Claire Stephenson

Mitral annular myocardial velocity assessment of segmental left ventricular diastolic function after prolonged exercise in humans

We assessed segmental and global left ventricular (LV) diastolic function via tissue‐Doppler imaging (TDI) as well as Doppler flow variables before and after a marathon race to extend our knowledge of exercise‐induced changes in cardiac function. Twenty‐nine subjects (age 18–62 year) volunteered to participate and were assessed pre‐ and post‐race. Measurements of longitudinal plane TDI myocardial diastolic velocities at five sites on the mitral annulus included peak early myocardial tissue velocity (E′), peak late (or atrial) myocardial tissue velocity (A′) and the ratio E′/A′. Standard pulsed‐wave Doppler transmitral and pulmonary vein flow indices were also recorded along with measurements of body mass, heart rate, blood pressures and cardiac troponin T (cTnT), a biomarker of myocyte damage. Pre‐ to post‐race changes in LV diastolic function were analysed by repeated measures ANOVA. Delta scores for LV diastolic function were correlated with each other and alterations in indices of LV loading. Diastolic longitudinal segmental and mean TDI data were altered post‐race such that the mean E′/A′ ratio was significantly depressed (1.51 ± 0.34 to 1.16 ± 0.35, P < 0.05). Changes in segmental and global TDI data were not related to an elevated post‐race HR, a decreased post‐race pre‐load or an elevated cTnT. The pulsed wave Doppler ratio of peak early transmitral flow velocity (E)/peak late (or atrial) flow velocity (A) was also significantly reduced post‐race (1.75 ± 0.46 to 1.05 ± 0.30, P < 0.05); however, it was significantly correlated with post‐race changes in heart rate. The lack of change in E/E′ from pre‐ to post‐race (3.4 ± 0.8 and 3.3 ± 0.7, respectively) suggests that the depression in diastolic function is likely to be due to altered relaxation of the left ventricle; however, the exact aetiology of this change remains to be determined.

Impact of marathon running on cardiac structure and function in recreational runners

The present study examined the relationship between LV (left ventricular) function, markers of cardiac-specific damage and markers of oxidative stress in recreational runners following a marathon. Runners (n=52; 43 male and nine female; age, 35+/-10 years; height, 1.74+/-0.08 m; body mass, 75.9+/-8.9 kg) were assessed pre- and immediately post-marathon. LV function was assessed using standard M-mode two-dimensional Doppler echocardiography and TDI (tissue-Doppler imaging) echocardiography. Serum was analysed for cTnT (cardiac troponin-T), TEAC (Trolox equivalent antioxidant capacity; a measure of total antioxidant capacity), MDA (malondealdehyde) and 4-HNE (4-hydroxynonenal). A strong relationship was observed between standard and TDI echocardiography for all functional measures. Diastolic function was altered post-marathon characterized by a reduction in E (peak early diastolic filling: 0.79+/-0.11 compared with 0.64+/-0.16 cm/s; P<0.001), an increase in A (peak late diastolic filling: 0.48+/-0.11 compared with 0.60+/-0.12 cm/s; P<0.001) and a resultant decrease in E/A (ratio of E to A; 1.71+/-0.48 compared with 1.10+/-0.31; P<0.001). Ejection fraction remained unchanged post-marathon. Thirty-two runners presented with cTnT values above the lower limit of detection for the assay (0.01 microg/l), and 20 runners presented post-marathon with cTnT values above the acute myocardial infarction cut-off value (0.05 microg/l). No significant correlations were observed between cTnT and any functional measurements. MDA (2.90+/-1.58 compared with 3.59+/-1.47 micromol/l) and TEAC (1.80+/-0.12 compared with 1.89+/-0.21 mmol/l) were significantly increased post-marathon, but were unrelated to changes in function or cTnT. In conclusion, the present study demonstrated a reduction in diastolic function and widespread evidence of minimal cardiac damage following a marathon in recreational runners. The mechanism(s) underpinning the altered function and appearance of cTnT appear unrelated to reactive oxygen species.

A study of presbycardia, with gender differences favoring ageing women

BACKGROUND The impact of ageing on the human cardiovascular system has been the subject of several studies in recent years, but with insufficient emphasis on defining sex-specific differences. To rectify this, gender-specific differences in structure and function in the human cardiovascular system were studied in a European population during natural ageing. METHODS Cardiac power output (CPO) was measured and integrated with changes in left ventricular (LV) mass, diastolic, systolic and limb blood flow, blood pressure and exercise capacity in 93 health-screened men and 122 women, aged 20 to 75 years. RESULTS Correlating with a 21% loss of LV mass, maximum cardiac pumping (i.e. CPOmax=QmaxxMAPmax) and reserve (CR=CPOmax-CPOrest) capacities decreased 20-25% with age in male hearts. In contrast, CPOmax, CR and LV mass were all preserved in ageing women. Maximum cardiac output (Qmax; 26-32%), peak forearm blood flow (FBFpeak; 61%) and exercise capacity (40-50%) all decreased, but more so in men than women. In contrast, systemic vascular resistance (68-75%) and mean arterial pressure (MAPmax; 14-26%) increased in both sexes. CPOrest decreased 27% in men, but was unchanged in women, despite lower early:late diastolic filling (48-51%), Qrest (19-23%) and FBFrest (56%) in both sexes. CONCLUSIONS Understanding sex-specific differences in cardiovascular ageing is important for public health and biomedical research, given increasingly larger older populations and the need to prevent and treat cardiovascular disease.

The effect of weightlifting upon left ventricular function and markers of cardiomyocyte damage

The purpose of this study was to assess left ventricular (LV) function and biochemical markers of myocyte after prolonged weightlifting activity. Seventeen male subjects (age range 20–34 years) performed a 90-min bout of weightlifting exercise consisting of three sets of 8–10 repetitions at 70% one-repetition maximum. Body mass, heart rate, systolic blood pressure (SBP) and echocardiographically determined indices of LV loading (LV internal diameter during diastole, LV meridonial wall stress), systolic function (stroke volume (SV), ejection fraction (EF), end-systolic pressure volume relationship; SBP/ESV) and diastolic filling (ratio of early to late; E:A) were obtained pre-exercise, immediately after and 24 h post-exercise. A 5-ml venous blood sample was obtained for the assessment of cardiac troponin T (cTnT) via third generation electrochemiluminescence assay. Data were assessed via one-way ANOVA and Pearsons correlation. Although SV declined (80.9 ± 18.3 vs. 66.9 ± 17.2, p < 0.05) there was no alteration in LV contractility (EF 62 ± 6 vs. 59 ± 7; SBP/ESV 3.51 ± 1.4 vs. 3.51 ± 1.4, p > 0.05). The E:A ratio was significantly decreased following exercise (1.78 ± 0.41 vs. 1.33 ± 0.37, p < 0.05). This decrease was not fully explained by loading conditions (r2 = 0.05 to 0.24). All values returned to baseline 24 h post-exercise. No cTnT was reported in any of the blood samples. In conclusion, there was no significant evidence of any LV contractile depression and no cTnT was observed post exercise. The small reduction in diastolic filling could not be explained by changes in haemodynamic loading or the post-exercise elevation in heart rate.