficial effects of endurance exercise participation in senior hearts

Evaluation of right and left ventricular function using speckle tracking echocardiography in patients with arrhythmogenic right ventricular cardiomyopathy and their first degree relatives

<p>Abstract</p> <p>Introduction and aim</p> <p>The identification of right ventricular abnormalities in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC) in early stages is still difficult. The aim of this study was to investigate if longitudinal strain based on speckle tracking can detect subtle right (RV) or left ventricular (LV) dysfunction as an early sign of ARVC.</p> <p>Methods and results</p> <p>Seventeen male patients, fulfilling Task force criteria for ARVC, 49 (32–70) years old, nineteen male first degree relatives 29 (19–73) y.o. and twenty-two healthy male volunteers 36 (24–66) y.o participated in the study. Twelve-lead and signal-averaged electrocardiograms were recorded. All subjects underwent echocardiography. LV and RV diameters, peak systolic velocity from tissue Doppler and longitudinal strain based on speckle tracking were measured from the basal and mid segments in both ventricles. RV longitudinal strain measurement was successful in first degree relatives and controls (95 resp. 86%) but less feasible in patients (59%). Results were not systematically different between first degree relatives and controls. Using discriminant analysis, we then developed an index based on echocardiographic parameters. All normal controls had an index < l while patients with abnormal ventricles had an index between 1–4. Some of the first degree relatives deviated from the normal pattern.</p> <p>Conclusion</p> <p>Longitudinal strain of LV and RV segments was significantly lower in patients than in relatives and controls. An index was developed incorporating dimensional and functional echocardiographic parameters. In combination with genetic testing this index might help to detect early phenotype expression in mutation carriers.</p

Ankyrin-B dysfunction predisposes to arrhythmogenic cardiomyopathy and is amenable to therapy

Arrhythmogenic cardiomyopathy (ACM) is an inherited arrhythmia syndrome characterized by severe structural and electrical cardiac phenotypes, including myocardial fibrofatty replacement and sudden cardiac death. Clinical management of ACM is largely palliative, owing to an absence of therapies that target its underlying pathophysiology, which stems partially from our limited insight into the condition. Following identification of deceased ACM probands possessing ANK2 rare variants and evidence of ankyrin-B loss of function on cardiac tissue analysis, an ANK2 mouse model was found to develop dramatic structural abnormalities reflective of human ACM, including biventricular dilation, reduced ejection fraction, cardiac fibrosis, and premature death. Desmosomal structure and function appeared preserved in diseased human and murine specimens in the presence of markedly abnormal β-catenin expression and patterning, leading to identification of a previously unknown interaction between ankyrin-B and β-catenin. A pharmacological activator of the WNT/β-catenin pathway, SB-216763, successfully prevented and partially reversed the murine ACM phenotypes. Our findings introduce what we believe to be a new pathway for ACM, a role of ankyrin-B in cardiac structure and signaling, a molecular link between ankyrin-B and β-catenin, and evidence for targeted activation of the WNT/β-catenin pathway as a potential treatment for this disease