Thyroid Pills Prevent Heart Attacks by Jeffrey Dach MD
The Low Thyroid Condition and Heart Disease
In 1976 Broda Barnes was the first to connect low thyroid function with heart attacks and heart disease. His book is called, Hypothyroidism The Unsuspected Illness by Broda Barnes, Click Here to read my Book Review. Above Left Image: Photo of WP Thyroid Pills Bottle courtesy of RLC labs Natural thyroid pills
Discovering the Connection
How did Broda Barnes discover the connection between low thyroid and heart disease? Barnes took summer vacations in Graz Austria every year to study the autopsy files. Graz had a high prevalence of thyroid disorders, and anyone in Graz who died over the past 100 years required an autopsy to determine cause of death, as mandated by the authorities. This rather large amount of autopsy data showed that low thyroid patients survived the usual childhood infectious diseases thanks to the invention of antibiotics, and years later develop heart disease. Barnes also found that thyroid treatment was protective in preventing heart attacks, based on his own clinical experience. Likewise for diabetes, Dr. Barnes found that adding thyroid medication was beneficial at preventing the onset of vascular disease in diabetics. Again, blood tests are usually normal.
New research like the Hunt Study confirms that Broda Barnes was right all along, creating a paradigm shift in thyroid treatment, and constituting a frontal assault on the Institution of Medicine’s thyroid dogma.
The Hunt Study – Thyroid Function and Heart Disease
TSH is short for thyroid stimulating hormone, made by the pituitary gland. TSH actually stimulates the thyroid gland to make more thyroid hormone, and can therefore be used as a barometer of thyroid function. If thyroid function is low, the pituitary sends out more TSH to stimulate the thyroid to make more thyroid hormone. Above Image: Hunting Dog Courtesy of Wikimedia Commons.
The TSH Test
Mainstream Medicine regards the TSH as the single most important test for determining thyroid function. High TSH means low thyroid function, and a Low TSH means normal or high thyroid function.
What Did The Hunt Study Find?
The Hunt Study from the April 2008 Archives of Internal Medicine examined mortality from coronary heart disease (CHD) and TSH level. The authors conclude,
“The results indicate that relatively low but clinically normal thyroid function may increase the risk of fatal CHD.”
Above Image: Thyroid Gland makes thyroid hormone.
The Hunt Study measured thyroid function with the TSH test in 17,000 women and 8,000 men with no known thyroid disease or heart disease. All patients had “normal TSH” levels meaning the TSH values were in the lab reference range of 0.5 to 3.5. The women were stratified into three groups, lower TSH, intermediate and upper TSH levels, and mortality from heart disease was recorded over an 8 year observation period.
(see chart below).
70% Increase in Heart Disease Mortality for TSH in Upper Normal Range
The Hunt study found that group with the higher TSH had a 70% increased mortality from heart disease compared to the lower TSH group. Remember all these TSH vales were in the normal lab range. See chart below for results of the Hunt Study:
Left Image: Heart with Occluded Coronary Artery and Infarction at the apex, courtesy of wikimedia commons.
Results of the Hunt Study:
|TSH||Death from Heart Disease|
|Group 1||0.50-1.4||baseline risk|
|Group 2||1.5-2.4||40% higher than baseline|
|Group 3||2.5-3.5||70% higher than baseline|
This Finding is Earthshaking !!
This means that merely by taking natural thyroid pills to reduce TSH to the low end of “normal” (0.5), one can reduce death from cardiovascular disease by 70 percent. This mortality benefit is mind boggling and far exceeds any drug intervention available.
Thyroid Hormone Also Improves LDL Lipo-Proteins
Another report from the Hunt Study published in 2007 showed that LDL cholesterol was linearly associated with TSH level. (see chart below).
Above chart shows linear increase in LDL cholesterol as TSH increases.
The Conclusion is Clear:
The best way to normalize lipoprotein profile and reduce mortality from heart disease is to reduce TSH to the lower end of the normal range with thyroid medication. A TSH in the upper end of the normal range is associated with increased cardiovascular mortality and elevations in LDL lipo-protein measurements. A TSH at the lower end of the normal range is associated with protection from heart disease.<
Statin Drugs or Thyroid to Prevent Heart Disease in Women?
