Key result
Depressed heart rate variability is linked to severe cardiac iron deposition in transfusion-dependent thalassemia.
Why the study?
Iron overload cardiomyopathy is the major cause of death in transfusion-dependent thalassemia, and cardiac T2 MRI is costly for detecting cardiac iron accumulation. Heart rate variability has been used to evaluate cardiac autonomic function and may serve as an early indicator of cardiac iron deposition.
Can heart rate variability be used as an indicator for early identification of cardiac iron deposition in patients with transfusion-dependent thalassemia?
Cross-Sectional (n=101)
No
Can heart rate variability be used as an indicator for early identification of cardiac iron deposition in patients with transfusion-dependent thalassemia?
Heart rate variability and mean serum ferritin over the last 12 months can serve as predictors for cardiac iron deposition in patients with transfusion-dependent thalassemia, potentially aiding in early risk evaluation.
Answers are grounded in this paper and cite their sources.
ASDNN may support noninvasive risk stratification in transfusion-dependent thalassemia; leaves open prospective validation before clinical use.
BACKGROUND: Iron overload cardiomyopathy remains the major cause of death in patients with transfusion-dependent thalassemia. Cardiac T2* magnetic resonance imaging is costly yet effective in detecting cardiac iron accumulation in the heart. Heart rate variability (HRV) has been used to evaluate cardiac autonomic function and is depressed in cases of thalassemia. We evaluated whether HRV could be used as an indicator for early identification of cardiac iron deposition. METHODS: One hundred and one patients with transfusion-dependent thalassemia were enrolled in this study. The correlation between recorded HRV and hemoglobin, non-transferrin bound iron (NTBI), serum ferritin and cardiac T2* were evaluated. RESULTS: The median age was 18 years (range 8-59 years). The patient group with a 5-year mean serum ferritin >5,000 ng/mL included significantly more homozygous β-thalassemia and splenectomized patients, had lower hemoglobin levels, and had more cardiac iron deposit than all other groups. Anemia strongly influenced all domains of HRV. After adjusting for anemia, neither serum ferritin nor NTBI impacted the HRV. However cardiac T2* was an independent predictor of HRV, even after adjusting for anemia. For receiver operative characteristic (ROC) curve analysis of cardiac T2* ≤20 ms, only mean ferritin in the last 12 months and the average of the standard deviation of all R-R intervals for all five-minute segments in the 24-hour recording were predictors for cardiac T2* ≤20 ms, with area under the ROC curve of 0.961 (p<0.0001) and 0.701 (p = 0.05), respectively. CONCLUSIONS: Hemoglobin and cardiac T2* as significant predictors for HRV indicate that anemia and cardiac iron deposition result in cardiac autonomic imbalance. The mean ferritin in the last 12 months could be useful as the best indicator for further evaluation of cardiac risk. The ability of serum ferritin to predict cardiac risk is stronger than observed in other thalassemia cohorts. HRV might be a stronger predictor of cardiac iron in study populations with lower somatic iron burdens and greater prevalence of cardiac iron deposition.
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Silvilairat et al. (2016) conducted a cross-sectional in Transfusion-dependent thalassemia (n=101). Heart rate variability (ASDNN) was evaluated on Prediction of severe cardiac iron deposition (cardiac T2 ≤ 20 ms) (AUC 0.701, p=0.05). Depressed heart rate variability (ASDNN) was a predictor of severe cardiac iron deposition (cardiac T2 ≤ 20 ms) in patients with transfusion-dependent thalassemia, with an area under the ROC curve of 0.701.
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