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Enalapril therapy and cardiac remodelling in sickle cell disease patients
Carmen S P Lima1, Osvaldo M Ueti, Adriana A Ueti
1Haematology and Haemotherapy Centre, State University of Campinas, Campinas, São Paulo, Brazil. carmenl@fcm.unicamp.br
Insights
Angiotensin-converting enzyme inhibitors (ACEi) prevent cardiac remodeling in sickle cell disease (SCD) patients. Enalapril treatment halted increases in left ventricular mass and wall thickness observed in untreated SCD individuals.
Area of Science:
- Cardiology
- Hematology
- Pharmacology
Background:
- Angiotensin-converting enzyme inhibitors (ACEi) are established treatments for cardiac dysfunction post-myocardial infarction.
- Cardiac complications are a concern in sickle cell disease (SCD).
Purpose of the Study:
- To investigate the cardiac effects of ACEi in patients with SCD.
- To assess enalapril's impact on cardiac structure in SCD patients.
Main Methods:
- Enalapril was administered to 9 SCD patients with microalbuminuria.
- A control group of 9 SCD patients without microalbuminuria was followed for 36 months.
- Echocardiograms were performed at baseline and after 36 months.
Main Results:
- Untreated SCD patients showed increased left ventricular mass, wall thickness, and aortic root diameter.
- Enalapril-treated SCD patients did not exhibit these cardiac remodeling changes.
- No significant changes in left ventricular dimensions or ejection fraction were observed in either group.
Conclusions:
- Enalapril appears to prevent cardiac remodeling in SCD patients.
- Further large-scale trials are needed to confirm enalapril's efficacy in SCD.
Introduction:
Angiotensin-converting enzyme inhibitors (ACEi) have been successfully used for patients with cardiac dysfunction after myocardial infarction.
Objective:
The aim of the present study was to investigate cardiac effects of ACEi in sickle cell disease (SCD) patients, as there are no previous reports regarding these effects.
Methods:
Enalapril was administered to 9 SCD patients with microalbuminuria. Nine SCD patients without microalbuminuria, matched according to age, diagnosis and levels of haemoglobin, haematocrit and foetal haemoglobin did not receive enalapril and were followed up as the control group during the same period of study. Echocardiograms were performed before the study entry and after 36 months of follow-up.
Results:
At 36 months of follow-up, significant increases in left ventricular mass, left ventricular mass index, posterior left ventricular wall thickness in end-diastole, interventricular septal wall thickness in end-diastole, and aortic root diameter values were seen in untreated, but not in enalapril-treated patients. No major changes were seen in left ventricular systolic diameter, diastolic dimension and ejection fraction, and left atrial diameter, in both groups, along the observational period.
Conclusion:
The results of this study suggest that enalapril prevents cardiac remodelling in SCD patients. However, a large trial concerning the response to enalapril in patients with SCD should be carried out to further clarify this issue.
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