Introduction
This case focuses on the fact, that not every individual presenting with chest discomfort and ECG changes has ACS and other factors such as metabolic disturbances should always be considered in the differential diagnosis of these patients. Furthermore, the importance of history and physical examination should never be underestimated.
As a clinician, it is our duty to recognize the common as well as the uncommon presentations of hypothyroidism to prevent misdiagnosis and improper treatment. In this case, for example, patient was initially thought to have ACS but we later realized that the presentation was due to uncontrolled hypothyroidism secondary to non-compliance with medications. Given patients low TIMI score, his probability of having an ACS was very low. Also, the reversal of ECG changes after starting levothyroxine therapy supports the diagnosis. It is essential to understand that all ECG changes don’t necessarily mean cardiac injury. We should always consider the possibility of non-cardiac causes whenever we see a new change on an ECG.
Case Report
60 year old male with past medical history of hypertension and hypothyroidism, presented to the Emergency Department because of dizziness and some chest discomfort. He had no headaches, nausea, vomiting or tinnitus. He denied loss of consciousness. Blood pressure on this presentation was slightly elevated. He was given three sublingual nitroglycerine for chest discomfort. ECG was done which showed new T wave inversion in leads V4, V5 and V6 [Fig.1]. There was mild troponins elevation with the presentation. Given ECG findings and elevated troponins, patient was started on heparin drip with anticipation of possible need for left heart catheterization. Of note, patient stated that he had not been taking his thyroid medication for past 6 months.
Physical examination revealed an elderly male, in no apparent distress, resting comfortably in bed. His heart rate was found to be 58/min and BP of 160/90 mmHg with no S3 or S4 on auscultation. Patient did not have any jugular venous distension or pitting edema. Patient’s voice was hoarse and thyromegaly was noted on physical examination. Lungs were clear on auscultation and there was no organomegaly on abdominal exam. Bowel sounds were normal. Neurological examination revealed slow but normal responses on questioning. There was a delayed relaxation phase of deep tendon reflexes. Repeat ECG done in our hospital showed the same findings on T wave inversion. Given the fact that patient’s troponins were minimally elevated and decreased on repeat testing, patient’s risk of non-ST elevation myocardial infarction was low. Patient underwent a 2D echocardiogram which did not show any wall motion abnormalities and a normal ejection fraction. Patient’s heparin drip was discontinued and was started on levothyroxine 100 mcg daily. Subsequently, patient’s ECG changes reversed within 48 hours after starting levothyroxine.
After treatment with levothyroxine, patient’s condition improved significantly and his symptoms resolved completely. The ECG changes in V4 and V5 reversed within the next 3 days [Fig.2]. Patient was ultimately discharged in a stable condition and was counseled in detail about proper medication compliance.
Troponin I level was found to be 0.06 ng/mL which on repeat testing was 0.07 and 0.04. Patient’s TSH was 39.67. Complete blood count and basic metabolic profile was found to be normal. 2D echocardiogram showed an ejection fraction of 59% with no wall motion abnormalities. Pulmonary arterial pressure was found to be normal (20 mm Hg).
Uncontrolled hypothyroidism should be considered given high TSH and history of medication non-compliance. Dizziness is not uncommon in people with uncontrolled hypothyroidism. Another differential would be non-ST elevation myocardial infarction given patient’s age and history of hypertension. However, we ruled this out because of pattern and degree of troponin elevation and a normal 2D echocardiogram with no wall motion abnormalities. Patient also had a low TIMI score. Pulmonary embolism can also present with dizziness and chest pain if the embolus is large enough. However, chest pain was non-pleuritic. There was no history of travel (or other factors suggestive of DVT) and there was no leg swelling. Patient’s pulse oximetry was normal throughout the hospital course and the patient did not have tachypnea or tachycardia on physical examination. Based on a very low Wells score and clinical presentation, pulmonary embolism was ruled out. Orthostatic hypotension is a fairly common cause of dizziness in elderly population. However, patient’s BP was actually high on presentation. Also, the improvement in symptoms after treatment with levothyroxine points towards hypothyroidism as the cause of this patient’s dizziness.
Patient’s condition improved significantly after administration of levothyroxine and his ECG changes revered. After 2 days of treatment, patient’s dizziness improved significantly and most of his ECG changes had reversed. Patient was ultimately discharged in a very stable condition and was scheduled for a follow-up within 1 week. Patient’s condition was stable at the follow-up appointment. As a part of the work-up for chest pain, patient also underwent exercise stress testing 8 weeks after being discharged which was found to be normal.
