Background: Patients with heart failure show a reduction in peak oxygen uptake (VO2), even with optimal medical therapy. In subjects with biventricular involvement, the main contributor to exercise limitation may be right or left heart failure. In these patients, the identification of the primary mechanism of exercise lmitation is a challenge. Simultaneous analysis of the metabolic and hemodynamic response during exercise may permit an improved differentiation of the primary mechanisms of limitation.
Aim: In this pilot study, we characterized the hemodynamic and metabolic response to exercise in stable patients with chronic, isolated left vs right heart failure, and determined whether there are specific response patterns in these two patient groups.
Methods: We analyzed a cohort of highly selected patients with isolated right heart failure (group 1, n=9) and isolated left heart failure (group 2, n=9). All patients were in functional class II and III, and under stable medical treatment according to current guidelines. All patients had received right heart catheterization before enrollment that reveiled elevated pulmonary vascular resistance (PVR) in all of the patients in group 1 and normal PVR in all of the patients in group 2. All patients received a cardiopulmonary exercise test (CPET) with a ramp protocol up to maximal exercise tolerance. During a second visit, a combined CPET / stress echocardiography was performed with a two step constant work rate protocol. For step 1, a workrate below the patients‘ anaerobic threshold was chosen. For step 2, 80% of the patients‘ maximum workrate from the ramp test was chosen. Each step was performed until a complete echocardiographic image acquisition was obtained. Gas exchange was measured breath-by-breath. Echocardiographic parameters were obtained once at rest and for each of the two exercise steps.
Results: There were no significant differences in demographic baseline characteristics. The absolute peak VO2 values, corrected for body weight, showed no significant difference. In both goups, exercise induced a significant increase of left ventricular (LV) ejection fraction and longitudinal LV function. In contrast, diastolic LV function deteriorated only in group 2, as demonstrated by increased E/A ratio and failure to reduce E/e’. Right ventricular function, as assessed by fractional area change, deteriorated under exercise exclusively in group 1, explained by substantial augmentation of paradoxical septal motion under exercise. Under exercise, PVR by echocardiography increased only in group 1, whereas in this group and in contrast to group 2, left ventricular stroke volume remained unchanged.
Conclusions: The non-invasive, simultaneous evaluation of hemodynamic and metabolic parameters by CPET and stress echocardiography is safe and reveals characteristic response patterns.Whereas cardiovascular limitation in left heart failure is mainly due to diastolic dysfunction, increase of PVR, paradoxical septal motion and deterioration of right ventricular function occur in right heart failure. Furthermore, patients with right heart failure seem to be less able to increase stroke volume during exercise.
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