My previous article discussed the issue of statin drugs for women. Decades of published statin drug studies show that statin drugs simply don’t work for women, and don’t reduce mortality from heart disease in women. But on the other hand, the HUNT study shows that TSH levels in the lower normal range provide a 70% reduction in heart disease mortality for women. This can be accomplished safely with inexpensive thyroid medication under a physician’s supervision. So for women concerned about preventing heart disease, this is good news, pointing out a natural alternative to statin drugs that works much better.
Natural Thyroid is Better
Rather than Synthroid, we prefer to use natural thyroid which is a dessicated porcine thyroid gland from RLC Labs. The reason for this is that we have seen better clinical results with the natural thyroid preparations compared to synthroid.
Above image: thyroid hormone Courtesy Wikimedia .
Natural Thyroid is Safer, but can Cause Adverse Effects of Palpitations
Although natural thyroid is safe, there is always the possibility of adverse effects from thyroid excess, defined as too much thyroid medication. The first sign of thyroid excess is usually a rapid heart rate at rest or perhaps palpitations (at rest). We spend about five minutes at the office going over this adverse effect before starting patients on thyroid medication. Usually patients will notice the heart rate going up or the heart beat sounding louder than usual as the first sign that can be easily recognized. Once recognized, the patient is instructed to stop the thyroid medication, and symptoms usually resolve within 6 hours (for natural thyroid). It is perfectly safe to stop the thyroid medication at any time, as there will be no acute changes, merely a gradual reversion to the original state that existed before starting the thyroid pills.
Some patients are very sensitive to thyroid medication and will have thyroid excess symptoms such as rapid heart rate and palpitations from small amounts of thyroid medication. These are usually the elderly with underlying heart disease and/or magnesium deficiency, and we usually avoid giving thyroid medication to these patients. We also liberally supplement everyone with magnesium if their RBC magnesium levels are low.
About 5 per cent of our patients initially started on thyroid will notice symptoms of thyroid excess with a rapid heart rate, and they will stop the medication for a day or two and restart at a lower dosage with no problem. This is more common in Hashimoto’s patients whose own production of thyroid hormones may fluctuate from month to month. Patients with magnesium deficiency or adrenal fatigue with low cortisol output on salivary testing will also tend to be more sensitive to small amounts of thyroid medication, so caution is advised in these groups as well.
Thyroid Excess Can Rarely Cause Atrial Fibrillation
So far, we have not had a patient go into atrial fibrillation from thyroid medication, probably because we spend so much time with each patient discussing the symptoms of thyroid excess, and the importance of stopping the thyroid medication if these symptoms are noted.
Mainstream Docs Don’t Have Time To Discuss Adverse Effects
One of the reasons the mainstream conventional docs will give only a minuscule amount of synthroid to the low thyroid patient is that they simply don’t have the time to discuss thyroid excess and can’t afford an adverse event which is more likely if the patient doesn’t have a clue about what to watch out for. In addition, mainstream medical docs don’t recognize the syndrome of adrenal fatigue or magnesium deficiency , so they can run into problems with thyroid excess without understanding why, and this also makes them very cautious, tending to under treat. Left Image: Doctor thinking about thyroid dosage.
In patients with underlying heart disease who are prone to cardiac arrhythmias, thyroid excess can cause atrial fibrillation with characteristic EKG appearance. Atrial fibrillation can be a problem, because if it becomes chronic and doesn’t go away on its own, the cardiologist will try a maneuver called cardioversion, the application of an electrical shock to restart a normal cardiac rhythm. Or, if that doesn’t work, prescribe blood thinners, all of which is not without risk. So it is better to avoid atrial fibrillation altogether by simply stopping the thyroid pills whenever symptoms of rapid heart rate or palpitations are noted while at rest. Exercise induced rapid heart rate, of course, doesn’t count since that is normal cardiovascular response to exercise.
How To Design A Better Hunt Study
How would I design an even better Hunt Study? That’s easy. Include another group of patients with TSH levels above and below the study group, namely, below 0.5, and above 3.5. I would also include data on annual CAT coronary calcium scores. I would predict that the lower TSH group (below 0.5) would have even less heart disease than the higher TSH group, and that coronary calcium score, indicating plaque burden, would go up as TSH went up.
