Atrial Histology And Connexin 43 Immunohistochemical Staining
Left atrial appendages were taken and immersion-fixed with 4% paraformaldehyde, processed, and paraffin embedded. Serial histological sections were cut and stained with hematoxylin and eosin and Massonâs trichrome stain.
A separate group of sections were immunostained with a monoclonal antibody against rat connexin-43 . Connexin-43 antibody was visualized using goat-anti-mouse Rhodamine Red-X-conjugated antibody and cell nuclei were counterstained with DAPI .
Stained sections were examined using an Olympus BX53 microscope and high-resolution digital images captured at x40 magnification with an Olympus DP72 digital camera. Morphometric and stereological analyses of digitized images were performed in a blinded manner using Image-Pro Analyzer 7.0 software .
The mean cross-sectional area and diameter of cardiac myocytes were estimated using optical fields in which cardiac myocytes showed a relatively circular outline and presence of a round-shaped nucleus. On average, about 60 to 80 nucleated myocyte profiles were examined in each appendage.
Interstitial fibrosis was estimated using Masson-stained sections and expressed as percentage of the total area occupied by interstitial tissue and cardiac myocytes.
Density of Cx43 was estimated using the sections immunostained with anti-Cx43 antibody. Cx43 is best viewed and was examined in areas of longitudinally-oriented cardiac myocytes and expressed as percentage of area examined.
T3 Thyroid Hormone & The Heart
In mainstream medicine, Levothyroxine is the most commonly prescribed thyroid hormone replacement drug, with brand names including Synthroid, Levoxyl, Oroxine and Eltroxin. Levothyroxine drugs contain the synthetic form of only ONE thyroid hormone, T4. T4 is only one portion of the thyroid hormone complex. Yes the majority of thyroid hormones produced by the human thyroid gland are T4, however T3 is the most active useable form of thyroid hormone that can be used in the cells of the body. The conversion of T4 to T3 is a critical element in this puzzle. By doctors strictly relying on T4-only medications, they are under the assumption that our bodies are properly converting the T4 to active T3. For many hypothyroid sufferers like me, our bodies dont convert T4 to T3 properly. Please read my post Top 5 Reasons Doctors Fail To Diagnose Hypothyroidism.
TSH is the gold standard for thyroid diagnosis and treatment in mainstream medicine. Traditional doctors will test TSH and sometimes T4 levels when they suspect thyroid dysfunction, however many do NOT test Free T3 levels. Many traditional doctors will NOT treat patients with natural desiccated thyroid or synthetic T3 drugs even if their patients are not doing well on their T4-only drugs. This focus on TSH and T4 in mainstream medicine is particularly disturbing to me considering the studies published linking low Free T3 levels to heart disease.
Low T3 syndrome is a strong predictor of death in cardiac patients.
Effects Of Different T4 Dosages On Echocardiographic Parameters
LV function and cardiac dimensions acquired by echocardiography before terminal experiments are reported in . LV fractional shortening and wall thickness were reduced in the hypothyroid group compared with the euthyroid group and hyperthyroid group. Although hypothyroid rats had larger LV chamber dimension in systole, the LV diastolic chamber dimension was not yet increased at this relatively early stage. These data indicate cardiac atrophy with reduced ventricular contractility rather than heart failure, which can occur with long-term hypothyroidism. The hyperthyroid group had increased LV fractional shortening, indicating increased ventricular contractility.
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Why People With Hypothyroidism Get Heart Symptoms
The first thing to say is that the thyroid hormone thyroxine controls other enzymes which regulate, firstly, how fast our heart beats and, secondly, how strongly the heart contracts. Thirdly, thyroxine also controls how responsive our heart is to the hormone adrenaline. Another thing to know about thyroxine is that it relaxes all our blood vessels. It does this by its own effects but also by controlling the release of something called endothelial-derived relaxing factor which, again, opens up our blood vessels. And all of these processes can get affected if we are deficient in thyroid hormone.
