Increased Myocardial Wall Thickness in a Patient with Severe Hypothyroidism, Showed Complete Reversibility

Dr. Areeg Magzoub Babiker El Tayeb^1, Dr. Omnia Mutaz Mamoon Yousif^2, Dr. Mohamed Alaa Eldin Mohamed Ahmed^3,  Dr. Abdelazez Allaeldin Mohamed Ahmed^4,

1. Gezira University, Sudan; Consultant Physician and Adult Cardiologist; Department of Medicine and Cardiology, Alfajr College for Medical Science and Technology, Khartoum, Sudan; Department of Medicine and Cardiology, Ribat University Hospital, Khartoum, Sudan; Department of Medicine and Cardiology, Fedail Hospital, Khartoum Sudan
2. National University, Sudan; Master of Public Health and Tropical Disease, University of Medical Science and Technology, Sudan
3. Sudan International University, Sudan; Imperial Hospital, Sudan
4. Sudan international University, Sudan; Ribat University Hospital

OPEN ACCESS

PUBLISHED: 30 December 2024

CITATION: TAYEB, Dr. Areeg Magzoub Babiker El et al. “Increased Myocardial Wall Thickness in a Patient with Severe Hypothyroidism, Showed Complete Reversibility After Thyroid Hormone Replacement Therapy” Case Report and Literature Review. Medical Research Archives, [S.l.], v. 12, n. 12, dec. 2024. Available at: <https://esmed.org/MRA/mra/article/view/6095>.

COPYRIGHT: © 2025 European Society of Medicine. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

DOI: https://doi.org/10.18103/mra.v12i12.6095

ISSN 2375-1924

Abstract

Hypothyroidism affects the cardiovascular system in various ways. This may include reduced stroke volume, decreased cardiac output, and increased systemic vascular resistance (SVR), decreased heart rate, and increased myocardial wall thickness. We present a case of a 72-year-old female patient with severe hypothyroidism who showed complete reversibility of increased myocardial wall thickness following thyroid hormone replacement therapy.

Keywords

• Hypothyroidism
• Myocardial wall thickness
• Thyroid hormone replacement
• Cardiovascular effects

Introduction

Thyroid disease is a common medical condition. It affects the cardiovascular system and is more prevalent in females compared to males, namely Grave’s and Hashimoto’s disease. Estimates showed that thyroid disease affects around 9-15% of the adult female population and a smaller percentage of adult males. However, around the eighth decade of life, the incidence of disease in males is almost equal to that of females. Symptoms of hypothyroidism can vary from simple fatigue to its extreme presentation with myxedema coma. The most common age group affected in women is 40-50 years.

Hypothyroidism is a clinical syndrome resulting from thyroid hormone deficiency, which in turn results in slowing down of the metabolism, causing multiple organ dysfunction. It is estimated that 2% of adults suffer from hypothyroidism. 10% of patients with hypothyroidism have hypercholesterolemia. In this case report, we present a 72-year-old female who was known to have hypothyroidism and presented with increased myocardial wall thickness.

Case Report and Literature Review

The patient is a 72-year-old female who was known to have hypothyroidism for the past 10 years. She was on levothyroxine replacement therapy but was not compliant with her medication. She presented to the emergency department with complaints of shortness of breath and fatigue. Initial transthoracic echocardiography showed severe left ventricular hypertrophy (LVH) with a left ventricular wall thickness of 18 mm. The patient was started on thyroid hormone replacement therapy, and her TSH levels were monitored.

Table 1 summarizes the timeline of cardiac measurements and findings with the change of TSH levels.

