C 2012, Wiley Periodicals, Inc.
DOI: 10.1111/j.1540-8175.2012.01719.x
Assessment of Left Atrial Function in Hypertrophic Cardiomyopathy and Athlete’s Heart: A Left Atrial Myocardial Deformation Study ´ ˜ ez, M.D., Luigi Gabrielli, M.D., Andr´es Enr´ıquez, M.D., Samuel Cordova, M.D., Fernando Y´an Iv´an Godoy, M.D., and Ramon Corbal´an, M.D. ´ Cardiovascular Diseases Division, School of Medicine, Pontificia Universidad Catolica de Chile, Santiago, Chile
Background: Hypertrophic cardiomyopathy (HCM) is a common cause of sudden death in athletes and differentiating this condition from the nonpathological “athlete’s heart” remains a challenge. The development of pathological left ventricular hypertrophy (LVH) is associated with left atrial (LA) dilatation and dysfunction. LA strain and strain rate by two-dimensional (2D) speckle tracking are novel indices of LA function and might contribute to differentiate physiological from pathological LVH among athletes with underdiagnosed HCM. Methods: We evaluated 20 patients with nonobstructive HCM, 20 highly trained athletes and 20 healthy controls matched for age, gender, and body surface area. All patients underwent a transthoracic echocardiogram with evaluation of LA strain: s-wave (LASs); and strain rate: s-wave (LASRs) and a-wave (LASRa). Results: LV mass index, LA volume index, and ejection fraction were comparable between patients with HCM and athletes. Patients with HCM had a significantly lower LASs (19 + 8% vs. 43 + 8%, P < 0.01), LASRs (0.7 + 0.2 s-1 vs. 1.6 + 0.2 s-1, P < 0.01), and LASRa (–0.8 + 0.1 s-1 vs. –1.4 + 0.3 s-1, P < 0.01) compared to athletes. Among hypertrophic subjects, independent predictors of hypertrophy related to HCM were LASs and E/´e ratio. Conclusions: LA myocardial deformation is significantly impaired in patients with HCM compared to athletes and healthy controls. LA strain and strain rate assessed by 2D speckle tracking should be incorporated in the evaluation of trained athletes with LVH and LA dilatation. (Echocardiography 2012;29:943-949) Key words: athlete’s heart, hypertrophic cardiomyopathy, strain-strain rate Sudden death in young athletes is a dramatic event and carries a significant social impact.1 Hypertrophic cardiomyopathy (HCM) is one of the leading causes, accounting for about one-third of sudden death.2,3 Therefore, distinguishing HCM from the nonpathological “athlete’s heart” is critically important.4 Echocardiography plays a key role in the differential diagnosis, but significant overlap exists between both conditions and its differentiation remains challenging.4,5 Pathological left ventricular hypertrophy (LVH) is associated with progressive left atrial (LA) dilatation and dysfunction. Echocardiographic assessment of LA myocardial function might contribute to differentiate between pathological and physiological LVH.6 In recent years, LA strain and strain rate analysis by two-dimensional (2D) speckle tracking has emerged as a novel method to evaluate LA function. Speckle tracking is an echocardiographic tool that tracks the speckle patterns Address for correspondence and reprint requests: Luigi ´ de Enfermedades Cardiovasculares, Gabrielli, M.D., Division ´ Escuela Medicina, Pontificia Universidad Catolica de Chile, Marcoleta 367 Piso 8, Santiago, Chile. Fax: 6392037; E-mail:
[email protected]
frame by frame in standard B-mode images for the quantification of myocardial deformation. It has important advantages over tissue Doppler imaging, including the angle independence and the avoidance of tethering by the left ventricle.7,8 Normal LA function consists of three components: (1) contractile function, which actively empties the atria before the end of left ventricle (LV) diastole; (2) reservoir function, which stores pulmonary venous return during LV systole and isovolumic relaxation time; and (3) conduit function, which empties its content into the LV after the mitral valve opens and during LV diastole.9 The objective of this study was to evaluate LA myocardial function using 2D speckle tracking in patients with HCM and highly trained athletes, and assess its potential role in the differential diagnosis between these two entities. Methods: Study Design and Population: This was a cross-sectional study comparing three groups of subjects: 20 patients with nonobstructive HCM, 20 highly trained athletes, and 20 sedentary healthy controls matched for age, gender, and body surface area. All participants 943
Gabrielli, et al.