Update: 2014: A study by Dr Zhu from China shows low Free T3 (FT3) level is associated with increased coronary artery calcification and increased major cardiac (MACE) events.(16) The authors conclude:
“FT3 levels are associated with coronary artery calcification scores and the incidence rate of MACE in patients with suspected coronary artery disease. A low FT3 level is considered as an important risk factor of high calcification scores and MACE.”(16)
Update 2015: Arch Intern Med. 2012 May 28;172(10):811-7.Razvi S, Weaver JU, Butler TJ, Pearce SH.Levothyroxine treatment subclinical hypothyroidism cardiovascular events mortality Razvi Salman Archives of internal medicine 2012
CONCLUSIONS Treatment of Subclinical Hypothyridism with levothyroxine was associated with fewer Ischemic heart disease events in younger individuals, but this was not evident in older people.
Upper Left Image : L-thyroxine treatment and ischaemic heart disease events in people aged 40-70 years, with subclinical hypothyroidism; HR=0.56 (0.39 – 0.81); p=0.002 (Razvi S et al, Arch Intern Med 2012)
Above Image Figure 2 from Razvi 2012. Above Image : L-thyroxine treatment and ischaemic heart disease events in people aged 40-70 years, with subclinical hypothyroidism; (Razvi S et al, Arch Intern Med 2012)
Read More About the Hunt Study from William Davis MD and Jacob Teitelbaum MD:
Is normal TSH too high? by William Davis MD
Low Thyroid (Even if Tests are Normal) is a Major Cause of Heart Attacks by Jacob Teitelbaum, MD.
Credit and Thanks is given to William Davis MD and Jacob Teitelbaum MD for bringing the Hunt Study to my attention.
Excellent Summary Article on Use of Thyroid to Prevent Heart Disease: Thyroid Hormones: The Ultimate Weapon Against Heart Disease? by Vladimir Heiskanen
For more information on thyroid and heart disease, read my previous articles:
Saving Time Russert and George Carlin
Healthy Men Should Not Take Statin Drugs
Heart Disease Vitamin C and Linus Pauling
Getting Off Statin Drug Stories
How to Reverse Heart Disease with the Coronary Calcium Score (part one)
Reversing Heart Disease Part Three
Cholesterol Lowering Drugs for the Elderly, Bad Idea
Cholesterol Lowering Statin Drugs for Women Just Say No
Jeffrey Dach MD
7450 Griffin Road Suite 190
Davie Florida 33314
(c) 2013 Jeffrey Dach MD All Rights Reserved, This article may be reproduced on the internet without permission, provided there is a link to this page and proper credit is given.
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Links and References:
1) Broda Barnes: Solved the Riddle of Heart Attacks…click here for full -pdf file Broda_Barnes_Solved_Riddle_Heart_Attacks
2) Åsvold, Bjørn O., et al. “Thyrotropin levels and risk of fatal coronary heart disease: the HUNT study.” Archives of internal medicine 168.8 (2008): 855-860.
Background Recent studies suggest that relatively low thyroid function within the clinical reference range is positively associated with risk factors for coronary heart disease (CHD), but the association with CHD mortality is not resolved.
Methods In a Norwegian population-based cohort study, we prospectively studied the association between thyrotropin levels and fatal CHD in 17,311 women and 8,002 men without known thyroid or cardiovascular disease or diabetes mellitus at baseline.
Results During median follow-up of 8.3 years, 228 women and 182 men died of CHD. Of these, 192 women and 164 men had thyrotropin levels within the clinical reference range of 0.50 to 3.5 mIU/L. Overall, thyrotropin levels within the reference range were positively associated with CHD mortality (P for trend = .01); the trend was statistically significant in women (P for trend = .005) but not in men. Compared with women in the lower part of the reference range (thyrotropin level, 0.50-1.4 mIU/L), the hazard ratios for coronary death were 1.41 (95% confidence interval [CI], 1.02-1.96) and 1.69 (95% CI, 1.14-2.52) for women in the intermediate (thyrotropin level, 1.5-2.4 mIU/L) and higher (thyrotropin level, 2.5-3.5 mIU/L) categories, respectively.
Conclusions Thyrotropin levels within the reference range were positively and linearly associated with CHD mortality in women. The results indicate that relatively low but clinically normal thyroid function may increase the risk of fatal CHD.
