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The heart is very sensitive to even small changes in the levels of thyroid hormones. The heart is a muscle and contains receptors for thyroid hormone, hence heart muscle growth and cardiac function may be influenced by too much or too little thyroid hormone. There is increasing evidence that even small changes in levels of thyroid hormone may be associated with measurable changes in how well the heart functions. For an overview of the literature, see Thyroid hormone and heart failure. Curr Heart Fail Rep. 2006 Sep;3(3):114-9 and Effects of subclinical thyroid dysfunction on the heart. Ann Intern Med. 2002 Dec 3;137(11):904-14. For more data on specific conditions, read on below.
Hypothyroidism and your heart
In modest cases of hypothyroidism, the heart rate may be slowed, although heart function is generally normal. With more significant and prolonged deficiency of thyroid hormone, cardiac function may become abnormal. In persons who have normal heart function and no history of heart disease to begin with, these mild changes in heart function associated with hypothyroidism are usually imperceptible. Although there are very few large randomized studies examining the effect of treating mild hypothyroidism on cardiac function, there is some data that correction of even mild hypothyroidism may improve objective parameters of cardiac function, as demonstrated in Assessment of left ventricular diastolic function by radionuclide ventriculography at rest and exercise in subclinical hypothyroidism, and its response to L-thyroxine therapy. Am J Cardiol. 2003 Jun 1; 91 (11): 1327-1330 and Does subclinical hypothyroidism affect cardiac pump performance? Evidence from a magnetic resonance imaging study. J Am Coll Cardiol. 2005 Feb 1; 45 (3): 439-45.
In some patients with pre-existing heart disease, hypothyroidism may be associated with decreased cardiac function, producing a mild exacerbation or deterioration in the underlying heart condition, occasionally leading to shortness of breath, or rarely, congestive heart failure Risk for ischemic heart disease and all-cause mortality in subclinical hypothyroidism. J Clin Endocrinol Metab. 2004 Jul;89(7):3365-70. In such patients, treatment with thyroid hormone may improve several parameters of cardiac function, even after only a few weeks of treatment. For example, see Thyroid Hormone Substitution Therapy Rapidly Enhances Left-Ventricular Diastolic Function in Hypothyroid Patients. Cardiology. 2001 Dec;96(2):59-64.
Although treatment of hypothyroid patients who have heart disease may ultimately increase energy and improve cardiac function, treatment must be initiated slowly, and low doses of thyroid hormone should be used, especially in patients who have or who are at risk for development of coronary artery disease.
Many patients with significant degrees of hypothyroidism may have a reduced heart rate, and occasionally reduced function of the heart due to the lack of the beneficial action of thyroid hormone on the heart muscle. Patients with more severe hypothyroidism may develop fluid around the heart, a condition known as a pericardial effusion. Treatment of patients with thyroid hormone will usually gradually improve the normal function of the heart muscle, however caution is indicated in such instances. It is usually better to err on the side of caution when heart disease is suspected or present, and start replacement, if indicated, with very low doses of thyroid hormone, in the range of 25 ug of thyroxine daily. The dose of thyroid hormone can then be gradually increased every 3-6 weeks, as long as the thyroid hormone replacement is well tolerated. As even small amounts of thyroid hormone can speed up the metabolic activity and oxygen consumption of your heart, treatment with even small doses of thyroid hormone may cause angina, shortness of breath or palpitations and rapid heart beats in some susceptible patients. Accordingly, even though it may take longer to build up to normal levels of thyroid hormone, it is best to be cautious about the timetable for replacing thyroid hormone in hypothyroid patients with heart disease.
Are there benefits to treating asymptomatic subclinical hypothyroidism in patients with heart disease, especially in the setting of coronary artery disease?