The simplest way to think of this is that when we are deficient in thyroid hormone everything slows down and everything gets a bit stiffer. The contraction of the heart becomes less effective. Our heart rate slows down. The reason the blood pressure goes up is because of the stiffness of the blood vessels. The blood pressure goes up because the heart is having to pump against this stiffer system. Although less blood is going around because the heart is beating less strongly and more slowly and because of the stiffness, less blood is going around. This doesnt really manifest as a major problem because the oxygen requirements become less because everything has slowed down in the hypothyroid person so all the tissues dont need as much oxygen.
Irregular Heartbeat Linked To Higher Thyroid Hormone Levels
- American Heart Association
- Individuals with higher levels of thyroid hormone circulating in the blood were more likely than individuals with lower levels to develop irregular heartbeat, even when the levels were within normal range. Blood levels of thyroid-stimulating hormone , which regulates the production of thyroid hormones and is primarily measured in clinical practice to assess thyroid function, however, were not associated with an increased risk of irregular heartbeat.
Individuals with higher levels of thyroid hormone circulating in the blood were more likely than individuals with lower levels to develop irregular heartbeat, or atrial fibrillation, even when the levels were within normal range, according to new research in the American Heart Association’s journal Circulation.
“Our findings suggest that levels of the thyroid hormone, free thyroxine, circulating in the blood might be an additional risk factor for atrial fibrillation,” said study lead author Christine Baumgartner, M.D., specialist in General Internal Medicine from the University Hospital of Bern, Switzerland, and currently a postdoctoral scholar at University of California San Francisco. “Free thyroxine hormone levels might help to identify individuals at higher risk.”
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Causes Of An Underactive Thyroid
An underactive thyroid is when your thyroid gland doesn’t produce enough of the hormone thyroxine .
Most cases of an underactive thyroid are caused by the immune system attacking the thyroid gland and damaging it, or by damage that occurs as a result of treatments for thyroid cancer or an overactive thyroid.
Should We Anticoagulate And Attempt Cardioversion In Those With Af
The published data examining AF and embolic risk in thyrotoxicosis are limited but considered together suggest that the rate of embolism in thyrotoxic AF exceeds that for nonthyrotoxic AF not associated with rheumatic heart disease . Furthermore, the majority of clinically evident emboli in thyrotoxic AF involves the central nervous system and occurs most commonly early in the course of the disease . These findings are in keeping with data demonstrating highest rates of mortality from cerebrovascular causes within the first year following treatment for thyrotoxicosis .
It is generally recommended that anticoagulation be considered in those with AF and thyrotoxicosis there are, however, no published data specifically examining the use of anticoagulants in thyrotoxic AF, so the risk/benefit ratio of such therapy remains to be established. The decision to treat patients who have thyrotoxicosis-induced AF with short- or long-term anticoagulation remains one to be made on an individual basis, taking into consideration age, associated heart disease, and risks of such therapy. Antiplatelet and anticoagulant agents differentially affect cardioembolic and noncardioembolic stroke in AF . Aspirin has a greater effect on noncardioembolic stroke than cardioembolic but may offer some degree of protection against cardioembolic stroke in AF patients, although these are more effectively prevented by anticoagulant therapy .
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Electrophysiology Study And Af Inducibility Test
Under anesthesia, a 1.6F octopolar Millar electrophysiology catheter was inserted through right jugular vein and advanced into the right atrium with 8 poles recording atrial electrograms. Standard surface ECG lead II and 3 right atrial electrocardiograms from 3 pairs of electrodes were displayed and recorded using a PowerLab data acquisition system . The purpose of recording 3 atrial electrograms from distal, middle, and proximal pairs was to facilitate determination of atrial capturing and AF pattern. Poles 5 and 6 were used for pacing.
Regular pacing and standard S1S2 pacing protocols were used to determine sinus node recovery time and atrial effective refractory period . The atria were paced at 3x threshold at cycle length of 150 ms or 20 ms shorter than the spontaneous sinus cycle length . Atrial ERP was defined as the longest coupling intervals which did not capture the atria.
Burst pacing containing 200 impulses at 50 Hz was used to induce AF. The duration of the subsequent spontaneous AF after burst pacing was documented. The median AF duration based on 5 such tests was used to reflect the AF substrate in each animal. If induced spontaneous AF lasted more than 10 minutes, AF was considered permanent.