European Journal of Endocrinology, Vol 156, Issue 2, 181-186, 2007 CLINICAL STUDY The association between TSH within the reference range and serum lipid concentrations in a population-based study. The HUNT Study by Bjørn O Åsvold1,2, Lars J Vatten1, Tom I L Nilsen1 and Trine Bjøro3 1 Department of Public Health, Faculty of Medicine, Norwegian University of Science and Technology, N-7489 Trondheim, Norway, 2 St Olavs Hospital, Trondheim University Hospital, Trondheim, Norway and 3 Department of Medical Biochemistry, Rikshospitalet-Radiumhospitalet Medical Center, Oslo, Norway (Correspondence should be addressed to L J Vatten
Jacob Teitelbaum MD
Jacob Teitelbaum, MD. Low Thyroid (Even if Tests are Normal) is a Major Cause of Heart Attacks,
5) Int Homrone Soc References Consensus 9 Treatment Clinically Hypothyroid Biochemically Euthyroid Patients
International Hormone Society, Concensus 9 references, clinically hypothyroid , lab euthyroid
6) Suh, Sunghwan, and Duk Kyu Kim. “Subclinical Hypothyroidism and Cardiovascular Disease.” Endocrinology and Metabolism 30.3 (2015): 246.
Strong evidence points to a link between SCH and CV risk factors such as alterations in blood pressure, lipid levels, and atherosclerosis. Additionally, accumulating evidence indicates that SCH is associated with metabolic syndrome and heart failure. The present review proposes that SCH may be a potentially modifiable risk factor of CV disease and mortality.
7) Kvetny, J., et al. “Subclinical hypothyroidism is associated with a low-grade inflammation, increased triglyceride levels and predicts cardiovascular disease in males below 50 years.” Clinical endocrinology 61.2 (2004): 232.
The main findings were a high incidence of subclinical hypothyroidism (19.7%) in a general population. Subclinical hypothyroidism was associated with higher concentrations of triglycerides and C-reactive protein. Below 50 years of age cardiovascular disease was more frequent in males with subclinical hypothyroidism compared to euthyroid males. Subclinical hypothyroidism was a predictor of cardiovascular disease in males below 50 years with an odds ratio of 3.4 (95% confidence interval 1.6-6.8) for developing cardiovascular disease compared to euthyroid age-matched males.
CONCLUSION:Our study demonstrates that patients with subclinical hypothyroidism have increased levels of triglycerides and signs of low-grade inflammation (raised C-reactive protein levels) and that subclinical hypothyroidism might be a risk factor for development of cardiovascular disease in younger males.
8)Hak, A. Elisabeth, et al. “Subclinical Hypothyroidism Is an Independent Risk Factor for Atherosclerosis and Myocardial Infarction in Elderly Women: The Rotterdam Study.” Ann Intern Med 132 (2000): 270-278.Subclinical hypothyroidism risk factor for myocardial infarction in elderly women Rotterdam Hak Elisabeth Ann int med 2000
Subclinical hypothyroidism was present in 10.8% of participants and was associated with a greater age-adjusted prevalence of aortic atherosclerosis (odds ratio, 1.7 [95% CI, 1.1 to 2.6]) and myocardial infarction (odds ratio, 2.3 [CI, 1.3 to 4.0]). Additional adjustment for body mass index, total and high-density lipoprotein cholesterol level, blood pressure, and smoking status, as well as exclusion of women who took beta-blockers, did not affect these estimates. Associations were slightly stronger in women who had subclinical hypothyroidism and antibodies to thyroid peroxidase (odds ratio for aortic atherosclerosis, 1.9 [CI, 1.1 to 3.6]; odds ratio for myocardial infarction, 3.1 [CI, 1.5 to 6.3]). No association was found between thyroid autoimmunity itself and cardiovascular disease. The population attributable risk percentage for subclinical hypothyroidism associated with myocardial infarction was within the range of that for known major risk factors for cardiovascular disease.
CONCLUSION: Subclinical hypothyroidism is a strong indicator of risk for atherosclerosis and myocardial infarction in elderly women.
9) Imaizumi, Misa, et al. “Risk for ischemic heart disease and all-cause mortality in subclinical hypothyroidism.” The Journal of Clinical Endocrinology & Metabolism 89.7 (2004): 3365-3370.
Our results indicate that subclinical hypothyroidism is associated with ischemic heart disease and might affect all-cause mortality in men.