Given the caveats noted above, it is also clear that patients with hypothyroidism may have increased levels of cholesterol and triglycerides, and correction of the hypothyroid state may have a modest beneficial effect on these parameters. A study published in 1999 suggests another intriguing link between homocysteine and thyroid status. Levels of plasma homocysteine appear to be an independent risk factor for coronary artery disease. Patients with hypothyroidism have elevated levels of plasma homocysteine, and these levels decrease significantly once the hypothyroidism is corrected. See Normalization of hyperhomocysteinemia with L-thyroxine in hypothyroidism. Ann Intern Med. 1999 Sep 7;131(5):348-51. Although the study was small and carried out over a short period of time, the results are intriguing, have been confirmed in follow-up studies such as Homocysteine, hypothyroidism, and effect of thyroid hormone replacement. Thyroid. 1999 Dec;9(12):1163-6. and suggest the relationship between hypothyroidism, homocysteine, and the development and/or treatment of heart disease, deserves further scrutiny. Moreover, there is evidence that treatment of subclinical hypothyroidism produces small but significant improvements in plasma lipids, waist-hip ratio, and endothelial function, as outlined in The beneficial effect of L-thyroxine on cardiovascular risk factors, endothelial function and quality of life in subclinical hypothyroidism: randomised, crossover trial. J Clin Endocrinol Metab. 2007 Feb 13; [Epub ahead of print]
Similarly, levels of C Reactive Protein (CRP), a circulating protein that also indirectly correlates with the risk of heart disease, are elevated in patients with overt or subclinical hypothyroidism. However, CRP levels do not correlate perfectly with the extent of hypothyroidism, and treatment of the hypothyroidism frequently has no effect on the levels of CRP. See Elevated C-reactive protein and homocysteine values: cardiovascular risk factors in hypothyroidism? A cross-sectional and a double-blind, placebo-controlled trial. Atherosclerosis. 2003 Feb;166(2):379-86.
Although there is a questionable correlation between levels of TSH and mean blood pressure even in individuals with normal thyroid function Thyroid function and blood pressure homeostasis in euthyroid subjects. J Clin Endocrinol Metab. 2004 Jul;89(7):3455-61, there is little evidence that treating very modest levels of TSH elevation produces independent lowering of blood pressure. Nevertheless, in some studies, even mild subclinical hypothyroidism is associated with an increased risk of cardiovascular events Subclinical thyroid dysfunction as a risk factor for cardiovascular disease. Arch Intern Med. 2005 Nov 28;165(21):2467-72. Indeed, some studies do show a modest correlation between the level of TSH and diastolic blood pressure as outlined in Association between blood pressure and serum TSH concentration within the reference range: a population-based study. J Clin Endocrinol Metab. 2007 Jan 2; [Epub ahead of print]. Although a very large prospective study (The EPIC-Norfolk prospective population study) demonstrated a modest but detectable correlation between levels of TSH and blood pressure and lipid levels, there was no link between the detection of subclinical hypothyroidism at the start of the study, and the subsequent development of coronary artery disease or all cause mortality in over 11,500 individuals Initial thyroid status and cardiovascular risk factors: The EPIC-Norfolk prospective population study Clin Endocrinol (Oxf). 2009 May 25. [Epub ahead of print]
For an overview of the cardiac abnormalities that may be present in patients with mild hypothyroidism, and opinions about treatment, see Cardiovascular and atherogenic aspects of subclinical hypothyroidism Thyroid 2000 Aug;10(8):665-79 and Cardiovascular and medical ramifications of treatment of subclinical hypothyroidism. Curr Atheroscler Rep. 2003 Jan;5(1):73-7 and Effects of thyroxin therapy on cardiac function in patients with subclinical hypothyroidism: index of myocardial performance in the evaluation of left ventricular function. Int J Cardiol. 2004 Jun;95(2-3):135-43.
Hypothyroidism and Cholesterol
Many studies have documented a relationship between hypothyroidism, and an increase in the levels of cholesterol and triglycerides in some hypothyroid subjects. This link can be confusing, as some patients may have been told that their cholesterol is elevated largely as a result of their associated hypothyroidism. While this may indeed be the case in rare individuals, for most subjects, hypothyroidism actually contributes only modestly to the total abnormality in cholesterol and LDL that may be present. To review the average changes in levels of cholesterol that might be expected in hypothyroid patients see Clinical review 115: effect of thyroxine therapy on serum lipoproteins in patients with mild thyroid failure: a quantitative review of the literature. J Clin Endocrinol Metab. 2000 Sep;85(9):2993-3001.