AF was defined as irregular, rapid atrial activations with varying electrogram morphology lasting â¥0.5second. The atrial rates were typically > 1500bpm in rats.
Cellular Mechanisms Determining Arrhythmogenesis
Cardiac myocytes constitute only one-third of the total cells that make up the myocardium. Fibroblasts, smooth muscle cells, endothelial cells, and other cell types constitute the majority of cardiac cells. Thyroid hormone-responsive proteins that have been investigated are largely of myocytic origin, and thyroid hormone influences on nonmyocytic cardiac cells have not been investigated in detail.
The biologically active hormone T3 mediates thyroid hormone action. Once inside the cardiac myocyte, T3 enters the nucleus and binds to nuclear receptors that are bound to DNA response elements of target genes. T3-responsive genes encode both structural and regulatory proteins in the heart. Several cardiac genes are modulated by thyroid hormone at transcriptional and posttranscriptional levels .
After commencing antithyroid therapy, biochemical euthyroidism may be achieved after 46 wk the excess vascular mortality noted following treatment of thyrotoxicosis might be related to the persistence of cellular effects, despite the restoration of biochemical euthyroidism. There is evidence that the on-rate or induction of transcription of specific genes by thyroid hormones differs from the off-rate of transcription with the latter taking more time. Cellular changes could thus persist with continuing arrhythmic consequences because of electrical remodeling, especially of the atria.
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Effect Of Hypothyroid Treatment On The Heart
Treatment with levothyroxine in those with overt thyroid dysfunction has been shown to improve LDL cholesterol, total cholesterol, triglycerides, hypertension, diastolic dysfunction, heart rate, and heart rate variability in exercise and to delay progression of atherosclerosis. Patients with cardiomyopathies may demonstrate improved cardiac contractility and stroke volume with levothyroxine treatment. One of the main concerns with starting levothyroxine replacement is the precipitation of myocardial ischemia or arrhythmias, which, although rare, are known to occur. The recommendation for these patients is usually to start with low doses and gradually escalate until euthyroid status is achieved.
Treating An Underactive Thyroid
Treatment for an underactive thyroid involves taking daily hormone replacement tablets, called levothyroxine, to raise your thyroxine levels. You’ll usually need treatment for the rest of your life. However, with proper treatment, you should be able to lead a normal, healthy life.
If an underactive thyroid isn’t treated, it can lead to complications, including heart disease, goitre, pregnancy problems and a life-threatening condition called myxoedema coma .
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How Too Much Thyroid Hormone Affects Your Heart
An overactive thyroid gland hyperthyroidism can cause the irregular heartbeat of atrial fibrillation.
The thyroid, which is a small gland in your neck, could throw your heart out of its natural rhythm and increase your risk for heart failure or stroke. This is because thyroid hormone has a profound effect on the hearts function and may cause atrial fibrillation.
About 2.7 million Americans have atrial fibrillation, according to the American Heart Association . It’s the most common arrhythmia, which is an irregular heartbeat that can have many different causes.
Diagnosing and treating atrial fibrillation is important because the condition can cause blood to pool in the heart and form a dangerous clot, increasing stroke risk fivefold, according to the National Stroke Association.
But to get the best treatment, you need to know the origins of this condition. Atrial fibrillation can be caused by several factors, including underlying heart disease, high blood pressure, sleep apnea, and older age, according to the AHA.
Symptoms Of An Underactive Thyroid
Many symptoms of an underactive thyroid are the same as those of other conditions, so it can easily be confused for something else.
Symptoms usually develop slowly and you may not realise you have a medical problem for several years.
Common symptoms include:
- pain, numbness and a tingling sensation in the hand and fingers
- irregular periods or heavy periods
Elderly people with an underactive thyroid may develop memory problems and depression. Children may experience slower growth and development. Teenagers may start puberty earlier than normal.
If you have any of these symptoms, see your GP and ask to be tested for an underactive thyroid.
