ISSN: 1223-1533

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Authors: Florina Parv, M. Balint, Melania Balas, Rodica Avram

Received for publication: 25th of July, 2013
Revised: 6th of August, 2013

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SUMMARY: (Hide the summary)

It is presented a case of a young male subject diagnosed in emergency room with severe cardiothyreosis and thyroid goiter. During the hospitalization Graves’ disese is confirmed with concomitant severe heart failure. In this paper are presented clinical and paraclinical findings, diagnostic   and   treatment   management,   ethiological   aspects and   case particularities.

Key Words:

cardiothyreosis, heart failure, Graves' disease




Effects  of hyperthyroidism  on the cardiovascular system and especially on heart manifest even at small changes in serum thyroid hormones. In the context of cardiothyreosis  while supraventricular  arrhythmias (especially atrial fibrillation) and unmasked ischemic heart disease are found more frequently, heart failure rarely occurs and denotes a severe pathological heart condition  or intense  and  prolonged  effect of thyroid hormones.



Male patient,  26 years  old, currently unemployed, former  undertaker, without  prior  cardiovascular disorders, presented himself in the emergency room of County Emergency Hospital Timisoara for malaise, rapid palpitations for about a month, small and medium effort dyspnea during last two weeks, accentuated in the last 3 days,  12h fever, sweats,  significant  weight loss. On physical examination we have found warm and wet skin, mild exophthalmia,  peripheral  tremor of extremities, enlarged thyroid gland, tachyarrhythmic  heart sounds with heart rate 210/min,  grade 3 systolic  murmur in mitral  focus,  blood pressure of 140/80 mmHg; turgid jugular veins, decreased vesicular murmur basal in right pulmonary area, also liver was sensitive and palpable 4 cm below the costal margin and lower splenic pole was palpable.

Electrocardiogram at presentation in emergency room showed atrial fibrillation with rapid heart rate (Fig.1).

The first biological  investigations  revealed mild normocytic  normochromic  anemia (Hb=10.5 g/dl), a slightly increased CKMB = 26 U/l, but normal troponin (TnI   = 0.008 ng/ml) and   mild cholestasis   (total bilirubin=2.38  mg/dl). At chest radiography we noted global cardiomegalyin  and mild central pulmonary stasis.



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Fig.1. The resting electrocardiogram on admission: atrial fibrillation, HR 216 b/min;  QRS axis 00; electric alternance; rSr in ‘V1.


Based on history, objective clinical examination and primary emergency investigations  we estabilshed the following diagnosis:

  • Recent atrial fibrillation with rapid heart rate. Heart failure NYHA class III. Suspicion of Graves’ disease with cardiothyreosis.

The    determinatin     of   thyroid  hormone serum concentrations showed the following: FT3 > 35 pmol/l (normal  values:   3.39-6.80  pmol/l),  FT4 > 90 pmol/l (normal  values: 10.55-22.77  pmol/l),  TSH < 0.015 mUI/L. (normal values ranged between 0.27-4.20 mUI/L), antiTPO antibodies 230 IU/mL (normal <12 IU/mL), anti TSH  receptor  antibodies:   25.2 IU/mL  (normal  <1.5 IU/mL).

Echocardiography has brought additional elements of subsequent  cardiac  disturbance:  dilation  of the four chambers with right ventricle of 3.6 cm, left ventricle end-diastolic   diameter of  6.8  cm,  left  ventricle end-sistolic diameter of 5.5 cm, left atrium of 6.3 cm and right atrium of 5.2 cm, a significant systolic dysfunction with LVEF=34% , severe mitral regurgitation, tricuspid regurgitation grade    II,    moderate pulmonary hypertension, without pericardial fluid (Fig.3,4,5,6); also at ultrasound we found  pleural fluid in small amount in right side, hepatomegaly and splenomegaly (14 cm in lenght).

Thyroid ultrasound confirmed a diffuse goiter (thyroid volume of  47.2 ml  )  with  marked hipoechogenic homogeneous appearance of parenchyma and intense, diffuse vascularization at Doppler ultrasound (Fig.7)



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Fig . 2 . Chest X-ray(antero-posterior incidence): cardiomegaly, pulmonary stasis


The final diagnostic was:

  • Graves’ disease with severe cardiothyreosis.

Persistent atrial fibrillation. Mitral insuficiency grade III. Functional tricuspid insufficiency grade II. Moderate secondary pulmonary hypertension. Idiopathic dilated cardiomyopathy. Heart failure NYHA II. Small right sided hidrothorax.



