Thyroid and Heart Connection: Known for Decades

UPDATE 3 July, 2010
Larry Frieders, the compounder, THYROID MADNESS DEFINITION:

1.Treating hypothyroid patients solely with T4-only meds (synthroid)
2.Dosing solely by the TSH and the total T4, or using the outdated "Thyroid Panel"
3.Prescribing anti-depressants in lieu of evaluating and treating the free T3
4.Telling thyroid patients that desiccated natural thyroid like Armour is "unreliable", "inconsistent", "dangerous" or "outdated".
5.Making lab work more important than the hypo symptoms which scream their presence
6.Failing to see the OBVIOUS symptoms of poorly treated thyroid, and instead, recommending a slew of other tests and diagnoses.

9/23/08 - I am pleased to see this topic in the medical article arena. I'd like it more if I saw it in mainstream news. This way there might be some hope that patients would pressure their doctors to run annual thyroid panels, especially for the over 35 crowd, as the AMA recommended about 15 years ago or more.

Endocrine function is closely related to heart function. This is very true for good thyroid health and good gallbladder health, among related issues.

I don't agree that the TSH alone is sufficient for good thyroid evaluation. A Free T3 and a Free T4 are very necessary. If you've never had a reverse T3 (rT3) it's not a bad idea to add that in for baseline, as it does relate to autoimmune issues that are becoming more common today.

Does Your Doctor Know About the New TSH Lab Standards?

I'd be happier too if providers would get current on the TSH et al ranges: The Clinical Endocrinologists (AACE) are currently suggesting that TSH is 0.3-3.0 mU/L.
Over 13 Million Americans with Thyroid Disease Remain Undiagnosed

It is also a good idea to refer to the National Academy of Clinical Biochemistry, part of the Academy of the American Association for Clinical Chemistry (AACC), Laboratory Medicine Practice Guidelines: Laboratory Support for the Diagnosis and Monitoring of Thyroid Disease

"It is likely that the current upper limit of the population reference range is skewed by the inclusion of persons with occult thyroid dysfunction."

"In the future, it is likely that the upper limit of the serum TSH euthyroid reference range will be reduced to 2.5 mIU/L because >95% of rigorously screened normal euthyroid volunteers have serum TSH values between 0.4 and 2.5 mIU/L."

"A serum TSH result between 0.5 and 2.0 mIU/L is generally considered the therapeutic target for a standard L-T4 replacement dose for primary hypothyroidism."

"Thyroxine requirements increase during pregnancy. Thyroid status should be checked with TSH + FT4 during each trimester of pregnancy. The L-T4 dose should be increased (usually by 50 micrograms/day) to maintain a serum TSH between 0.5 and 2.0 mIU/L and a serum FT4 in the upper third of the normal reference interval."

Optimally, cardiologists have a lot to gain by talking cross-specialty.

Patients have much more to lose if they don't.

From this article, ranges not current with ACCE recommendations. "Normal thyroid function (euthyroid; TSH 0.45 - 4.5 mU/L), those with subclinical hypothyroidism (divided into moderate, TSH 4.5 - 9.9 mU/L, and severe, ≥ 10.0 mU/L), and those with subclinical hyperthyroidism (TSH < 0.45 mU/L)."

3 July, 2010 - And consider this article on thyroid and heart health

From Heartwire — a professional news service of WebMD

September 22, 2008 — A new study has found that older adults with severe subclinical hypothyroidism had almost double the risk of developing heart failure (HF) compared with those with normal thyroid function over a 12-year follow-up period [1]. Dr Nicolas Rodondi (University of Lausanne, Switzerland) and colleagues report their findings in the September 30, 2008 issue of the Journal of the American College of Cardiology.

Rodondi told heartwire that these results were in line with those of the only other study to have looked at subclinical hypothyroidism and HF incidence, which also found an increased HF risk only in those with high levels of thyroid-stimulating hormone (TSH).

