Limits...
Second degree AV block and severely impaired contractility in cardiac myxedema: a case report.

Chatzitomaris A, Scheeler M, Gotzmann M, Köditz R, Schildroth J, Knyhala KM, Nicolas V, Heyer C, Mügge A, Klein HH, Dietrich JW - Thyroid Res (2015)

Bottom Line: Although magnetic resonance imaging of the heart demonstrated decreased cardiac contractility and pericardial effusion, suggesting peri-myocarditis, plasma levels for BNP and troponin I were low.Additionally, bradycardiac episodes abated, although intermittent second degree AV block was still occasionally present during the night.In conclusion, overt hypothyroidism may be associated by cardiac myxedema affecting both electrophysiology and contractility, observations that underscore the necessity of thyroid testing in different phenotypes of heart failure.

View Article: PubMed Central - PubMed

Affiliation: Department of Endocrinology and Diabetes, Medical Hospital I, Bergmannsheil University Hospitals, Ruhr University of Bochum, Bochum, NRW Germany.

ABSTRACT
The heart is a major target organ for thyroid hormone action. Severe overt hypothyroidism can result in diastolic hypertension, lowered cardiac output, impaired left ventricular contractility and diastolic relaxation, pericardial effusion and bradycardia. However, the function of the atrial pacemaker is usually normal and the degree by which the heart rate slows down is often modest. Here we report the case of a 20 year old male Caucasian with severe overt hypothyroidism. He presented with syncopation due to second degree atrioventricular block type Mobitz 2 and heart failure with reduced ejection fraction (38 %). Laboratory testing revealed a severe overt hypothyroidism with markedly elevated TSH (>100 mIU/L) and reduced fT3 and fT4 levels. The condition was caused by hypothyroid Graves' disease (Graves' disease with Hashimoto component). Although magnetic resonance imaging of the heart demonstrated decreased cardiac contractility and pericardial effusion, suggesting peri-myocarditis, plasma levels for BNP and troponin I were low. A possible infectious cause was unlikely, since testing for cardiotropic viruses was negative. The patient was treated with intravenous levothyroxine and after peripheral euthyroidism had been achieved, left ventricular ejection fraction returned to normal and pericardial effusion dissolved. Additionally, bradycardiac episodes abated, although intermittent second degree AV block was still occasionally present during the night. In conclusion, overt hypothyroidism may be associated by cardiac myxedema affecting both electrophysiology and contractility, observations that underscore the necessity of thyroid testing in different phenotypes of heart failure.

No MeSH data available.


Related in: MedlinePlus

ECG monitoring in overt hypothyroid state
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
getmorefigures.php?uid=PMC4440534&req=5

Fig1: ECG monitoring in overt hypothyroid state

Mentions: A 20-year-old Caucasian male was admitted to the emergency department of an external secondary care hospital after he collapsed with syncopation while he watched a football match in the stadium. He had lost consciousness for less than a minute. Two years before he was diagnosed to have hypothyroidism, and the prescribed medication consisted of low dose levothyroxine and, for unknown reasons, low dose of carbimazole, potentially because of high TRAb titers. He was, however, taking his medication irregularly. Upon hospital admission he complained of increasing fatigue over the last two months. Dyspnea, chest pain, weight gain and stool irregularity were denied as well as symptoms and signs of previous viral infection in the last months. At arrival, the patient was awake and amenable, without showing any signs of alcohol consumption. His body temperature was 35.8 °C, heart rate was 52 bpm and the blood pressure was 80/40 mmHg. The physical examination was otherwise unremarkable. His initial electrocardiography (ECG) showed sinus bradycardia without atrioventricular block and ST-segment abnormalities. Echocardiography in the emergency department demonstrated impaired cardiac contractility with ejection fraction (LVEF) of 38 % and a pericardial effusion with maximal thickness of 15 mm without hemodynamic relevance. All valves were well visualized and appeared to be normal. Initial laboratory findings revealed a TSH level of over 100 mIU/L, therefore the patient was moved to our hospital in face of imminent myxedema coma. We confirmed hypothyroidism with reduced levels of plasma free thyroxine (fT4, < 3.9 pmol/L, see Table 1 for reference ranges) and plasma free triiodothyronine (fT3, 2.4 pmol/L) associated with massive rise in plasma thyrotropin (TSH, 108 mIU/L). Creatin kinase (CK) was 437 U/L (normal < 172) and CK-MB was 34 U/l (normal < 24). However, troponin I and BNP concentrations were low. Serum electrolytes, complete blood count, and basal levels of cortisol and ACTH were normal. The patient was transferred to the ICU, where treatment with intravenous infusion of levothyroxine (500 μg over the first 24 h) was commenced. ECG monitoring revealed an intermittent atrioventricular block type Mobitz 2 (Fig. 1). In order to evaluate the pericardial effusion and the impaired left ventricular ejection fraction, magnetic resonance imaging was performed, which confirmed the echocardiographic findings. A potential peri-myocarditis was susptected because of the increased signal intensity in the epicardial layer, suggesting local edema, in the T2-weighted and late gadolinium enhancement images (Fig. 2 and Additional file 1). Therefore, to rule out a peri-myocarditis, serologic studies, including parvovirus-B19, streptococcus, influenza-virus, mycoplasma, adenovirus, enterovirus, herpes virus type 6 and cytomegalovirus were performed, which did not support the diagnosis.Table 1


Second degree AV block and severely impaired contractility in cardiac myxedema: a case report.