Read more about getting tested for an underactive thyroid
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Thyroid Problems Linked To Irregular Heart Rhythm
People with an overactive thyroid gland carry a greater risk of developing irregular heart rhythm than those with normal thyroid function, finds a study published on bmj.com today.
As such, the researchers suggest there should be an increased focus on atrial fibrillation in patients with raised thyroid function.
Hyperthyroidism occurs when the thyroid gland makes too much thyroxine , causing many of the body’s functions to speed up. About 1 in 100 women and 1 in 1,000 men develop hyperthyroidism at some stage of their life and it can happen at any age.
It is well known that overt hyperthyroidism is associated with atrial fibrillation, but its still not clear whether milder hyperthyroidism has a similar effect. Data on the risk of atrial fibrillation in patients with an underactive thyroid is also limited.
So a team of researchers in Denmark set out to examine the risk of atrial fibrillation in relation to the whole spectrum of thyroid disease in a large group of patients.
Using nationwide registries, they identified 586,460 patients who had consulted a general practitioner in Copenhagen from 2000 to 2010 and had a thyroid function blood test. This measures the amount of thyroid-stimulating hormone circulating in the blood. In people with hyperthyroidism the level of TSH will usually be low, whereas in people with hypothyroidism the level of TSH will usually be high.
In contrast, hypothyroidism was associated with a lower risk of atrial fibrillation.
Effects Of Thyroid Status On The Autonomic Nervous System
Several symptoms and signs in patients with hyperthyroidism suggest an abnormality of the autonomic nervous system. Alterations in vagal and sympathetic innervation can influence the development of arrhythmias with areas of sympathetic supersensitivity being conducive to the development of arrhythmias. Although the effect of thyroid hormone on the autonomic nervous system has been the subject of study for many years, there remain doubts about the nature of this interaction. It has been suggested that there is high adrenergic and low vagal activity in thyrotoxicosis, but circulating concentrations of catecholamines in hyperthyroidism suggest that secretion is normal or even reduced . To explain this paradox, some have suggested that thyroid hormones and catecholamines can exert similar effects because of their structural similarity . Increased tissue sensitivity to catecholamines, secondary to increased -adrenoceptors and reduced parasympathetic activity , have also been put forward as possible explanations.
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Cardiac Symptoms Of Hypothyroidism
Cardiac symptoms that we see in patients with hypothyroidism include a slow heart rate. It usually manifests as a sinus bradycardia, meaning it is a normal rhythm just a little bit slower.
Secondly, sometimes we see exertional breathlessness, shortness of breath on exertion. They arent able to do as much without getting extremely tired.
The third thing that we see often in hypothyroidism is high blood pressure. In particular, we see both values, the top value and the bottom value , go up but the diastolic blood pressure goes up much more than the systolic blood pressure.
It is also worth noting that patients with hypothyroidism may develop swelling of their legs. What is typical about this swelling is that it tends to be non-pitting. When you press the swelling, the finger doesnt leave a massive indentation behind.
Another thing we sometimes see in patients with hypothyroidism is the development of fluid around the heart. Up to 25 percent of hypothyroid patients may develop fluid which accumulates in the sac that the heart sits in, the pericardial sac. This accumulation of fluid around the heart is termed pericardial effusion. Pericardial effusions can grow quite big but usually they dont have to be manually drained out because, as you treat the hypothyroidism, the fluid gets less.
How Can Thyroid Conditions Affect Pregnancy
If you have a thyroid condition, be sure to tell the health care provider who will take care of you during your pregnancy. It’s best if you do this before you become pregnant.
If you are already pregnant, continue taking your medication and talk to your provider as soon as possible. Many medications used to treat thyroid disease in pregnancy are safe for a baby. But radioactive iodine, which is sometimes used to treat hyperthyroidism, should not be taken during pregnancy. In addition, your blood levels need to be monitored and the amount of medication you take may need to be adjusted as your pregnancy progresses.
Health care providers do not routinely perform thyroid screening for women who are planning to get pregnant or who are newly pregnant. If you think you might have a thyroid conditionor if you have a family history of thyroid diseaseask your provider if you should be tested.
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