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J Am Coll Cardiol, 2003; 42:527-532, doi:10.1016/S0735-1097(03)00642-9 © 2003 by the American College of Cardiology Foundation |








* Service of Nephrology, Hospital Universitario de Canarias e Instituto Reina Sofía de Investigación, La Laguna, Tenerife, Spain
Service of Cardiology, Hospital Universitario de Canarias e Instituto Reina Sofía de Investigación, La Laguna, Tenerife, Spain
Service of Sports Medicine, Hospital Universitario de Canarias e Instituto Reina Sofía de Investigación, La Laguna, Tenerife, Spain
Research Unit, Hospital Universitario de Canarias e Instituto Reina Sofía de Investigación, La Laguna, Tenerife, Spain
Manuscript received January 17, 2003; revised manuscript received March 28, 2003, accepted April 17, 2003.
* Reprint requests and correspondence: Dr. Domingo Hernández, Servicio de Nefrologia, Hospital Universitario de Canarias, Ofra s/n. 38320, La Laguna, Tenerife, Spain.
dhmarrero{at}hotmail.com
OBJECTIVES: We studied the impact of the angiotensin-converting enzyme (ACE)/DD genotype on morphologic and functional cardiac changes in adult endurance athletes.
BACKGROUND: Trained athletes usually develop adaptive left ventricular hypertrophy (LVH), and ACE gene polymorphisms may regulate myocardial growth. However, little is known about the impact of the ACE/DD genotype and D allele dose on the cardiac changes in adult endurance athletes.
METHODS: Echocardiographic studies (including tissue Doppler) were performed in 61 male endurance athletes ranging in age from 25 to 40 years, with a similar period of training (15.6 ± 4 h/week for 12.6 ± 5.7 years). The ACE genotype (insertion [I] or deletion [D] alleles) was ascertained by polymerase chain reaction (DD = 27, ID = 31, and II = 3). Athletes with the DD genotype were compared with their ID counterparts.
RESULTS: The DD genotype was associated with a higher left ventricular mass index (LVMI) than the ID genotype (162.6 ± 36.5 g/m2 vs. 141.6 ± 34 g/m2, p = 0.031), regardless of other confounder variables. As a result, 70.4% of DD athletes and only 42% of ID athletes met the criteria for LVH (p = 0.037). Although systolic and early diastolic myocardial velocities were similar in DD and ID subjects, a more prolonged E-wave deceleration time (DT) was observed in DD as compared with ID athletes, after adjusting for other biologic variables (210 ± 48 ms vs. 174 ± 36 ms, respectively; p = 0.008). Finally, a positive association between DT and myocardial systolic peak velocity (medial and lateral peak Sm) was only observed in DD athletes (p = 0.013, r = 0.481).
CONCLUSIONS: The ACE/DD genotype is associated with the extent of exercise-induced LVH in endurance athletes, regardless of other known biologic factors.
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