Subclinical hypothyroidism is defined as an elevated serum thyroid-stimulating 
hormone (TSH) level in the face of normal free thyroid hormone values. The 
overall prevalence of subclinical hypothyroidism is 4-10% in the general 
population and up to 20% in women aged >60 years. The potential benefits and 
risks of therapy for subclinical hypothyroidism have been debated for 2 decades, 
and a consensus is still lacking. Besides avoiding the progression to overt 
hypothyroidism, the decision to treat patients with subclinical hypothyroidism 
relies mainly on the risk of metabolic and cardiovascular alterations. 
Subclinical hypothyroidism causes changes in cardiovascular function similar to, 
but less marked than, those occurring in patients with overt hypothyroidism. 
Diastolic dysfunction both at rest and upon effort is the most consistent 
cardiac abnormality in patients with subclinical hypothyroidism, and also in 
those with slightly elevated TSH levels (>6 mIU/L). Moreover, mild thyroid 
failure may increase diastolic blood pressure as a result of increased systemic 
vascular resistance. Restoration of euthyroidism by levothyroxine replacement is 
generally able to improve all these abnormalities. Early clinical and autopsy 
studies had suggested an association between subclinical hypothyroidism and 
coronary heart disease, which has been subsequently confirmed by some, but not 
all, large cross-sectional and prospective studies. Altered coagulation 
parameters, elevated lipoprotein (a) levels, and low-grade chronic inflammation 
are regarded to coalesce with the hypercholesterolemia of untreated patients 
with subclinical hypothyroidism to enhance the ischemic cardiovascular risk. 
Although a consensus is still lacking, the strongest evidence for a beneficial 
effect of levothyroxine replacement on markers of cardiovascular risk is the 
substantial demonstration that restoration of euthyroidism can lower both total 
and low-density lipoprotein-cholesterol levels in most patients with subclinical 
hypothyroidism. However, the actual effectiveness of thyroid hormone 
substitution in reducing the risk of cardiovascular events remains to be 
elucidated. In conclusion, the multiplicity and the possible reversibility of 
subclinical hypothyroidism-associated cardiovascular abnormalities suggest that 
the decision to treat a patient should depend on the presence of risk factors, 
rather than on a TSH threshold. On the other hand, levothyroxine replacement 
therapy can always be discontinued if there is no apparent benefit. 
Levothyroxine replacement therapy is usually safe providing that excessive 
administration is avoided by monitoring serum TSH levels. However, the 
possibility that restoring euthyroidism may be harmful in the oldest of the 
elderly population of hypothyroid patients has been recently raised, and should 
be taken into account in making the decision to treat patients with subclinical 
hypothyroidism who are aged >85 years.