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Fig. 3. Echocardiography (four chambers view, Color Doppler): severe mitral regurgitation



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Fig. 4. Echocardiography (four chambers view, 2D mode): dilation of the four cardiac chambers suggesting dilated cardiomyopathy



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Fig. 5. Echocardiography (four chambers view, continuous doppler): velocity and gradient of mitral regurgitation



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Fig. 6. Echocardiography (four chambers view, continuous doppler): velocity and gradient of tricuspid regurgitation



We initiated treatment with antithyroid drug (Thyrozol 40 mg/day), beta-blocker (metoprolol in progressively increasing doses),    diuretic, injectable    then  oral anticoagulant. The     patient  evolution     during hospitalization  was favourable  with improvement  of symptoms, hemodynamic control, INR control.

Given  the  large  size  of the  heart  dimensions  we considered also    other  etiologies such  as tachycardiomyopathy,   because of undefined onset  of arrhythmia, a    preexisting     (non)familial dilated cardiomyopathy,  a dilated  cardiomyopathy.  We have taken into account  a  postmiocarditis   viral etiology, ethanol or drug abuse, infectious etiology. Markers of B, C hepatitis  and HIV serology  were  negative,  full blood count analysis,  erythrocytes  sedimentation  rate and inflammation markers  were   normal.  Additional immunological  dosing  and cardiac  MRI could  not be performed. Hepato-splenomegaly and association of cholestatic syndrome could be an expression of the liver ischemia in the context of heart failure or a chronic liver preexisting pathology.



The  most important  hemodynamic  effects of the thyroid hormones include peripheral   vasodilation, increased  heart  rate,  increased  cardiac and  stroke output, increased myocardial contractility  and improved ventricular relaxation.

Tachycardiomyopathy   occurs in  the  context of persistent supraventicular   tachyarrhythmia    (atrial fibrillation or atrial tachycardia) and is characterized by persistent ventricular dysfunction. Severity of the heart failure depends on the duration of arrhythmia  and the heart rate and improves after controlling the frequency and/or heart rate, the duration ranging from several days to several months (1).



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Fig. 7. 2D thyroid ultrasound: right thyroid lobe increased in volume, homogeneous appearance, transonic region of about 10 mm.



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Fig. 8. The resting electrocardiogram at discharge: atrial fibrillation, HR 88/min


Graves’  disease,  the most common  cause  of hyperthyroidism,  is an  autoimmune   thyroid disorder which often affects middle-aged women.

Atrial  fibrillation occurs in about 10 %  of cases of Graves’ disease, especially in young people. Embolic risk is reduced  to this category (<2  %  / year)  and it is recommended only antiplatelet therapy. In this case, the significant systolic  dysfunction and    associated cardiomegaly  imposed  the anticoagulation  treatment. Excepting the cases with hemodynamic instability, the conversion to sinus rhythm it is not recommended as the risk of recurrence lasts until the thyroid function returns to normal. The euthyroidism  is restored usually in few (3-4) months of  antithyroid treatment. Restoring euthyroid  status  leads to spontaneous  conversion  to sinus rhythm in about 6-12 weeks to more than 50 % of patients newly diagnosed with atrial fibrillation (3), the main contributing factor being the duration of arrhythmia, patient  age  and  the  absence  of cardiac  disease.  In patients who do not recover the sinus rhythm in more than four months after restoring  the euthyroid status cardioversion  may attempted  if the necessary  CHA2 DS-VAS 2C criteria are met.

Heart failure  in a patient  with hyperthyroidism per primam  is the expression  of overt  increased cardiac output  but often unmask  a  latent cardiopathy, most frequently coronary heart disease. Other cardiac failure mechanisms are: the shortening of diastole by loss of the atrial pump when atrial fibrillation occurs, myocardial structural  changes  with the appearance  of diastolic dysfunction,  deficit between  demand  and  myocardial oxygen consumption, ventricular systolic dysfunction by direct toxic action of excess thyroid hormones on cardiac myocytes.(2).  The recommended treatment  is classic, primarily beta -blockers,   but  also   ACE   inhibitors, diuretics, digitalis are used in severe systolic dysfunction and lack  of adequate control  of heart rate.  The most severe complication of thyrotoxicosis is represented by thyroid storm, characterized by impairment of general health, associating fever, nausea, vomiting, diarrhea, dehydration and coma appearance.



  • Relatively good clinical  tolerance to a very rapid heart rate and a previously damaged heart
  • Cardiac dilation associated to Graves’ disease with atrial fibrillation in  a   young patient, which customizes  the therapeutic  management  and evolution
  • Graves’  disease   occurrence   in   a  young   male subject.



  1. Carmen Ginghina. Mic tratat de cardiologie. Ed. Academiei Romana, 2010
  2. Pereira N, Parisi A. Myocardial stunning in hyperthyroidism. Clin Cardiol , 2000, 23: 298-300
  3. Nakazawa K, Sakurai K, Hamada N. Management of atrial fibrillation in the post-thyrotoxic state. Am J Med 72: 903-906, 1982

Correspondence to:
Correspondence to: Florina Parv, MD, PhD Clinic of Cardiology, Timișoara County Hospital, 10 Iosif Bulbuca St., 300736