The cardiac effects of subclinical hypothyroidism (SCH i.e. increased circulating TSH with normal T4) have been documented. While overt hypothyroidism causes increased central arterial stiffness (CAS) and augmentation gradient (AI) 1, there are only limited data in SCH. We have measured CAS, AG and augmentation Index (AI) (AG/Pulse pressure x 100) in patients with SCH before and after L-thyroxine (synthroid) therapy.
Peripheral pulse pressure waveforms were studied non-invasively using pulse wave analysis (PWA) with a pencil shaped tonometer applied to the radial artery in 23 females with SCH (ethical committee approval obtained) by applanation tonometry (sphygmocor). PWA was measured at 0,6,12 and 24 weeks and incremental doses of Synthroid were given after each measurement.
Mean age of patients at recruitment was 50.8 plus/minus 4.1yrs, mean FT4 concentration 12.9 plus/minus 0.22 pico mols per litre [NR 9.8-23.1 pico mols per litre].Median TSH was 7.75 milliunits per litre, range 5.7-21.64 milliunits per litre [NR up to 5.5 milliunits per litre]
In 11 patients (all TPO Antibody positive) after 6 months of Synthroid therapy (mean dose 107 micrograms) the median TSH fell from 8.2 to 1.1 milliunits per litre (p<0.01) and the mean FT4 concentration rose from 12.9 to 20.6 pico mols per litre (p<0.01) accompanied by a significant fall in AI (AG /PP x 100) from 28.7% to 23.5% (p<0.02)
SCH is associated with an increase in arterial stiffness and central arterial pressure compared to control values. The improvement in AI following T4 therapy underpins the pathophysiological evidence for T4 treatment in SCH even with values between 5.5 and 10 millimols per litre.
Ref 1:Obuobie K et al, Increased Central Arterial Stiffness in Hypothyroidism, The
Journal of Clinical Endocrinology and Metabolism.87: 4662-4666,2003
22 - 24 Mar 2004
British Endocrine Societies