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      Vigorous physical activity impairs myocardial function in patients with arrhythmogenic right ventricular cardiomyopathy and in mutation positive family members

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          Abstract

          Aims

          Exercise increases risk of ventricular arrhythmia in subjects with arrhythmogenic right ventricular cardiomyopathy (ARVC). We aimed to investigate the impact of exercise on myocardial function in ARVC subjects.

          Methods and Results

          We included 110 subjects (age 42 ± 17 years), 65 ARVC patients and 45 mutation-positive family members. Athletes were defined as subjects with ≥4 h vigorous exercise/week [≥1440 metabolic equivalents (METs × minutes/week)] during a minimum of 6 years. Athlete definition was fulfilled in 37/110 (34%) subjects. We assessed right ventricular (RV) and left ventricular (LV) myocardial function by echocardiography, and by magnetic resonance imaging (MRI). The RV function by RV fractional area change (FAC), RV global longitudinal strain (GLS) by echocardiography, and RV ejection fraction (EF) by MRI was reduced in athletes compared with non-athletes (FAC 34 ± 9% vs. 40 ± 11%, RVGLS –18.3 ± 6.1% vs. –22.0 ± 4.8%, RVEF 32 ± 8% vs. 43 ± 10%, all P < 0.01). LV function by LVEF and LVGLS was reduced in athletes compared with non-athletes (LVEF by echocardiography 50 ± 10% vs. 57 ± 5%, LVEF by MRI 46 ± 6% vs. 53 ± 8%, and LVGLS –16.7 ± 4.2% vs. –19.4 ± 2.9%, all P < 0.01). The METs × minutes/week correlated with reduced RV and LV function by echocardiography and MRI (all P < 0.01). The LVEF by MRI was also reduced in subgroups of athlete index patients (46 ± 7% vs. 54 ± 10%, P = 0.02) and in athlete family members (47 ± 3% vs. 52 ± 6%, P < 0.05).

          Conclusion

          Athletes showed reduced biventricular function compared with non-athletes in ARVC patients and in mutation-positive family members. The amount and intensity of exercise activity was associated with impaired LV and RV function. Exercise may aggravate and accelerate myocardial dysfunction in ARVC.

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          Most cited references9

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          Physical Activity and Public Health: Updated Recommendation for Adults From the American College of Sports Medicine and the American Heart Association

          In 1995 the American College of Sports Medicine and the Centers for Disease Control and Prevention published national guidelines on Physical Activity and Public Health. The Committee on Exercise and Cardiac Rehabilitation of the American Heart Association endorsed and supported these recommendations. The purpose of the present report is to update and clarify the 1995 recommendations on the types and amounts of physical activity needed by healthy adults to improve and maintain health. Development of this document was by an expert panel of scientists, including physicians, epidemiologists, exercise scientists, and public health specialists. This panel reviewed advances in pertinent physiologic, epidemiologic, and clinical scientific data, including primary research articles and reviews published since the original recommendation was issued in 1995. Issues considered by the panel included new scientific evidence relating physical activity to health, physical activity recommendations by various organizations in the interim, and communications issues. Key points related to updating the physical activity recommendation were outlined and writing groups were formed. A draft manuscript was prepared and circulated for review to the expert panel as well as to outside experts. Comments were integrated into the final recommendation. To promote and maintain health, all healthy adults aged 18 to 65 yr need moderate-intensity aerobic (endurance) physical activity for a minimum of 30 min on five days each week or vigorous-intensity aerobic physical activity for a minimum of 20 min on three days each week. [I (A)] Combinations of moderate- and vigorous-intensity activity can be performed to meet this recommendation. [IIa (B)] For example, a person can meet the recommendation by walking briskly for 30 min twice during the week and then jogging for 20 min on two other days. Moderate-intensity aerobic activity, which is generally equivalent to a brisk walk and noticeably accelerates the heart rate, can be accumulated toward the 30-min minimum by performing bouts each lasting 10 or more minutes. [I (B)] Vigorous-intensity activity is exemplified by jogging, and causes rapid breathing and a substantial increase in heart rate. In addition, every adult should perform activities that maintain or increase muscular strength and endurance a minimum of two days each week. [IIa (A)] Because of the dose-response relation between physical activity and health, persons who wish to further improve their personal fitness, reduce their risk for chronic diseases and disabilities or prevent unhealthy weight gain may benefit by exceeding the minimum recommended amounts of physical activity. [I (A)]
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            Metabolic equivalent: one size does not fit all.