A randomized study examined the impact of correcting mild subclinical hypothyroidism in women. The subjects, women with a mean TSH of ~ 11.7 were treated with placebo or thyroxine for 48 weeks. A modest but significant reduction in total and LDL cholesterol was observed in the group receiving sufficient thyroxine to correct the TSH to normal. See TSH-controlled l-thyroxine therapy reduces cholesterol levels and clinical symptoms in subclinical hypothyroidism: a double blind, placebo-controlled trial (basel thyroid study). J Clin Endocrinol Metab. 2001 Oct;86(10):4860-6.
Although modest variations of thyroid hormones within the normal range have been shown to weakly correlate with the extent of coronary artery calcification detected in patients undergoing angiography, there is no evidence treating patients with slightly lower levels of thyroid hormone may influence the development of coronary artery disease. See Thyroid function is associated with presence and severity of coronary atherosclerosis. Clin Cardiol. 2003 Dec; 26(12): 569-73.
Hyperthyroidism and your heart
A rapid heart beat, or irregular skipped beats (palpitations) is a common complaint in patients with hyperthyroidism. Some subjects notice that their basal resting heart rate is a bit higher than normal; other patients observe that their heart rate goes up much faster and takes longer to return to normal when they exercise. Increases in systolic blood pressure are common in hyperthyroid patients Ambulatory blood pressure monitoring in patients with hyperthyroidism before and after control of thyroid function. Clin Endocrinol (Oxf). 2005 Jul;63(1):66-72
In some older patients, or in patients with existing heart disease, hyperthyroidism may increase the risk of developing an abnormal heart rhythm, such as atrial fibrillation. In fact, there seems to be a correlation between levels of thyroid hormones, and the risk of developing atrial fibrillation, even in subjects who do not have overt biochemical hyperthyroidism, as outlined in High-normal thyroid function and risk of atrial fibrillation: the Rotterdam study Arch Intern Med. 2008 Nov 10;168(20):2219-24.
Several large studies have shown that the risk of developing hyperthyroidism can be up to 5-fold greater in subjects with a suppressed TSH, who feel otherwise well, compared to control subjects with a normal TSH. See Subclinical hyperthyroidism as a risk factor for atrial fibrillation. Am Heart J. 2001 Nov;142(5):838-842. Furthermore subclinical hyperthyroidism also appears to be a risk factor for the development of left ventricular hypertrophy, as described in The association of thyroid function with cardiac mass and left ventricular hypertrophy. J Clin Endocrinol Metab. 2004 Nov 2; [Epub ahead of print]
Indeed, the diagnosis of previously unsuspected hyperthyroidism is not uncommon in older patients with rapid irregular heart rhythms who present to the emergency room. It may be difficult to maintain the heart in normal rhythm until the hyperthyroidism is brought under satisfactory control. For some patients with sustained irregularities in heart rate and rhythm, the possibility of anticoagulation should be considered until the abnormal heart rate and rhythm can be corrected. For an evaluation of how even mild hyperthyroidism can affect the heart, see Endogenous Subclinical Hyperthyroidism Affects Quality of Life and Cardiac Morphology and Function in Young and Middle-Aged Patients. J Clin Endocrinol Metab. 2000 Dec;85(12):4701-4705. For a review of how hyperthyroidism can cause cardiac problems in older patients see Cardiac risks of hyperthyroidism in the elderly. Thyroid. 1998 Dec;8(12):1165-9. and Cardiac dysrhythmias and thyroid dysfunction - the hidden menace? J Clin Endocrinol Metab. 2002 Mar;87(3):963-7. Shortness of breath in hyperthyroid patients may also be attributable to effects on the lungs, likely as a partial result of weakness in the muscle used for breathing. Alternatively, a reversible form of pulmonary hypertension may be more common than previously recognized in subjects with hyperthyroidism as described in Hemodynamic Changes in Hyperthyroidism Related Pulmonary Hypertension: A Prospective Echocardiographic study. J Clin Endocrinol Metab. 2007 Feb 27; [Epub ahead of print]. A direct effect on oxygen exchange in the lungs remains a possibility. See Ineffective cardiorespiratory function in hyperthyroidism. J Clin Endocrinol Metab. 1998 83(11):4075-8.
A low TSH and excess cardiovascular mortality
Although treated thyroid disease does not appear to be associated with an increased risk of mortality, both hypothyroidism and hyperthyroidism may, under some circumstances, place a patient at increased risk for the development of heart problems Mortality and Vascular Outcomes in Patients Treated for Thyroid Dysfunction. J Clin Endocrinol Metab. 2006 Mar 14; [Epub ahead of print] and Thyroid status, cardiovascular risk, and mortality in older adults. JAMA. 2006 Mar 1;295(9):1033-41.
