Arterial Stiffness and Central Hemodynamics in Thyroidectomized Patients on Long-Term Substitution Therapy with Levothyroxine.

Abstract

Long-term levothyroxine (LT4) therapy targeting thyrotropin (TSH) suppression in hypothyroid patients treated for thyroid cancer has been associated with increased arterial stiffness and increased cardiovascular mortality. However, most patients with hypothyroidism receive LT4 therapy targeting TSH in the reference range. The long-term vascular effects of this strategy have never been evaluated. Arterial stiffness and central hemodynamics were studied in 30 thyroidectomized patients (Mage = 54.5 ± 10.2 years; 80% female) on long-term (median = 11 years; range 3-41 years) LT4 replacement therapy targeting TSH in the reference range and 30 sex- and age-matched controls. Arterial stiffness was evaluated by carotid-femoral pulse wave velocity (PWV) and central hemodynamics by pulse wave analysis using the SphygmoCor system. TSH levels were comparable in patients and controls (median = 1.99 × 10(3) IU/L [range 0.24-5.64 × 10(3) IU/L] vs. median = 2.13 × 10(3) IU/L [range 0.59-5.63 × 10(3) IU/L]; p = 0.69), but patients had higher plasma thyroxine and lower plasma triiodothyronine levels than controls (median = 108 nmol/L [range 84-149 nmol/L] vs. 86 nmol/L [range 59-141 nmol/L]; p < 0.001 and median = 1.49 nmol/L [range 1.00-2.37 nmol/L] vs. 1.62 nmol/L [range 1.18-2.09 nmol/L]; p = 0.04, respectively). PWV was not significantly higher in patients compared to controls (8.2 ± 1.9 vs. 7.9 ± 1.9 m/s, p = 0.69). Similarly, no group differences were observed in central systolic/diastolic blood pressure (120 ± 16 mmHg vs. 119 ± 12 mmHg, p = 0.77; and 80 ± 11 mmHg vs. 80 ± 10 mmHg, p = 0.98, respectively), the augmentation index (28 ± 13% vs. 29 ± 8%, p = 0.72), or the pulse pressure amplification ratio (129 ± 17% vs. 124 ± 13%, p = 0.18). Despite subtle differences in plasma levels of thyroid hormones, long-term LT4 replacement therapy targeting TSH in the reference range does not seem to cause adverse effects on arterial stiffness and central hemodynamics.