Discussion
Normal heart contractility requires a normally functioning thyroid gland [
1]. It is related to proper tri-iodothyronine stimulated transcription of the myosin alpha gene and inhibition of the beta gene. Moreover, tri-iodothyronine also contributes to beta receptor expression on cardiac tissue and also determines its response to catecholamines. The disruption of any of these mechanisms can result in cardiac abnormalities seen in hypothyroidism [
2]. In less severe cases, sinus bradycardia is the most common abnormality seen in these patients, but in a small number of patients, other, more serious cardiac problems can also be seen such as prolong QT interval and rarely even fatal arrhythmias like Torsades de pointes [
3]. There is evidence to suggest that subclinical hypothyroidism is related to increased QT interval dispersion in females [
4]. Treatment of hypothyroid patient with levothyroxine results in correction of these ECG abnormalities in most of the patient [
5]. There is also evidence to suggest that even short periods of hypothyroidism (as short as 10 days) might be sufficient to have effects on the heart. A small study that looked at patients with acute hypothyroidism (after thyroidectomy or radioactive iodine ablation) found that short periods of hypothyroidisms may be sufficient to affect cardiac reserves, mainly through metabolic alteration and without any structural abnormalities [
6]. Hypothyroidism also has an association with atrio-ventricular block. Most common types of blocks associated with thyroid disease are Type II and Type III AV block. However, unlike the QT changes on ECG which reverse after sufficient treatment with levothyroxine, AV block associated with thyroid disease almost always requires the placement of a permanent pacemaker even after normalization of thyroid status [
7]. Another mechanism by which hypothyroidism can result in QT prolongation indirectly is after thyroid surgery. A well know complication of thyroid surgery is unrecognized parathyroidectomy, which in turn can lead to hypocalcemia and subsequent QT prolongation [
8].
There have been similar case reports in which patients presenting with chest discomfort, ECG changes and even mild elevation in cardiac enzymes were subsequently found to have thyroid disease rather than an actual MI [
9]. 30-50% of patient with hypothyroidism can have ST and T-wave changes on ECG and can be reversed when they are treated with thyroid hormones [
10]. However, care must be undertaken not to treat too rapidly as such an action has been shown to precipitate acute myocardial infarction or heart failure in hypothyroid patients. Another article published in Probl Endokrinol Gormonoter Journal showed that patient with hypothyroidism tend to have dystrophic disorders of the myocardium secondary to metabolic derangements [
11]. The study also showed an absence of disturbed perfusion processes in the myocardium and a diffuse decrease in metabolic activity of myocardial tissue. One case report in Dtsch Med Wochenschr presents a similar case when a middle age male presented with strongly elevated cardiac enzymes along with proximal myopathy of the limbs and was found to have overt hypothyroidism secondary to Hashimoto’s thyroiditis [
12]. Subsequently, the patient’s condition improved after treatment with levothyroxine.
Conclusion
Detailed history and physical examination is one of the biggest strengths of a physician, and their importance should never be underestimated. Always rule out metabolic/electrolyte abnormalities in patients with ECG changes suggestive of myocardial ischemia. Patients with thyroid dysfunction (hypothyroidism or hyperthyroidism) can have an abnormal ECG which does not require further work-up unless clinical presentation is suggestive of a cardiac issue. Patients who are non-compliant with their medications should always be counseled about the regular use of their medications to avoid unnecessary hospital readmissions.
References
- Weinbrenner C, Gerbert B, Strasser RH. Thyroid hormone and the cardiovascular system. Deutsche medizinische Wochenschrift (1946). 2005;130(39):2215-2219.
- Erdogan E, Akkaya M, Bacaksiz A, Tasal A, Ilhan M, Kul S, et al. Electrocardiographic and echocardiographic evidence of myocardial impairment in patients with overt hypothyroidism. Annales d’endocrinologie. 2013;74(5-6):477-482.
- Kandan SR, Saha M. Severe primary hypothyroidism presenting with torsades de pointes. BMJ Case Reports. 2012;2012.
- Bakiner O, Ertorer ME, Haydardedeoglu FE, Bozkirli E, Tutuncu NB, Demirag NG. Subclinical hypothyroidism is characterized by increased QT interval dispersion among women. Medical principles and practice: International Journal of the Kuwait University, Health Science Centre. 2008;17(5):390-394.
- Kweon KH, Park BH, Cho CG. The effects of L-thyroxine treatment on QT dispersion in primary hypothyroidism. Journal of Korean Medical Science. 2007;22(1):114-116.
- Donaghue K, Hales I, Allwright S, Cooper R, Edwards A, Grant S, et al. Cardiac function in acute hypothyroidism. European Journal of Nuclear Medicine. 1985;11(5):147-149.
- Ozcan KS, Osmonov D, Erdinler I, Altay S, Yildirim E, Turkkan C, et al. Atrioventricular block in patients with thyroid dysfunction: prognosis after treatment with hormone supplementation or antithyroid medication. Journal of Cardiology. 2012;60(4):327-332.
- Rentoukas E, Lazaros G, Sotiriou S, Athanassiou M, Tsiachris D, Deftereos S, et al. Extreme but not life-threatening QT interval prolongation? Take a closer look at the neck! Journal of Electrocardiology. 2013;46(2):128-130.
- Minutiello L. The enzymatic and electrocardiographic changes falsely indicative of an acute myocardial infarct during hypothyroidism. Minerva Cardioangiologica. 1993;41(12):597-602.
- Hylander B, Ekelund LG, Rosenqvist U. The cardiovascular response at rest and during exercise in hypothyroid subjects to thyroxine substitution. Clinical Cardiology. 1983;6(3):116-124.
- Kotova GA, Livshits G. Myocardial involvement in hyper- and hypothyroidism. Problemy Endokrinologii. 1992;38(1):24-27.
- Harbeck B, Berndt MJ, Lehnert H. Cardiac myopathy due to overt hypothyroidism]. Deutsche medizinische Wochenschrift (1946). 2014;139(10):483-485.