Reduced right ventricular myocardial strain in the elite athlete may not be a consequence of myocardial damage. "Cream masquerades as skimmed milk".

BACKGROUND: Latest research shows that the lower resting values of right ventricular (RV) myocardial % strain may represent a physiologic change rather than subclinical myocardial damage. Therefore, we assessed load-independent changes to the RV as a consequence of high intensity training by measuring the Isovolumic acceleration (IVA) of the free wall of the RV in conjunction with NT pro-BNP measured by an electrochemiluminescence assay. METHODS: Seventeen controls (mean age 27 ± 4), 24 soccer footballers (mean age 24 ± 4), and 18 elite rowers (mean age 22 ± 4) were studied. Left ventricular (LV) and RV % strain were measured using two-dimensional (2D) speckle based automated functional imaging (AFI) software. RV free wall IVA was measured using pulsed-wave tissue Doppler at the lateral tricuspid annulus. Standard 2D echo were used to measured RV parameters including the Tei index (systolic and diastolic function) and the total annular plane systolic excursion (TAPSE) of the RV annulus. NT pro-BNP was measured by an electrochemiluminescence assay. RESULTS: The RV diameter was increased in the footballers and elite rowers compared with controls (P < 0.001). RV wall size was greater in the elite rowers compared with controls and footballers (P = 0.002). The peak IVA of the RV was higher in the rowers, compared with the footballers and to controls (P < 0.001). The mean LV and RV % myocardial strain were lower in the elite athletes and the footballers compared with controls (P < 0.001). There was no difference in RV Tei index, levels of BNP, and TAPSE across all subjects. CONCLUSIONS: This study showed a significant increase in IVA of the RV of athletes despite reduced myocardial % strain and normal levels in NT-proBNP. This suggests that the decrease in % strain is not a consequence of myocardial damage, but may represents a part of the physiological response to endurance exercise. Therefore, a reduced IVA in a remodeled RV could herald a pathological response.

Myocardial stiffness and the timing difference between tissue Doppler imaging Ea and peak mitral valve opening can distinguish physiological hypertrophy in athletes from hypertrophic cardiomyopathy.

AIM: To differentiate between physiological and pathological left ventricular hypertrophy in athletes using echocardiography. METHODS AND RESULTS: Eleven patients with mild hypertrophic cardiomyopathy were compared against 17 international rowers with mild left ventricular hypertrophy, and 30 age matched controls. The time difference between peak Ea (Doppler tissue imaging) and peak mitral valve opening (using M-mode) was measured simultaneously. A novel index (E/Ea)/LVEDD, as a measure of left ventricular stiffness was recorded. In athletes the peak Ea preceded peak mitral opening by: median (interquartile range) 20 ms (10,20), control group 15 ms (0,30), compared with HCM where Ea followed peak mitral opening by 10 ms (0,20), P<0.0001. In athletes the index of left ventricular stiffness was lower than controls 1.2 (0.93,1.4) versus 1.5 (1.3,1.6), and HCM 2.2 (2.0,2.3), P<0.0001. CONCLUSION: Physiological hypertrophy can be differentiated from hypertrophic cardiomyopathy in athletes using the Ea-peak mitral opening difference, and our index of ventricular stiffness.