What should the approach be to patients who are otherwise well, but have a low TSH indicative of biochemical, often "subclinical" hyperthyroidism. Clearly, the approach needs to be individualized for each patient. A population-based study examining the relationship between TSH and mortality found a small but significant increase in mortality from cardiovascular causes in 1191 persons not being actively treated with thyroxine or anti-thyroid medications. The results of this study do not prove treatment of the thyroid problem would reduce the risk of mortality, but they do provide further evidence linking hyperthyroidism to adverse cardiovascular (heart-related) events. However, a subsequent study did not replicate the conclusions of a link between increased cardiovascular mortality and subclinical hyperthyroidism Thyroid status, cardiovascular risk, and mortality in older adults. JAMA. 2006 Mar 1;295(9):1033-41. Furthermore, if one has a suppressed TSH for another reason (hyperthyroidism, treatment of thyroid nodules, pituitary problems or thyroid cancer), there is no evidence suggesting that the TSH level correlates with increased mortality in these settings. Indeed, patients with thyroid cancer and a suppressed TSH exhibited a reduced risk of cancer-related mortality. To review the data linking a low TSH to excess cardiovascular mortality, see Prediction of all-cause and cardiovascular mortality in elderly people from one low serum thyrotropin result: a 10-year cohort study. Lancet 2001 Sep 15;358(9285):861-5. Furthermore, it appears that the risk of increased mortality in patients with hyperthyroidism is significantly diminished once patients are treated appropriately and thyroid status is returned to normal, as described in Thyroid function and mortality in patients treated for hyperthyroidism. JAMA. 2005 Jul 6;294(1):71-80. However, other studies have suggested that it a history of previously treated hyperthyroidism is associated with a small but significant increase in mortality in women older than 65 Thyroid hormone use, hyperthyroidism and mortality in older women. Am J Med. 2007 Apr;120(4):343-9
I have been diagnosed with atrial fibrillation and hyperthyroidism. Should I be anticoagulated to reduce the risk of a stroke?
This therapeutic area remains somewhat controversial, and there is no universal answer that is correct for all patients. The risk of stroke in patients with hyperthyroidism and irregular heart rhythms increases with age. Nevertheless, so does the risk of bleeding. Some physicians are more aggressive about anticoagulation in elderly patients with additional risk factors for stroke. A careful consideration of the advantages and disadvantages and theoretical risks of all options is indicated in this situation, which should be discussed with your physician.
My TSH is 20, I am tired, and I have coronary artery disease and angina. Will I feel better and have less chest pain if I am treated for my hypothyroidism?
This clinical scenario calls for extreme caution, and a careful assessment of the risks and benefits of initiating thyroid hormone replacement. Although some patients will indeed experience clinical improvement if their thyroid status is optimized, other patients may experience exacerbation of their heart disease with even a few small doses of thyroid hormone. Given the complexity of this clinical dilemma and the potential danger of thyroid hormone in some patients with severe coronary artery disease, the pros and cons of this decision should be carefully discussed with your physician in the context of your individual health and heart problem.
I need to take amiodarone for a heart condition. Will this make my thyroid condition worse?
Patients requiring institution of amiodarone often have a history of serious heart problems for which amiodarone can be a life-saving treatment. Although amiodarone may exacerbate or unmask a preexisting tendency to develop an underactive or overactive thyroid, the thyroid problems can usually be managed effectively by a skilled physician, although careful monitoring may be required. Patients started on amiodarone should have their TSH monitored on a regular basis, every 3-4 months, so any potential thyroid problem may be detected early before clinical difficulty arises.
My blood pressure is high; is this related to my thyroid?
Although many patients assume that an overactive thyroid gland will frequently cause high blood pressure, it is actually hypothyroidism that seems to be associated with an increased risk of high blood pressure, possibly due to sympathetic nervous system activation. See The role of thyroid hormone in blood pressure homeostasis: evidence from short-term hypothyroidism in humans. J Clin Endocrinol Metab. 2002 May;87(5):1996-2000.