The findings are important to inform the debate about subclinical hypothyroidism, he says. "There is a big controversy about whether we should screen and treat people with subclinical hypothyroidism. We know that people with overt hypothyroidism with symptoms need to get treated, but about those with no symptoms and just subclinical disease, there is debate. And within this debate about whether to treat or not is another controversy about the threshold at which you should treat."

These and other results from prior studies support the recommendations of several guidelines that those with subclinical hypothyroidism and no symptoms should be treated with thyroxine only if their TSH is 10.0 mU/L or more, Rodondi says. However, he points out that some endocrinologists disagree and advocate treating such patients at lower TSH levels. The debate is important, he says, because it is has been shown that monitoring of TSH levels under thyroxine is not always accurate in clinical practice, with overtreatment having its own attendant risks.

"Indirect evidence" that thyroxine might prevent HF

Rodondi and colleagues studied 3044 adults who were 65 or older participating in the Cardiovascular Health Study, all of whom were free of HF at baseline. They compared adjudicated HF events over a mean of 12 years of follow-up and changes in cardiac function over the course of five years among those with normal thyroid function (euthyroid; TSH 0.45 - 4.5 mU/L), those with subclinical hypothyroidism (divided into moderate, TSH 4.5 - 9.9 mU/L, and severe, ≥ 10.0 mU/L), and those with subclinical hyperthyroidism (TSH < 0.45 mU/L). Over the follow-up period, 736 people developed HF events. Those with TSH 10.0 mU/L or more had a greater incidence of HF compared with euthyroid participants (adjusted HR 1.88, p=0.01). No such increased risk was seen in those with TSH 4.5 - 9.9 mU/L or in those with subclinical hyperthyroidism compared with euthyroid participants. Baseline peak E velocity — an echocardiographic measure of diastolic function associated with incident heart failure in the cohort — was also greater in those with TSH 10.0 mU/L or more compared with euthyroid participants (0.80 m/s vs 0.72 m/s; p=0.002). And over the course of five years, left ventricular mass increased among those with TSH 10.0 mU/L or more, although other echocardiographic measures were unchanged. In a further exploratory analysis, the researchers stratified people with TSH 10.0 mU/L or more into those who received thyroxine replacement therapy and those who didn't. They found that those who got thyroxine did not have an increased risk of HF, "providing indirect evidence that [thyroxine] might work to prevent development of HF in those with TSH 10.0 mU/L or more," said Rodondi. He stressed, however, that "to definitively prove a link between subclinical thyroid dysfunction and HF, a randomized clinical trial would be needed in which one group is treated with thyroxine vs placebo to see if the former reduces the risk. That would be proof of concept, but it has not been done as yet." Overtreatment with thyroxine has risks too Rodondi said their findings — that those with less severe subclinical hypothyroidism do not seem to be at risk of HF — are "important," because a high proportion of older adults fit into this category and are treated with thyroxine in clinical practice, without consistent evidence that this is of benefit. Monitoring of TSH levels under thyroxine is not always accurate in clinical practice, he explains, and it is estimated that around 20% to 30% of people receiving thyroxine are overtreated. This in itself has risks, as subclinical hyperthyroidism has been associated with atrial fibrillation and increased fracture risk. "In aggregate, our findings might help refine a treatment threshold at which clinical benefit would be expected and demonstrate a subpopulation at risk for a life-threatening condition," he and his colleagues say in their paper. "Clinical trials should examine the efficacy of screening for and treating subclinical thyroid dysfunction and assess whether the risk of HF might be ameliorated by thyroxine replacement in individuals with TSH levels above 10 mU/L," they conclude. Source: Rodondi N, Bauer DC, Cappola AR, et al. Subclinical thyroid dysfunction, cardiac function and the risk of heart failure. The Cardiovascular Health Study. J Am Coll Cardiol. 2008;52:1152-1159.

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