Time	TSH	Septal LV wall thickness at end diastole	Posterior LV wall thickness at end diastole	PE size	Diastolic function	LA size	Cardiac HF
Day 0	59	18 mm	18 mm	6.5 cm	Grade 2	4.7 cm	Yes
Day 60	10	14 mm	14 mm	5.1 cm	Grade 1	4.3 cm	No
Day 180	2	12 mm	12 mm	4.5 cm	Normal	4.1 cm	No

Discussion

Hypothyroidism is a clinical syndrome resulting from thyroid hormones deficiency, which in turn results in slowing down of the metabolism, causing multi-organ dysfunction. Hypothyroidism affects 2% of adult women and 0.1–0.2% of adult men. Thyroid hormones have direct cellular functions on almost all tissues of the body

Atherosclerosis and coronary artery disease are the result of dyslipidemia and diastolic hypertension.
This explains that hypothyroid patients also have an increased risk of stroke. The cardiovascular changes in hypothyroidism — namely the blood pressure, lipid profile, cardiac contractility, and increased SVR — are caused by decreased thyroid hormone action on the heart, liver, and peripheral vasculature. They are reversible after thyroid hormone replacement. 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 delay progression of atherosclerosis.

3. Left ventricular increased thickness and/or hypertrophy:

Cardiac hypertrophy is reported in both humans and experimental animals diagnosed with hyperthyroidism. The reason is primarily due to the increased cardiac performance to cope with the hemodynamic load caused by hyperdynamic circulation seen in hyperthyroidism. However, in hypothyroidism, the dynamic situation is the opposite.

The heart beats slower but against increased vascular and pulmonary resistance. Thus, the presence of increased myocardial thickness needs to have a different and/or an additional etiology and composition than just myocardial hypertrophy. Both increased interventricular septum (IVS) thickness and increased left ventricular posterior wall (LVPW) thickness were reported.

Cianciulli et al. reported a case in 2021 of hypothyroidism leading to septal asymmetric hypertrophy and a “cherry on the top” strain pattern similar to the pattern in hypertrophic cardiomyopathy and cardiac amyloid. However, unlike them, it recovered after thyroid hormone replacement therapy. Autopsy findings in another study found acid mucopolysaccharide deposition and resulting edema in the myocardium of a hypothyroid patient after sudden cardiac death.

4. Cardiac Magnetic Resonance in hypothyroidism and new promising evidence:

Recent evidence showed that native T1 mapping (MOLLI sequence without contrast administration) in CMR has significantly increased values in the myocardium of hypothyroid patients. This suggests the presence of edema and diffuse fibrosis. These effects were not seen using T2 or late gadolinium enhancement (LGE) (Figure 3).

It is a non-invasive way to prove the consistency and explain the diastolic and systolic dysfunction linked to hypothyroidism. They also found significantly reduced peak filling rate (PFR) and prolonged peak filling time (PFT) in hypothyroid patients, as well as reduced stroke volume and cardiac index.

Cardiac MRI comparing a patient with hypothyroidism (bottom row) and a control patient (upper row). T1 signals (middle column), unlike T2 and (LGE), showed increased values in the hypothyroid patient. T1 time in the hypothyroid patient is 1301 ms (orange range of the color scale) while in the control it is 1040 ms (purple range of the color scale).

5. Arrhythmia:

Prolongation of the QT interval in hypothyroid patients is well documented in several studies. This predisposes the patients to ventricular irritability that may rarely proceed to a reversible Torsade de Pointes.

6. Pericardial effusion:

Severe hypothyroidism can cause pericardial and pleural effusion. This can be small or huge. It usually accumulates slowly and rarely causes cardiac tamponade. Though the mechanism is unclear, increased capillary permeability and reduced lymphatic drainage from the pleural and pericardial space have been suggested. Most of the pericardial and pleural changes and effusion secondary to hypothyroidism are reversible with thyroxin replacement. The effusion is well known to be protein rich.

7. Diastolic dysfunction:

Diastolic dysfunction in some studies was found in 27% of patients, while systolic dysfunction is seen in 7% of patients. The decreased cardiac contractility associated with hypothyroidism results from the reduced expression of the sarcoplasmic reticulum Ca²⁺-ATPase and the increased expression of its inhibitor, phospholamban. In hypothyroidism, these two proteins function in intracellular calcium cycling and thus regulate diastolic function, particularly slowing the isovolumic relaxation phase of diastolic function. Isovolumic relaxation time increases proportionately to the severity.  is not affected by pulse rate or blood pressure and is mainly affected by the thyroid hormone. Values can range between the normal 50–90 ms and up to 150 ms.

