Key result
Athyreotic patients treated with TSH-suppressive doses of L-Thyroxine had a higher left ventricular mass index compared to controls (117 vs 92 g/m2).
Why the study?
Does TSH-suppressive L-Thyroxine therapy increase left ventricular mass index in asymptomatic athyreotic patients?
Does TSH-suppressive L-Thyroxine therapy increase left ventricular mass index in asymptomatic athyreotic patients?
Answers are grounded in this paper and cite their sources.
The author cautions that the increase in left ventricular mass index observed with TSH-suppressive L-Thyroxine therapy may be a marker of adverse cardiac effects and should not be dismissed as benign.
In their paper on the cardiac effects of TSH suppressive doses of L-Thyroxine in athyreotic patients, Shapiro et al. (1) found no significant differences between patients and controls in the cardiac indices studied. The single exception was an increase in left ventricular mass index (LVMi) in patients (patients 117 ± 35 g/m2, controls 92 ± 31, mean ± sd), but ventricular wall thicknesses were normal. The authors state that an increase in LVMi, without other associated cardiac abnormalities has no prognostic value. This is an optimistic interpretation of the available data. In population studies, left ventricular (LV) mass is a strong predictor of mortality. Calculated LV mass correlates better with LV mass at necropsy than the separate measurements of LV wall thickness (2). In the Framingham study, follow up of 3220 subjects free of clinically apparent heart disease showed that an increase in LV mass correlated with increased death from all causes as well as deaths from cardiovascular disease (3). LV hypertrophy predicted mortality in patients with and without coronary artery disease (4). The reasons for this are not clear. An increase in LV mass may have adverse effects on cardiac function. Alternately, LV mass may simply be a sensitive marker of cardiac end organ damage. Although the LVMi in TSH-suppressed patients are not sufficiently high to be classified as LV hypertrophy, it is prudent to assume that, in keeping with population data, an increase in LVMi is more likely to be harmful than beneficial. Human and animal studies show that thyroid hormone produces an increase in LV mass or even LV hypertrophy, and that this is mediated by an increase in cardiac work (5). Further, the benefits of TSH suppressive therapy are moderate at best. It is therefore necessary to be sure that it is safe. Until we have good mortality data on TSH suppressed patients, we will need to relay on surrogate markers of mortality such as LV mass. Future studies in this area may profit from the additional determination of LV geometry, as the patterns of ventricular remodeling or hypertrophy seem to affect prognosis (6).
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Sebastian J. Padayatty (1998) conducted a letter in Athyreotic patients. TSH suppressive doses of L-Thyroxine vs. Controls was evaluated on Left ventricular mass index (LVMi). Athyreotic patients treated with TSH-suppressive doses of L-Thyroxine had a higher left ventricular mass index compared to controls (117 vs 92 g/m2).
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