“Athlete’s heart” describes a symmetrical enlargement of all four cardiac chambers in response to exercise training. However, the uniformity of chamber dilation and the degree to which each contributes to enhanced fitness has not been interrogated. 214 current and former endurance athletes (75% men), aged 16-80 years, underwent a resting echocardiogram and maximal bicycle cardiopulmonary exercise test. Left ventricular volumes (LVEDV) and left atrial volumes (LAESV) were measured using 3D echocardiography and 2D biplane methods, respectively. LVEDV was significantly related to peak VO2 (r=0.643 p<0.001) whereas there was no association between LAESV and exercise capacity (r=0.013 p=0.844). LA/LV ratio (median 0.54) was negatively related to peak VO2 (r=-0.513, p<0.001). Furthermore, a higher LA/LV ratio was observed in athletes with a history of atrial fibrillation (AF, n=19, 0.86±39) compared to those without AF (0.55±14, p<0.001). Athletic remodelling affects the left atrium and ventricle differently, with the latter increasing proportionately to exercise capacity. On the other hand, left atrial enlargement appears to be somewhat maladaptive, with no influence on exercise capacity and associated with the development of AF. The novel ratio of LA/LV volumes warrants further evaluation as a potential predictor of AF.

Introduction: There is limited clinical evidence of pulmonary microvascular disease (PMD) in DM. We hypothesized that (1) a novel echocardiographic marker quantifying the pulmonary transit of agitated colloid contrast bubbles (PTAC) may identify pulmonary capillary disease; and (2) that low-PTAC may be associated with exercise limitation. Methods: A repeated measures cross-over trial of sixty participants (40 DM and 20 age/sex-matched controls [C]) receiving sildenafil 50 mg or placebo in randomized order prior to each of two exercise tests (VO 2max and exercise echocardiography) was performed. PMD was assessed by measuring the degree of PTAC traversing the pulmonary vasculature during incremental exercise. Bubbles reaching the left ventricle were quantified and categorized as low-PTAC or high-PTAC (see Figure 1). Sildenafil’s effect on VO 2max was observed, as were non-invasive measures of central hemodynamic parameters including cardiac output (CO) and pulmonary artery systolic pressure (PASP) to derive pulmonary vascular resistance (PVR). Results: DM and C subjects were of similar age (44 ± 13 vs. 43 ± 13 years, p=0.87) and gender (70% vs. 65% male, p=0.7). Mean DM duration was 16 ± 10 years and glycemic control was moderate (HbA1c: 7.7 ± 1.3%). At peak exercise, low-PTAC was present in more DM than C subjects (low-PTAC: 41 vs. 12.5%, χ 2 P=0.041). When only considering DM subjects, there was a further trend to low-PTAC in those with vs. without microvascular complications (low-PTAC: 55% vs. 26.3%, χ 2 P=0.069). Sildenafil increased CO and reduced PVR in DM, without altering the frequency of low-PTAC or improving VO 2max . On multiple regression, neither PTAC nor sildenafil predicted maximal VO 2 . Conclusion: PTAC was lower in DM compared to C subjects thereby suggesting that PTAC may be a novel marker of PMD. However, PTAC was not associated with exercise capacity and nor was it influenced by pulmonary vasodilator therapy.

Background: Subclinical left ventricular (LV) dysfunction is more commonly reported in diabetes mellitus (DM). We sought to assess in DM whether resting LV function is impaired, and if exercise attenuates these differences. Methods: Forty subjects with DM were grouped into Type 1 (T1DM) or T2DM, and presence/absence of microvascular complications. Twenty controls were age/sex- matched in a 2:1 fashion. Echocardiography was performed at rest and during supine bike exercise. Results: Mean age was 44±13 years with 70% male composition. DM subjects were overweight (BMI 28±4 vs. 25±3 kg/m2, P=0.005). Overall, LV systolic function was similar (LVEF: 60±5 vs. 59±5%, P=0.74). Estimated left-sided filling pressure was numerically greater without clinical significance in DM (E/e’: 11±4 vs. 9±3, P=0.046) however left atrial volume index was paradoxically lower (34±9 vs. 40±9 ml/m2, P=0.01). The differences in diastolic parameters were driven solely by the T2DM group (compared to their matched controls). The additional presence of microvascular disease tended to increase the observed differences on post hoc analysis. Peak exercise resistance was lower only for T2DM compared to their controls (102±32 vs. 142±32W, P=0.003), but was not accounted for by reduced LVEF augmentation or higher E/e’. Conclusion: This comprehensive assessment of LV function at rest and during exercise failed to show systolic or diastolic dysfunction as the cause for lower exercise performance in T2DM. Importantly, there was no difference in exercise or LV function in T1DM. T1DM and T2DM are phenotypically different, and peripheral causes rather than diabetic cardiomyopathy may explain reduced exercise performance in T2DM.

A 77 year-old man presented with dyspnoea. A left sternal edge systolic ejection murmur was noted. He underwent coronary artery bypass grafting with a vein graft(SVG) to the LAD 34 years prior, complicated by graft degeneration 10 years later, necessitating repeat surgery (LIMA to LAD). A rest/exercise echocardiogram demonstrated normal rest and exercise left ventricular function with no ischaemia demonstrated. The right ventricle(RV) was mildly dilated at rest with mild systolic impairment and further dilatation and hypokinesis with exercise. The resting RV systolic pressure was 50 mmHg + right atrial pressure(RAP), increasing to 100 mmHg + RAP with exercise, falling to 60 mmHg + RAP post exercise. The PA systolic pressure gradients at rest and exercise were 50mmHg and 95mmHg respectively. Invasive investigations revealed a PA gradient 20 mmHg, RV systolic pressure 40 mmHg, PA pressure 20/4 mmHg and a large, partially thrombosed aneurysm of the original vein graft. The LIMA graft to the LAD was patent. Computed tomography (figure) confirmed a 6.3 cm graft aneurysm compressing the PA (arrow). Accordingly, he had the aneurysm coiled with abolition of flow. Breathlessness subsequently improved. Exercise echocardiography seventeen months later revealed normal resting RV systolic pressure (21 mmHg + RAP), increasing to 32 mmHg + RAP with exercise and a peak systolic PA gradient at maximum exercise of only 22 mmHg. This case represents a rare example of a SVG aneurysm causing dynamic PA compression as arterial pressure within the aneurysm rose with exercise.

Introduction: Biochemical markers of myocardial damage seen post-IPE have not been explained by cardiac function studies, but RV abnormalities have not been considered.

Aims: Pulmonary transit of agitated contrast (PTAC) occurs to variable extents during exercise. We tested the hypothesis that PTAC signifies exercise-induced dilation of the pulmonary microvasculature, resulting in reduced pulmonary vascular resistance (PVR) and/or improved pulmonary vascular compliance (PVC).

Introduction: The physiological load of intense exercise results in cardiac remodelling. We hypothesized that both acute load and remodelling may be greater in the right ventricle (RV) than the left ventricle (LV) of athletes.