Chatzitomaris A, Scheeler M, Gotzmann M, Köditz R, Schildroth J, Knyhala KM, Nicolas V, Heyer C, Mügge A, Klein HH, Dietrich JW - Thyroid Res (2015)

ECG monitoring in overt hypothyroid state
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4440534&req=5

Fig1: ECG monitoring in overt hypothyroid state
Mentions: A 20-year-old Caucasian male was admitted to the emergency department of an external secondary care hospital after he collapsed with syncopation while he watched a football match in the stadium. He had lost consciousness for less than a minute. Two years before he was diagnosed to have hypothyroidism, and the prescribed medication consisted of low dose levothyroxine and, for unknown reasons, low dose of carbimazole, potentially because of high TRAb titers. He was, however, taking his medication irregularly. Upon hospital admission he complained of increasing fatigue over the last two months. Dyspnea, chest pain, weight gain and stool irregularity were denied as well as symptoms and signs of previous viral infection in the last months. At arrival, the patient was awake and amenable, without showing any signs of alcohol consumption. His body temperature was 35.8 °C, heart rate was 52 bpm and the blood pressure was 80/40 mmHg. The physical examination was otherwise unremarkable. His initial electrocardiography (ECG) showed sinus bradycardia without atrioventricular block and ST-segment abnormalities. Echocardiography in the emergency department demonstrated impaired cardiac contractility with ejection fraction (LVEF) of 38 % and a pericardial effusion with maximal thickness of 15 mm without hemodynamic relevance. All valves were well visualized and appeared to be normal. Initial laboratory findings revealed a TSH level of over 100 mIU/L, therefore the patient was moved to our hospital in face of imminent myxedema coma. We confirmed hypothyroidism with reduced levels of plasma free thyroxine (fT4, < 3.9 pmol/L, see Table 1 for reference ranges) and plasma free triiodothyronine (fT3, 2.4 pmol/L) associated with massive rise in plasma thyrotropin (TSH, 108 mIU/L). Creatin kinase (CK) was 437 U/L (normal < 172) and CK-MB was 34 U/l (normal < 24). However, troponin I and BNP concentrations were low. Serum electrolytes, complete blood count, and basal levels of cortisol and ACTH were normal. The patient was transferred to the ICU, where treatment with intravenous infusion of levothyroxine (500 μg over the first 24 h) was commenced. ECG monitoring revealed an intermittent atrioventricular block type Mobitz 2 (Fig. 1). In order to evaluate the pericardial effusion and the impaired left ventricular ejection fraction, magnetic resonance imaging was performed, which confirmed the echocardiographic findings. A potential peri-myocarditis was susptected because of the increased signal intensity in the epicardial layer, suggesting local edema, in the T2-weighted and late gadolinium enhancement images (Fig. 2 and Additional file 1). Therefore, to rule out a peri-myocarditis, serologic studies, including parvovirus-B19, streptococcus, influenza-virus, mycoplasma, adenovirus, enterovirus, herpes virus type 6 and cytomegalovirus were performed, which did not support the diagnosis.Table 1

Bottom Line: Although magnetic resonance imaging of the heart demonstrated decreased cardiac contractility and pericardial effusion, suggesting peri-myocarditis, plasma levels for BNP and troponin I were low.Additionally, bradycardiac episodes abated, although intermittent second degree AV block was still occasionally present during the night.In conclusion, overt hypothyroidism may be associated by cardiac myxedema affecting both electrophysiology and contractility, observations that underscore the necessity of thyroid testing in different phenotypes of heart failure.

View Article: PubMed Central - PubMed

Affiliation: Department of Endocrinology and Diabetes, Medical Hospital I, Bergmannsheil University Hospitals, Ruhr University of Bochum, Bochum, NRW Germany.

ABSTRACT
The heart is a major target organ for thyroid hormone action. Severe overt hypothyroidism can result in diastolic hypertension, lowered cardiac output, impaired left ventricular contractility and diastolic relaxation, pericardial effusion and bradycardia. However, the function of the atrial pacemaker is usually normal and the degree by which the heart rate slows down is often modest. Here we report the case of a 20 year old male Caucasian with severe overt hypothyroidism. He presented with syncopation due to second degree atrioventricular block type Mobitz 2 and heart failure with reduced ejection fraction (38 %). Laboratory testing revealed a severe overt hypothyroidism with markedly elevated TSH (>100 mIU/L) and reduced fT3 and fT4 levels. The condition was caused by hypothyroid Graves' disease (Graves' disease with Hashimoto component). Although magnetic resonance imaging of the heart demonstrated decreased cardiac contractility and pericardial effusion, suggesting peri-myocarditis, plasma levels for BNP and troponin I were low. A possible infectious cause was unlikely, since testing for cardiotropic viruses was negative. The patient was treated with intravenous levothyroxine and after peripheral euthyroidism had been achieved, left ventricular ejection fraction returned to normal and pericardial effusion dissolved. Additionally, bradycardiac episodes abated, although intermittent second degree AV block was still occasionally present during the night. In conclusion, overt hypothyroidism may be associated by cardiac myxedema affecting both electrophysiology and contractility, observations that underscore the necessity of thyroid testing in different phenotypes of heart failure.

No MeSH data available.


Related in: MedlinePlus