Journal of the American Society of Echocardiography
Clinical InvestigationMyocardial DisordersMyocardial Strain Assessment in Cystic Fibrosis
Section snippets
Study Population
We prospectively recruited patients with cystic fibrosis followed up at the Cystic Fibrosis Center of Basse-Normandie. Diagnoses had been confirmed using sweat chloride tests or molecular biology. To qualify for inclusion in the study, patients were required to be ≥16 years old, to be ambulatory and without signs of respiratory symptom worsening (no exacerbations requiring antibiotic therapy and no change in symptoms in the months before echocardiography), not to be on a lung transplantation
Patients
Overall, 42 consecutive patients (mean age, 24 ± 7.5 years; 52% men) diagnosed with cystic fibrosis and referred for echocardiographic assessment of cardiac function were enrolled in this prospective cohort. At the time of echocardiography, all patients were in stable respiratory condition and showed no signs of heart failure. Severe lung disease, defined as FEV1 < 30%, was present in 10 patients (23.8%), and oxygen supplementation was necessary in four patients (9.5%) with desaturation. The
Discussion
Using longitudinal strain measurements, we report for the first time to our knowledge an unexpectedly high rate of subclinical left ventricular functional changes in patients with cystic fibrosis and normal LVEFs.
Previous echocardiographic studies using standard two-dimensional, M-mode, and Doppler parameters have reported contradictory results concerning left ventricular systolic function in patients with cystic fibrosis.2 Our findings using longitudinal strain parameters suggest that left
Conclusions
Using longitudinal strain measurements, we found an unexpectedly high rate of subclinical left ventricular functional changes in patients with cystic fibrosis with normal LVEFs. These findings have potentially significant clinical implications for the outcomes and follow-up of patients with cystic fibrosis, meriting further studies.
Acknowledgments
We thank M. Hamon for helpful discussion. We thank Vaincre la Mucoviscidose (Paris, France) for support of French Cystic Fibrosis Centers.
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