Introduction:                                                     

Cardiomyopathies are diseases that involve the myocardium directly and not secondary to hypertension, congenital, valvular, coronary artery disease or pericardial disease¹. It has generally been accepted that thyrotoxicosis may be associated with high output high heart failure in patient with heart disease either symptomatic or not². Here we report two cases of dilated cardiomyopathies who presented with initial symptoms of  breathlessness & palpitations that did not resolve inspite of restoration of thyroid levels.                         

Case presentation 1:                                                                         

A 35 years old female patient presented with shortness of breath and bilateral pedal edema from 15 days. There was no history of shortthroat,paroxysmal nocturnal dysnea, chest pain, oliguria and hematuria.There was no history of any cardiac disease in the past. He was nonsmokers& nonalcoholic. He did not receive or intake of medicine.

On physical examination he was  afebrile,  pulse was 112/min irregularly irregular, blood pressure was110/70 mm of Hg and respiratory rate was 22/min.He had pallor, engorged neck vein with raised internal jugular venous pressure and bilateral pitting pedal edema. Fine tremors were present in both hands. There was bilateral thyroid swelling with tender hepatomegaly.The apex impulse was in 5^th intercostal space, hyper dynamic in nature just outside the midclavicular line. First heart sound was soft , S₂ audib le & S₃ gallop was present. There were grade 3 pan systolic flow murmur in mitral area. There was no rales in chest. The ski gram of chest showed cardiomegaly(Figure 1). The ECG showed left ventricular with left bundle branch block. Two dimension echocardiography was suggestive of dilated cardiomyopathy with left ventricular ejection fraction of 20% with severe mitral regurgitation, severe tricuspid regurgitation with global hypokinesia(Figure 2). On investigations Hb-8.6gm/dl TLC-7250/cumm with normal renal & liver profile.Troponin T was negative. ASLO titre was < 200 U. Blood culture was also negative.The thyroid hormone profile : Serum FT₃ was 7.75ng/dl ( 1.8-4.2 pg/ml), serum FT₄ was 4.48 microgram/dl( .89-1.76ng/dl)&Serum TSH  was .035(0.4- 4 micro IU/ml)

Case presentation 2  

A 65 years old male patient presented with chief complain of progressive dysnea on exertion and palpitation from 2 months. There was no history of orthopnea,paroxysmal nocturnal dysnea, chest pain, oliguria and hematuria.There was no history of any cardiac disease in the past. He was taking antithyroid drug from 1year.                                                                

On physical examination he was  afebrile,  pulse was 122/min irregularly irregular, blood pressure was110/70 mm of Hg and respiratory rate was 22/min.There was no thyroid swelling. Fine tremors were present in both hands. The apex impulse was in 5^th intercostal space, hyper dynamic in nature just outside the midclavicular line. First heart sound was loud, S₃ gallop was present. There were grade 3 pan systolic flow murmur in mitral area. There was no rales in chest. The ski gram of chest showed cardiomegaly. The ECG showed atrial fibrillation. Two dimension echocardiography was suggestive of dilated cardiomyopathy with left ventricular ejection fraction of 25% with severe mitral regurgitation, moderate tricuspid regurgitation & pulmonary hypertension with global hypokinesia(Figure 3). The thyroid hormone were evaluated serum T3 1.22 ( .6-1.81ng/ml), serum T4 11.01 microgram/dl(4.5-10.9 microgram/dl)&serum TSH .12(35-5.50 micro IU/ml.

Discussion                                                                                  

The cardiovascular manifestations of thyrotox-icosis may be due to direct effects of thyroid hormones at the cellular level, to their interactions with the sympathetic nervous system, or to alterations of peripheral circulation and metabolism¹.  Sinus tachycardia in thyrotoxicosis can occur at rest, during sleep, and during exercise. It is hypothesized that thyroid hormones have direct effects on the conduction system, possibly via cellular changes in cation transport,

Including a decrease of atrial excitation threshold, an increase of sinoatrial node firing, and a shortening of conduction tissue refractory time³. Atrial fibrillation  occurs in 5% to 15% of hyperthyroid patients⁴. It has been reported that approximately 6% of patients with hyperthyroidism present with congestive heart failure, half of whom have left ventricular systolic dysfunction⁵. Few cases of reversible dilated cardiomyopathy that recovered through the use of antithyroid medications ⁶. Possible mechanism may be chronic persistent tachyarrhythmias and cardiac sensitivity to b-adrenergic stimulation are likely to contribute to the development of left ventricular systolic dysfunction in patients with thyrotxicosis⁷. This case adds further evidence of association between thyrotoxicosis and dilated cardiomyopathy in adults. It is important to recognise that dilated cardiomyopathy may be initial manifestations of thyrotoxicosis because it can be reversed with of antithyroid drug⁶.

References                                                                                   

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