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Published on: July 14, 2021
Left ventricular reverse remodeling with infantile dilated cardiomyopathy and pitfalls of carvedilol therapy
Etsuko Tsuda1, Jun Negishi1, Kanae Noritake1
1Department of Pediatric Cardiology, National Cerebral and Cardiovascular Center, Osaka, Japan.
Insights
Idiopathic dilated cardiomyopathy (DCM) in infants may worsen with standard carvedilol doses. Careful titration of low-dose carvedilol, guided by BNP levels, is crucial for improving left ventricular reverse remodeling (LVRR) and heart failure outcomes.
Area of Science:
- Pediatric Cardiology
- Cardiovascular Research
- Pharmacology
Background:
- Idiopathic dilated cardiomyopathy (DCM) and its impact on infant heart function are not fully understood.
- Left ventricular reverse remodeling (LVRR) and carvedilol treatment efficacy in severe infantile heart failure require further investigation.
Purpose of the Study:
- To investigate LVRR in infants with DCM.
- To evaluate the role of carvedilol treatment in severe infantile heart failure due to DCM.
Main Methods:
- Retrospective review of medical records for 5 infants (around 12 months old) with severe heart failure from DCM.
- Defined LVRR by increased left ventricular fractional shortening (LVFS) >10% and percent of normal left ventricular end-diastolic dimension (%LVDd) <120%.
Main Results:
- Four out of five infants relapsed with worsening heart failure despite standard carvedilol doses.
- Brain natriuretic peptide (BNP) levels decreased upon carvedilol dose reduction.
- Over 24 months, significant improvements in LVFS (11±2% to 34±5%) and %LVDd (149±27% to 108±11%) were observed.
Conclusions:
- LVRR was observed two years post-DCM onset in infants.
- Standard carvedilol induction doses may exacerbate heart failure in some infants.
- Close monitoring and slow, low-dose carvedilol titration guided by BNP levels are essential for managing infantile DCM.
Background:
The left ventricular reverse remodeling (LVRR) in idiopathic dilated cardiomyopathy (DCM) and the treatment with carvedilol in infants with severe heart failure remain poorly understood.
Methods:
We reviewed the medical records of 5 infants around 12 months old referred to our hospital with severe heart failure due to DCM. Increased left ventricular fractional shortening (LVFS) by more than 10% and the percent of normal of left ventricular end-diastolic dimension (%LVDd) less than 120% were defined as LVRR in this study.
Results:
DCM onset ranged from 8 to 16 months. Initial treatment of their acute heart failure was successful in all 5 but 4 patients relapsed despite the usual dose of carvedilol (induction 0.02-maintenance 0.4mg/kg/day), and developed worsening heart failure. Brain natriuretic peptide (BNP) levels which increased again after the acute treatment had fallen subsequent to discontinuing or decreasing carvedilol. Over 24 months, LVFS had increased from 11±2% (mean±SD) to 34±5% (p<0.05), and %LVDd decreased from 149±27% to 108±11% (p<0.05).
Conclusions:
LVRR was found at 2 years after the onset of DCM. Usual dose induction of carvedilol therapy can sometimes worsen heart failure after successful initial conventional treatment for the acute heart failure in DCM. Close control of carvedilol treatment may determine the prognosis of infantile DCM around 12 months old. It is prudent to increase low-dose carvedilol slowly corresponding with the BNP level.
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