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Nonthyroidal illness: a risk factor for coronary calcification and arterial stiffness in patients undergoing
Christiaan L Meuwese1, Juan J Carrero, Iván Cabezas-Rodríguez
1Department of Clinical Epidemiology, Leiden University Medical Centre, Leiden, The Netherlands; Baxter Novum, CLINTEC, Karolinska Institutet, Stockholm, Sweden.
Insights
Low free triiodothyronine (fT3) in dialysis patients is linked to vascular calcification and higher mortality. This suggests accelerated vascular calcification may explain the increased cardiovascular risk in nonthyroidal illness syndrome.
Area of Science:
- Nephrology
- Endocrinology
- Cardiology
Background:
- Low triiodothyronine (fT3) is common in dialysis patients, associated with increased cardiovascular mortality.
- The nonthyroidal illness syndrome may contribute to this elevated mortality risk.
Purpose of the Study:
- To investigate if vascular calcification mediates the relationship between low fT3 and mortality in peritoneal dialysis patients.
- To assess the association between fT3 levels, vascular calcification, arterial stiffness, and mortality.
Main Methods:
- 84 peritoneal dialysis patients were studied, measuring serum fT3, thyroxine, and TSH.
- Coronary artery calcium (CAC) scores and arterial stiffness surrogates were assessed.
- Patients were followed for mortality events.
Main Results:
- Higher CAC scores and arterial stiffness were observed in patients with low fT3 levels.
- Low fT3 and high CAC scores were independently associated with increased all-cause mortality.
- Associations persisted after multivariate regression analysis.
Conclusions:
- In peritoneal dialysis patients, low fT3 is strongly linked to arterial stiffness, CAC, and mortality.
- Accelerated vascular calcification may partly mediate the mortality risk associated with nonthyroidal illness.
Objectives:
Low triiodothyronine levels, as part of the nonthyroidal illness syndrome, are common in dialysis patients and have repeatedly been shown to be associated with increased (cardiovascular) mortality rates. We hypothesized that increased vascular calcification may mediate this relationship.
Methods:
A total of 84 patients from the Stockholm region receiving maintenance peritoneal dialysis were included in the study. Serum concentrations of free triiodothyronine (fT3), thyroxine and thyroid-stimulating hormone were measured. Coronary artery calcium (CAC) scores were assessed by cardiac computed tomography scans. Surrogates of arterial stiffness included aortic diastolic and systolic blood pressures, pulse pressure, augmentation pressure and Buckberg's subendocardial viability ratio measured by pulse waveform analyses. Patients were subsequently followed, and events of death and censoring were recorded. Thyroid hormone concentrations were associated with CAC scores, measures of arterial stiffness and all-cause mortality. The associations between CAC scores and arterial stiffness surrogates and mortality were also determined to evaluate a possible causal pathway.
Results:
Both CAC scores and arterial stiffness surrogates were substantially higher in individuals with low fT3 levels. These associations persisted in multivariate logistic and linear regression analyses. During a median (interquartile range) follow-up of 32 (22-42) months, 24 patients died. Both fT3 levels below the median value [HR crude 4.1, 95% confidence interval (CI) 1.4-12.6] and CAC scores above the median value (HR crude 5.8, 95% CI 1.7-20.1) were strongly associated with mortality.
Conclusions:
In patients undergoing peritoneal dialysis, fT3 levels were strongly associated with arterial stiffness, coronary artery calcification and mortality. We speculate that the association between nonthyroidal illness and mortality may be partly mediated by acceleration of vascular calcification.
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