8. Dyslipidaemia:

90% of patients with hypothyroidism had hypercholesterolemia. High total, LDL, VLDL, and triglycerides and low HDL are all noted in hypothyroidism, with elevated triglycerides being in almost all patients. The hypercholesterolemia in hypothyroidism results from reduced catabolism of lipoproteins and decreased lipoprotein receptors and activity in the liver. A hypothyroid state results in decreased hepatic LDL receptors and reduced activity of the enzyme cholesterol-α-monooxygenase, resulting in decreased LDL clearance. Also noted are elevations in both C-reactive protein and homocysteine.

Females with subclinical and overt hypothyroidism had significantly higher total and LDL cholesterol. Females with total cholesterol greater than 7 mmol/L had about a 7 times higher risk of hypothyroidism. The catabolism of cholesterol into bile is mediated by the enzyme cholesterol 7-hydroxylase. This liver enzyme is negatively regulated by T3 and may add to the decreased catabolism and increased serum cholesterol seen in hypothyroidism. The increased lipid levels in subclinical hypothyroidism as well as in overt disease are potentially associated with increased cardiovascular risk. Treatment with thyroid hormone replacement reverses the risk.

9. Electrocardiogram:

ECG mainly shows bradycardia, low voltage, and electrical alternans, especially in the presence of pericardial effusion.

10. Echocardiography:

Echocardiography can be normal, with increased LV mass, pericardial effusion, and systolic or diastolic dysfunction.

11. Hypothyroidism and Heart Failure:

Review of multiple cross-sectional studies showed that 30% of patients with congestive cardiac failure have low T3 levels. The decrease in serum T3 is proportional to the severity of the heart disease. Low T3 syndrome is defined as a low serum T3 together with normal serum T4 and TSH. The syndrome results from defective hepatic conversion of T4 to T3 by 5-monodeiodination. The cardiac myocyte has no deiodinase activity and relies on the plasma T3.

Heart failure is found to be associated with iodine-induced hypothyroidism diagnosed within 60 days of exposure to iodine-containing contrast media. Females were affected more than males. There are several possible mechanisms accounting for the adverse prognosis of hypothyroidism on HF patients. The link between hypothyroidism and pulmonary hypertension is well reported, which accordingly increases mortality of HF patients. Hypothyroidism can significantly reduce preload, increase afterload, and thus reduce stroke volume and cardiac output. Anemia secondary to hypothyroidism can lead to reduced exercise tolerance and worsening HF. Hypothyroidism can also lead to altered lipid metabolism, elevated C-reactive protein, and increased prevalence of aortic atherosclerosis, which can all increase the prevalence of myocardial infarction and mortality in HF patients. Both subclinical hypothyroidism and subclinical hyperthyroidism are associated with adverse prognosis in HF patients. Subclinical hypothyroidism can increase the risk of both all-cause mortality and cardiac death and/or hospitalization in HF patients. Hypothyroidism caused severe, progressive systolic dysfunction and increased chamber diameter/wall thickness ratio in rats. It also resulted in impaired myocardial blood flow and dramatic loss of arterioles. This highlights two important mechanisms by which hypothyroidism may lead to heart failure.

12. Hypertension

In hypothyroidism, endothelial dysfunction and impaired vasomotor relaxation lead to increased SVR. These effects caused diastolic hypertension.in 30% of patients, and replacement therapy restored endothelial vasorelaxation and thus blood pressure to normal in most patients™,

 

13. Heart Block

Hypothyroidism is well-known to affect the chronotropic property of the cardiac conducting system through functional mechanisms. Cases of bradycardia and all degrees of atrioventricular (AV) block were reported with hypothyroidism. However, the response to treatment with thyroxin replacement have variable results. Few cases did recover whether due to primary hypothyroidism, hypothyroidism secondary to amiodarone treatment®, or subclinical hypothyroidism*”. A theory of hypothyroid induced oedema with recovery after thyroid hormone replacements was one of the explanations in patients with myxoedema”. However, most of the cases continued to have AV block and needed
permanent pacemakers (PPM) despite hormone replacement and normalization of the lab results”. These facts and data are against the general understanding that the condition is entirely reversible by treatment. It highlights the possibility that there is permanent damage caused by the lack of thyroxin, or that the heart block is not related to thyroxin deficiency from the start, especially that the incidence of heart block in hypothyroid patients is closer to that in the general population