were in sinus rhythm, normotensive, and did not have other cardiovascular risk factors. HCM was diagnosed in the presence of a positive family history, a septal wall thickness ≥13 mm and/or septal-to-posterior wall thickness ≥1.3, and exclusion of an underlying cardiac or systemic cause that might lead to LV hypertrophy. Patients with LV outflow tract obstruction (gradient ≥30 mmHg at rest) were excluded. The athletes group included 20 top-level, middle age competitive triathletes with evidence of LV hypertrophy by echocardiography. All of them had been training an average of 15 hours/week during the past year and past clinical diagnosis of hypertension and any drug use were an exclusion criteria. All subjects in the control group were healthy, asymptomatic, and did not participate in routine competitive or recreational sports. The study was approved by the ethics committee of our institution and written informed consent was obtained from all the subjects before participation. Echocardiography: Each patient had a complete 2D echocardiography study using a commercially available ultrasound equipment (Vivid 7, General Electric Medical Health, Horten, Norway) with a 2.5-MHz phased array transducer. Standard echocardiographic views, including apical four- and twochamber views, with the patient in the left lateral decubitus position, were obtained. LV and LA dimensions were measured according to recommendations of the American Society of Echocardiography.10 LV mass was determined using Devereux’s formula and indexed for body surface area and LV ejection fraction was measured us-
ing biplane Simpson’s method. Mitral inflow velocities were recorded by standard pulsed-wave Doppler at the tips of the mitral valve leaflets in an apical four-chamber view. Septal and lateral peak mitral annular velocities were measured. LA volumes were calculated from apical four- and two-chamber views of the LA using the biplane method of discs. LA emptying fraction was calculated using the maximal volume (just before the opening of the mitral valve) and minimal volume (at the closure of the mitral valve).11 All measurements were analyzed by two experienced sonographers. Left Atrial Strain and Strain Rate: To calculate LA strain and strain rate the images were analyzed offline by a computer software. The endocardial border was manually traced using a point-and-click technique. LA strain was calculated with the reference point set at the p-wave, which enabled the recognition of the peak positive strain (LASs), corresponding to the LA reservoir function. Similarly, in the LA strain rate curve we identified the peak positive strain rate (LASRs) at the beginning of LA systole and the peak negative strain rate (LASRa) during LA contraction (Fig. 1). The software divided the LA wall into six segments and the average LASs, LASRs, and LASRa were used for analysis.7 LA ejection fraction was obtained with the software by speckle tracking. Statistical Methods: Data were expressed as mean ± standard error for continuous variables and as percentages for categorical variables. Comparisons between the groups were performed using ANOVA
Figure 1. Two-dimensional left atrial (LA) speckle tracking. Longitudinal strain rate curve depicting the peak positive strain rate during left ventricular (LV) systole (LASRs), the peak negative strain rate at the beginning of LV diastole (LASRe), and the peak negative strain rate during LA contraction (LASRa).
944
Left Atrial Function in the Evaluation of Athlete’s Heart
TABLE I Clinical Characteristics
Age (years) Men (%) BMI (kg/m2 ) SAP (mmHg) HR (bpm) Creatinine (mg/dL) Hematocrite (%)
Controls (20)
Athletes (20)
HCM (20)
P (ANOVA)
45 ± 5 80 23 ± 2 121 ± 9 76 ± 6 0.8 ± 0.2 41 ± 3
43 ± 4 80 24 ± 2 117 ± 7 ∗ 55 ± 5 0.9 ± 0.3 44 ± 4
46 ± 5 80 25 ± 3 129 ± 9 ∗ 61 ± 6 1.1 ± 0.3 40 ± 5
NS NS NS NS