10) Safe Oral Triiodo-L-Thyronine Therapy Protects from Post-Infarct Cardiac Dysfunction and Arrhythmias without Cardiovascular Adverse Effects
Viswanathan Rajagopalan,1,* Youhua Zhang,1 Kaie Ojamaa,2 Yue-feng Chen,1 Alessandro Pingitore,3 Christine J. Pol,1 Debra Saunders,4 Krithika Balasubramanian,4 Rheal A. Towner,4 and A. Martin Gerdes1,*Yibin Wang, Editor
A large body of evidence suggests that thyroid hormones (THs) are beneficial for the treatment of cardiovascular disorders. We have shown that 3 days of triiodo-L-thyronine (T3) treatment in myocardial infarction (MI) rats increased left ventricular (LV) contractility and decreased myocyte apoptosis. However, no clinically translatable protocol is established for T3 treatment of ischemic heart disease. We hypothesized that low-dose oral T3 will offer safe therapeutic benefits in MI.
Methods and Results: Adult female rats underwent left coronary artery ligation or sham surgeries. T3 (~6 μg/kg/day) was available in drinking water ad libitum immediately following MI and continuing for 2 month(s) (mo). Compared to vehicle-treated MI, the oral T3-treated MI group at 2 mo had markedly improved anesthetized Magnetic Resonance Imaging-based LV ejection fraction and volumes without significant negative changes in heart rate, serum TH levels or heart weight, indicating safe therapy. Remarkably, T3 decreased the incidence of inducible atrial tachyarrhythmias by 88% and improved remodeling. These were accompanied by restoration of gene expression involving several key pathways including thyroid, ion channels, fibrosis, sympathetic, mitochondria and autophagy.
Conclusions: Low-dose oral T3 dramatically improved post-MI cardiac performance, decreased atrial arrhythmias and cardiac remodeling, and reversed many adverse changes in gene expression with no observable negative effects. This study also provides a safe and effective treatment/monitoring protocol that should readily translate to humans.
11) Tseng, Fen-Yu, et al. “Subclinical hypothyroidism is associated with increased risk for all-cause and cardiovascular mortality in adults.” Journal of the American College of Cardiology 60.8 (2012): 730-737. Subclinical Hypothyroidism Associated With Increased Risk Cardiovascular Mortality Tseng FenYu J Amer Coll Cardiology 2012
RESULTS:There were 3,669 deaths during the follow-up period; 680 deaths were due to CVD. Compared with subjects with euthyroidism, after adjustment for age, sex, body mass index, diabetes, hypertension, dyslipidemia, smoking, alcohol consumption, betel nut chewing, physical activity, income, and education level, the RRs (95% confidence interval) of deaths from all-cause and CVD among subjects with SCH were 1.30 (1.02 to 1.66), and 1.68 (1.02 to 2.76), respectively. CONCLUSIONS:Adult Taiwanese with SCH had an increased risk for all-cause mortality and CVD death.
12) Razvi, Salman, et al. “Levothyroxine treatment of subclinical hypothyroidism, fatal and nonfatal cardiovascular events, and mortality.” Archives of internal medicine 172.10 (2012): 811-817. Levothyroxine treatment subclinical hypothyroidism cardiovascular events mortality Razvi Salman Archives of internal medicine 2012
Background Subclinical hypothyroidism (SCH) has been associated with ischemic heart disease (IHD); however, it is unknown whether treatment of SCH with levothyroxine sodium will reduce the risk of IHD. The aim of this study was to investigate the association between levothyroxine treatment of SCH with IHD morbidity and mortality.
Methods We used the United Kingdom General Practitioner Research Database to identify individuals with new SCH (serum thyrotropin levels of 5.01-10.0 mIU/L and normal free thyroxine levels) recorded during 2001 with outcomes analyzed until March 2009. All analyses were performed separately for younger (40-70 years) and older (>70 years) individuals. Hazard ratios (HRs) for IHD events (fatal and nonfatal) were calculated after adjustment for conventional IHD risk factors, baseline serum thyrotropin levels, and initiation of levothyroxine treatment as a time-dependent covariate.
Results Subclinical hypothyroidism was identified in 3093 younger and 1642 older individuals. For a median follow-up period of 7.6 years, 52.8% and 49.9% of younger and older patients with SCH were treated with levothyroxine, respectively. There were 68 incident IHD events in 1634 younger patients treated with levothyroxine (4.2%) vs 97 IHD events in 1459 untreated individuals (6.6%) (multivariate-adjusted HR, 0.61; 95% CI, 0.39-0.95). In contrast, in the older group there were 104 events in 819 treated patients (12.7%) vs 88 events in 823 untreated individuals (10.7%) (HR, 0.99; 95% CI, 0.59-1.33).