            The metabolic equivalent (MET) is a widely used physiological concept that represents a simple procedure for expressing energy cost of physical activities as multiples of resting metabolic rate (RMR). The value equating 1 MET (3.5 ml O2 x kg(-1) x min(-1) or 1 kcal x kg(-1) x h(-1)) was first derived from the resting O2 consumption (VO2) of one person, a 70-kg, 40-yr-old man. Given the extensive use of MET levels to quantify physical activity level or work output, we investigated the adequacy of this scientific convention. Subjects consisted of 642 women and 127 men, 18-74 yr of age, 35-186 kg in weight, who were weight stable and healthy, albeit obese in some cases. RMR was measured by indirect calorimetry using a ventilated hood system, and the energy cost of walking on a treadmill at 5.6 km/h was measured in a subsample of 49 men and 49 women (26-45 kg/m2; 29-47 yr). Average VO2 and energy cost corresponding with rest (2.6 +/- 0.4 ml O2 x kg(-1) x min(-1) and 0.84 +/- 0.16 kcal x kg(-1) x h(-1), respectively) were significantly lower than the commonly accepted 1-MET values of 3.5 ml O2 x kg(-1) x min(-1) and 1 kcal x kg(-1) x h(-1), respectively. Body composition (fat mass and fat-free mass) accounted for 62% of the variance in resting VO2 compared with age, which accounted for only 14%. For a large heterogeneous sample, the 1-MET value of 3.5 ml O2 x kg(-1) x min(-1) overestimates the actual resting VO2 value on average by 35%, and the 1-MET of 1 kcal/h overestimates resting energy expenditure by 20%. Using measured or predicted RMR (ml O2 x kg(-1) x min(-1) or kcal x kg(-1) x h(-1)) as a correction factor can appropriately adjust for individual differences when estimating the energy cost of moderate intensity walking (5.6 km/h).
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              Transmural differences in myocardial contraction in long-QT syndrome: mechanical consequences of ion channel dysfunction.

              Long-QT syndrome (LQTS) is characterized by prolonged myocardial action potential duration. The longest action potential duration is reported in the endomyocardium and midmyocardium. Prolonged action potential duration in LQTS may cause prolonged cardiac contraction, which can be assessed by strain echocardiography. We hypothesized that myocardial contraction is most prolonged in subendocardial myofibers in LQTS patients and that inhomogeneous transmural contraction is related to the risk of spontaneous arrhythmia. We included 101 genotyped LQTS mutation carriers and 35 healthy individuals. A history of cardiac arrhythmias was present in 48 mutations carriers, and 53 were asymptomatic. Myocardial contraction duration was assessed by strain echocardiography as time from the ECG Q wave to peak strain in 16 LV segments. Strain was assessed along the longitudinal axis, predominantly representing subendocardial fibers, and along the circumferential axis, representing midmyocardial fibers. Mean contraction duration was longer in LQTS mutation carriers compared with healthy individuals (445 ± 45 versus 390 ± 40 milliseconds; P<0.001) and longer in symptomatic compared with asymptomatic LQTS mutation carriers (460 ± 40 versus 425 ± 45 milliseconds; P<0.001). Contraction duration by longitudinal strain was longer than by circumferential strain in symptomatic LQTS patients (460 ± 45 versus 445±45 milliseconds; P=0.008) but not in asymptomatic patients and healthy individuals, indicating transmural mechanical dispersion. This time difference was present in a majority of LV segments and was most evident in patients with LQT2 and the Jervell and Lange-Nielsen syndrome. Contraction duration in symptomatic LQTS mutation carriers was longer in the subendocardium than in the midmyocardium, indicating transmural mechanical dispersion, which was not present in asymptomatic and healthy individuals.
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                Author and article information

                Journal
                Eur J Heart Fail
                Eur. J. Heart Fail
                ejhf
                European Journal of Heart Failure
                John Wiley & Sons, Ltd (Oxford, UK )
                1388-9842
                1879-0844
                December 2014
                16 October 2014
                16 October 2014
                : 16
                : 12
                : 1337-1344
                Affiliations
                [1 ]Department of Cardiology, Institute for Surgical Research and Centre for Cardiological Innovation, Oslo University Hospital Rikshospitalet, PO Box 4950 Nydalen, N–0424, Oslo, Norway
                [2 ]University of Oslo Norway
                [3 ]Arrhythmia Clinic, Skåne University Hospital and Department of Cardiology, Clinical Sciences, Lund University Lund, Sweden
                [4 ]Department of Radiology and Nuclear Medicine, Oslo University Hospital, Rikshospitalet and University of Oslo Norway
                [5 ]Department of Cardiology, Rigshospitalet Copenhagen University Hospital Copenhagen, Denmark
                Author notes
                Corresponding author: Tel: +47 23071393; Fax: +47 23073530; E-mail: Kristina.Haugaa@ 123456rr-research.no
                Article
                10.1002/ejhf.181
                4278531
                25319773
                5fe83935-da68-4308-aeae-c149d1091418
                © 2014 The Authors. European Journal of Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.

                This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                : 03 July 2014
                : 09 September 2014
                : 12 September 2014
                Categories
                Exercise Psysiology

                Cardiovascular Medicine
                arrhythmogenic cardiomyopathy,heart failure,exercise,myocardial function,ventricular arrhythmia

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