Does echocardiography accurately reflect CMR-determined changes in left ventricular parameters following exercise training? A prospective longitudinal study

Cardiac adaptation in response to exercise has historically been described using echocardiography. Cardiac magnetic resonance (CMR), however, has evolved as a preferred imaging methodology for cardiac morphological assessment. While direct imaging modality comparisons in athletes suggest that large absolute differences in cardiac dimensions exist, it is currently unknown whether changes in cardiac morphology in response to exercise training are comparable when using echocardiography and CMR. Twenty-two young men were randomly assigned to undertake a supervised and intensive endurance or resistance exercise-training program for 24 wk. Echocardiography and CMR assessment of left ventricular (LV) mass, LV end-diastolic volume, internal cavity dimensions, and wall thicknesses were completed before and after training. At baseline, pooled data for all cardiac parameters were significantly different between imaging methods, while LV mass (r = 0.756, P < 0.001) and volumes (LV end-diastolic volume, r = 0.792, P < 0.001) were highly correlated across modalities. Changes in cardiac morphology data with exercise training were not significantly related when echocardiographic and CMR measures were compared. For example, posterior wall thickness increased by 8.3% (P < 0.05) when assessed using echocardiography, but decreased by 2% when using CMR. In summary, echocardiography and CMR imaging modalities produce findings that differ with respect to changes in cardiac size and volume following exercise training

Implications of exercise-induced pulmonary arterial hypertension

Purpose: To characterize the hemodynamic and ventilatory responses to exercise in a group of patients with unexplained dyspnea, increased risk for pulmonary arterial hypertension (PAH), and an elevated mean pulmonary artery pressure (mPAP; \u3e30 mm Hg) on exercise. Methods: A total of 37 symptomatic patients at risk of PAH and 20 healthy controls underwent a cardiopulmonary exercise test and were assessed for quality of life (QOL). Patients had a pulmonary artery catheter in situ during the exercise test. Results: Seventeen subjects had exercise-induced PAH (EIPAH), which we defined as mPAP \u3c= 25 mm Hg at rest, and mPAP \u3e 30 mm Hg and pulmonary artery wedge pressure \u3c20 mm Hg on exercise. These subjects had reduced peak exercise cardiac output (72% ± 19% predicted). Further, compared with matched controls, subjects with EIPAH had reduced peak oxygen consumption (1.2 ± 0.4 vs 1.7 ± 0.5 L·min-1, P \u3c 0.05), an elevated ventilatory equivalent for carbon dioxide (41.0 ± 7.3 vs 31.0 ± 2.9, P \u3c 0.05) and reduced end-tidal carbon dioxide tension (32.6 ± 3.6 vs 39.4 ± 2.7 mm Hg, P \u3c 0.05) at the anaerobic threshold. These exercise abnormalities were associated with impaired QOL (P \u3c 0.05). Conclusions: Elevated pulmonary artery pressure on exercise can be associated with hemodynamic and ventilatory abnormalities typical of PAH, along with impaired exercise capacity and reduced QOL