Conclusions Treatment of SCH with levothyroxine was associated with fewer IHD events in younger individuals,(40-70) but this was not evident in older people.\\
13) Rhee, Connie M., et al. “Hypothyroidism and mortality among dialysis patients.” Clinical Journal of the American Society of Nephrology (2012): CJN-06920712.
PDF FREE CHARTS
14) RAZVI, Salman, et al. “The Incidence of Ischemic Heart Disease and Mortality in People with Subclinical Hypothyroidism: Reanalysis of the Whickham Survey Cohort.” The Journal of clinical endocrinology and metabolism 95.4 (2010): 1734-1740.
The Whickham Survey evaluated vascular events over 20 yr in community-dwelling subjects stratified by thyroid function and thyroid autoantibody status. No association between ischemic heart disease (IHD) and a composite autoimmune thyroid disease group, comprising individuals with subclinical hypothyroidism (SCH), with positive thyroid antibodies or those using levothyroxine, was found. This result appears to be at odds with the findings of other cohort studies.
OBJECTIVE: The objective of the study was to evaluate incident IHD and mortality in participants in relation to their thyroid status. OUTCOMES, DESIGN, AND PARTICIPANTS: Data were reanalyzed assessing incident IHD events and mortality during 20 yr of follow-up in individuals with endogenous SCH (n = 97; TSH 6.0-15 mIU/liter) vs. the euthyroid group (n = 2279), who were IHD free at baseline.
RESULTS: Incident IHD was significantly higher in the SCH group [adjusted hazard ratio 1.76 (95% confidence interval 1.15-2.71); P = 0.01]. IHD mortality was also increased in the SCH group [hazard ratio of 1.79 (1.02-3.56); P = 0.05]. These findings lost their significance when subsequent treatment with levothyroxine was excluded from the regression model. There was no difference in all-cause mortality between the groups.
CONCLUSION: In the Whickham Survey, there is an association between incident IHD events and IHD-related mortality with SCH over the 20 yr of follow-up. Furthermore, subsequent treatment of SCH with levothyroxine appears to attenuate IHD-related morbidity and mortality, and this may explain why some other longitudinal studies of SCH have not shown such an association; properly designed controlled trials of treatment of SCH are required to answer this question definitively.
15) Rodondi, Nicolas, et al. “Subclinical Hypothyroidism and the Risk of Coronary Heart Disease and Mortality.” JAMA: the journal of the American Medical Association 304.12 (2010): 1365.
Conclusions; Subclinical hypothyroidism is associated with an increased risk of CHD events and CHD mortality in those with higher TSH levels, particularly in those with a TSH concentration of 10 mIU/L or greater.
16) Zhu, Lijie, et al. “Relationship of serum free T3 with the coronary artery calcification and major adverse cardiac events in patients with suspected coronary artery disease.” Zhonghua xin xue guan bing za zhi 42.12 (2014): 1017-1021.
To survey the association of serum free triiodothyronine (FT3) level with coronary artery calcification and major adverse cardiac events (MACE) in outpatients with suspected coronary artery disease (CAD).
METHODS: A total of 577 outpatients with suspected CAD, who underwent dual-source computed tomography and FT3 detection were included, patients were followed up for 8-29 months for the major adverse cardiac events (death, MI, PCI, CABG). These patients were divided into low FT3 ( < 3.5 pmol/L, n = 126) and normal FT3 ( ≥ 3.5 pmol/L, n = 451) group based on the FT3 level, and divided into CACS > 100 (n = 235) and CACS ≤ 100 (n = 342) group based on the coronary artery calcium score (CACS). Related factors to CACS and MACE were analyzed using logistic regression (stepwise) analysis.
RESULTS: CACS (146.7 (55.8, 599.1) vs. 34.8 (0, 261.9), P < 0.001) and MACE (7.9% (10/126) vs. 2.0% (9/451) , P = 0.003) were significantly higher in the low FT3 group than in normal FT3 group. Logistic regression analysis demonstrated that the FT3 levels are inversely associated with the CACS (OR = 0.442, 95%CI = 0.317-0.618, P < 0.001). Kaplan-Meier analysis displayed that patients with low FT3 levels had a lower cumulative survival rate than patients with normal FT3 levels (P = 0.005), and patients with CACS > 100 also had a lower cumulative survival rate than patients with CACS ≤ 100(P < 0.001).
CONCLUSIONS: FT3 levels are associated with coronary artery calcification scores and the incidence rate of MACE in patients with suspected coronary artery disease. A low FT3 level is considered as an important risk factor of high calcification scores and MACE.
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