Coronary vasoreactivity in subjects with thyroid autoimmunity and subclinical hypothyroidism before and after supplementation with thyroxine.
BACKGROUND
The association of subclinical hypothyroidism (SCH) with increased risk for cardiovascular disease is still controversial. This study aimed to examine coronary vascular reactivity by positron emission tomography (PET) in asymptomatic patients with SCH before and after levothyroxine (LT4) supplementation.


METHODS
Ten patients (7 women and 3 men; mean age 43±15 years) with untreated autoimmune SCH, defined by elevated levels of thyroid-stimulating hormone (mean TSH: 16.9±11.3 μU/mL), normal levels of free thyroxine (0.9±0.1 μg/mL), free triiodothyronine (3.2±0.4 pg/mL), and positive thyroid peroxidase antibodies were studied. Eight euthyroid subjects with similar low-risk cardiovascular risk profile served as controls. Myocardial blood flow (MBF) and coronary flow reserve (CFR) were quantitatively assessed with rest/stress N-13 ammonia PET at baseline and after 6 months of LT4 replacement therapy (given only to patients).


RESULTS
At baseline, stress MBF and CFR corrected (c) for rate pressure product (RPP) and myocardial vascular resistance (MVR) during stress were significantly reduced in SCH compared with controls (stress MBF: 2.87±0.93 vs. 4.79±1.16 mL/g/min, p=0.003; CFR: 2.6±0.73 vs. 4.66±1.38, p=0.004; MVR: 40.14±18.76 vs. 20.47±6.24 mmHg/mL/min, p=0.02). Supplementation therapy with LT4 normalized TSH in all subjects and was associated with an increase in CFR (2.6±0.73 vs. 3.81±1.19, p=0.003) and with a tendency toward a decrease in MVR. Differences in CFR between SCH and controls were also seen after correction of resting MBF for RPP.


CONCLUSIONS
In asymptomatic subjects with SCH due to thyroid autoimmunity, coronary microvascular function is impaired and improves after supplementation with LT4. This may partially explain the increased cardiovascular risk attributed to SCH.
Department of Nuclear Medicine, Medical University of Vienna, Vienna, Austria.
Tatjana
T
Traub-Weidinger
Senta
S
Graf
Mohsen
M
Beheshti
Sedat
S
Ofluoglu
Georg
G
Zettinig
Aliasghar
A
Khorsand
Stephan G
SG
Nekolla
Kurt
K
Kletter
Robert
R
Dudczak
Christian
C
Pirich
D000328:Adult; D000368:Aged; D001323:Autoantibodies / Q000097:blood; D016022:Case-Control Studies; D003326:Coronary Circulation / Q000187:drug effects*; D003331:Coronary Vessels / Q000000981:diagnostic imaging*; D005260:Female; D006801:Humans; D007037:Hypothyroidism / Q000188:drug therapy*; D007453:Iodide Peroxidase; D008297:Male; D008875:Middle Aged; D049268:Positron-Emission Tomography; D019275:Radiopharmaceuticals; D013961:Thyroid Gland / Q000000981:diagnostic imaging; D013963:Thyroid Hormones / Q000097:blood; D013967:Thyroiditis, Autoimmune / Q000188:drug therapy* / Q000503:physiopathology; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000627:therapeutic use*; D014655:Vascular Resistance / Q000187:drug effects*
D001323:Autoantibodies; D019275:Radiopharmaceuticals; D013963:Thyroid Hormones; D013972:Thyrotropin; D007453:Iodide Peroxidase; D013974:Thyroxine