14.Amiodarone

Amiodarone contains about 37% iodine by weight, and a 200-mg dose exposes the patient to about300 times the recommended daily allowance. Because of its high iodine content, amiodarone can cause either hypothyroidism (5% to 25% of treated patients) or hyperthyroidism (2% to 10% of treated patients)”, Amiodarone also inhibits the conversion of T4 to T3 by inhibition of 5-deiodin
leading to amiodarone-induced hypothyroidism leading to amiodarone-induced hypothyroidism. The tisk increases in the presence of preexisting thyroid disease” is activity,
In general, patients treated with amiodarone should have thyroid function testing (specifically TSH)
throughout therapy”. If hypothyroidism developed with a persistent rise in TSH, the patient should have thyroxine replacement™. Thyroxin replacement does not impair the antiarrhythmic effect, as the antiarrhythmic effects is independent of the effect of Amiodarone on thyroid hormone metabolism’

15. Anomia:

Serum erythropoietin levels are low in hypothyroidism, and it explain the normochromic, normocytic anemia found in almost 35% of those Patients” Hypothyroidism is associated with decreased insulin sensitivity due to downregulation of glucose transporters and direct effects on insulin secretion and clearance”,

 

17. Hemodynamics

Thyroid hormones have a variety of effects on the cardiovascular system that can greatly impact cardiac function. Bradycardia and smaller stroke volume are together the reason for reduced cardiac output while diminished heart sounds and cardiomegaly are mainly the result of poricardial effusion’. In hypothyroidism, cardiac output may decrease by 30-50%’*. The arterial compliance is reduced, which leads to increased SVR. Impaired endothelium dependent vasodilatation due to reduction in nitric oxide is seen in subclinical hypothyroidism as well” Hypothyroidism is often associated with high diastolic blood pressure, and because the cardiac output is low, the pulse pressure is narrowed. The increase in diastolic pressure occurs with low serum renin levels and is sodium sensitive”.

18. Subclinical Hypothyroidism

Subclinical hypothyroidism (SCH) is defined as a serum TSH concentration above the upper limit of the reference range (0.45-4.49mlU/L) ard serum free thyroxine (FT4) concentration within its reference range. This means TSH (4.5 to (6.9- 19.9) mIU/L) and normal Ta Several studies found that subclinical hypothyroidism is associated with an increased incidence and mortality of coronary heart disease”, systolic and diastolic cardiac dysfunction, especially with TSH levels greater than 10mlU/L**”. Atherosclerosis and myocardial infarction risk are increased in women with subclinical hypothyroidism’. hypothyroidism is associated with an increased risk of congestive heart failure in older patients with a TSH level of 7.0 mIU/L or more’. A recent study Subclinical confirms the cardiovascular benefits of therapy®. In a study of women with subclinical hypothyroidism, 18 months of treatment resulted in normalization of systolic and diastolic blood pressure and of total and LDL cholesterol as well as decreased carotid intima thickness®,

19. Carotid intimal Medial Thickness

Carotid intima-media thickness (C-IMT) is a generally agreed on measure of subclinical atherosclerotic. It is used to assess the efficacy of diseases and interventions that increase or reduce atherosclerosis”. CMT isa parameter of prophylax’s of cardiovascular disease in many guidelines. Progression of atherosclerosis is diagnosed when the value of C- IMT is over the threshold of 0.9 mm. The prospective risk of myocardial infarction increases from 10% to 15%, and stroke risk from 13% to 15% with a 0.1 mm increase in C-IMT™. A meta-analysis showed that high blood pressure is an independent risk factor for C-IMT®, A second one found that SCH isa cause of higher systolic and diastolic blood pressures”. Female sex, advanced age, and high cholesterol levels sub analysis significantly influenced the association between SCH and CIMT in a third meta-analysis. Interestingly, low lymphocyte-monocyte ratio, which is an inflammatory marker, is associated with increased hsCRP and CIMT in subclinical hypothyroidism patients”, Lithyroxine replacement fer one year led to decreased dyslipidemia and improved subclinical carotid atherosclerosis”. L-T4 treatment of SCH patients can reduce C-IMT, possibly due to the reduction in all lipid profile parameters, systolic and diastolic blood pressure, lipoprotein(a), and flow mediated dilatation. This effect was observed in meta- analysis after long-term (>6 months) treatment.

20. The Skin

Hypothyroidism is more prominent in females, and skin changes are seen more in hypothyroid females as well. Hypothyroidism can affect the skin in three. different ways. Direct skin changes due to lack of normal levels of thyroid hormones, auto-immune skin changes associated with hypothyroidism, and skin manifestations of other systems or diseases caused by hypothyroidism. auto-immune Xerosis and hair loss are the most common skin manifestations, followed by puffy oedema of the: face, hands, and feet, seen more in the younger population’. Direct thyroid hormone effects on the skin are carried through thyroid receptors (TR). These TR are distributed in almost every component of the skin, including hair follicles, muscle cells, Schwan cells, sebaceous gland cells, the epidermal keratocytes, skin fibroblasts and vascular endothelial
calls, Facial puffiness, periorbital oedema, and non-pitting oedema of hands and feet are due to tissue infiltration with muco-polysaccharides mainly in the papillary dermis around the vessels as well as increase in tissue sodium concentration and water retention”. The carotenemia is caused by carotene deposition in the dermis, this is more seen in the palms, feet, and nasolabial folds as a yellow tinge. The skin manifestation on the epidermis in hypothyroidism are dry palms and soles, and rough scaly skin that is seen histologically as thinning and hyperkeratosis”. Cold skin is caused by reduced cutaneous blood flow confirmed by nail fold capillaroscopy and laser doppler®®, The capillary constriction is a reflex to reduction in the body temperature, Thyroid dermopathy or the formally called protibial myxoedema are raised waxy yellow brown lesions. It is due to infiltration of hyaluric acid. The skin isnon-pitting and treatments with local steroids. Hyaluric acid is the main glycosaminoglycan that is deposited in the dermis of hypothyroid patients with myxedema’®. It can swell to one thousand times its dry weight when hydrated. Mucin deposition  involves the skin, tongue, myocardium, and kidneys. Increased transcapillary albumin loss and impaired lymphatic drainage leads to extravascular accumulation and increases the oedema⁷¹. The skin manifestations of other systems affected by lack of thyroid hormones are, pallor, cold intolerance, entrapments syndromes, drooping of the upper eye lids, and purpura⁴⁶. Direct skin changes in the sweat gland leads to decreased sweating and dry skin. Changes to the hair and nails include dry brittle nails, alopecia, dry brittle coarse hair, and loss of hair in the lateral third of the eyebrows. Associated skin manifestations in autoimmune diseases include dermopathy, acropathy, pruritic, vitiligo, pernicious anaemia, eczema, bullous disorders, and others⁷². The effect of hypothyroidism before and after treatment was proved on skin biopsies to reveal changes within 4 weeks of management with thyroid hormone replacement⁴⁶.

Conclusion

Hypothyroidism whether overt or subclinical has adverse cardiovascular effects. One of these effects is increased tissue thickness. This is seen in the skin, the left ventricular walls, and the carotid intima. The possible pathophysiology of increased thickness is one or a combination of tissue oedema, hypertrophy and substance infiltration with further water and salt entrapment. Fortunately, all forms of increased thickness showed response to treatment with thyroid hormone replacement. Further studies with tissue biopsy of the myocardial walls are needed to confirm the tissue consistency.

Disclosures:
None

Funding:
None

Conflict of interest:
None

Data availability:
Data is available on request from the corresponding Author

Acknowledgement:
Yousif Mutaz Yousif, Conestoga College, Canada for his contribution in image editing

Author contribution:
The corresponding author is the primary physician of the patient. She managed and followed up the case. She wrote the manuscript for the case report and literature review.

Author 2:
Data collection, literature collection, analysis, and referencing

Author 3:
Data collection, literature collection, and manuscript layout.

Author 4:
Data and literature collectio

 

 

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