Thyroxine and cardiac electrophysiology—a forgotten physiological duo?
© Ker; licensee BioMed Central Ltd. 2012
Received: 16 May 2012
Accepted: 20 August 2012
Published: 22 August 2012
Thyroid hormone exerts numerous effects on the cardiovascular system. Hypothyroidism can lead to various electrocardiographic and mechanical changes in the heart and blood vessels.
The potential risk for sudden cardiac death in patients with hypothyroidism have never been properly explored. However, numerous reports of various electrocardiographic changes indicative of such a risk has been published.
In this case report the occurrence of ventricular late potentials in a case of overt hypothyroidism is described and furthermore, the disappearance of these potentials with T4 treatment alone is shown.
It is concluded that the concept that undiagnosed and/or untreated hypothyroidism poses a risk for sudden cardiac death is worth exploring.
KeywordsHypothyroidism Late potentials Sudden cardiac death
Thyroid hormone has important physiological effects on the cardiovascular system . Cardiovascular effects of hypothyroidism can include electrocardiographic changes, such as bradycardia, right bundle branch block, flattened or inverted T waves, QRS prolongation and even torsades de pointes ventricular arrhythmia .
Mechanical cardiovascular effects of hypothyroidism include a remarkable increase in peripheral vascular resistance , an increase in arterial stiffness , an impairment in left ventricular diastolic function as characterized by a slowing of myocardial relaxation and impaired early ventricular filling  and pericardial effusion .
Currently, there is an interesting electrocardiographic contrast between thyrotoxicosis and hypothyroidism : In thyrotoxicosis atrial tachyarrhythmias are common and ventricular arrhythmias are rare. However, in hypothyroidism QT interval prolongation and ever QT dispersion can occur and lead to ventricular arrhythmias, such as torsade de pointes ventricular tachycardia which can be resolved with T4 treatment alone [2, 7].
In this case report it is shown that severe, primary hypothyroidism can present with an abnormal signal averaged electrocardiogram and that this can be corrected with T4 treatment alone. To date this is the only report of primary hypothyroidism presenting with an abnormal signal-averaged electrocardiogram corrected with T4 treatment alone.
At no stage did the patient experience any symptoms suggestive of hypothyroidism or any other disease.
The serum TSH (thyroid stimulating hormone) measured 76.11 mIU/L and was indicative of severe, primary hypothyroidism (normal range 0.27 – 4.20 mIU/L).
No other pathology was found. Specifically no secondary hyperlipidemia was present and the serum glucose level was normal. No classical signs of hypothyroidism were present. Thyroid ultrasonography revealed a small and hypoechogenic thyroid gland with the typical appearance of advanced Hashimoto thyroiditis with no nodules present.
The patient remains well with a normal signal-averaged electrocardiogram after one year of clinical follow-up.
Three aspects of this case merit discussion. Firstly, this is the first case report in the literature which describes the presence of ventricular late potentials in the myocardium of a patient with overt hypothyroidism. The signal-averaged electrocardiogram is a technique used to detect the presence of ventricular late potentials . Ventricular late potentials correspond to areas in the ventricular myocardium where there is slowed conduction velocity and these cause delayed ventricular activation . These ventricular late potentials indicate an increased risk for the occurrence of ventricular arrhythmias . These observed ventricular late potentials disappeared in this patient after T4 treatment alone.
Secondly, other parameters indicating an increased ventricular arrhythmic risk has been described in hypothyroidism [9–11]. An increase in the QTc interval have been described in hypothyroidism and that this increase is directly related to the severity of hypothyroidism . TSH levels have also been shown to be directly related to QT prolongation and QT dispersion . QT dispersion is the interlead variability of the QT interval on the surface ECG that reflects regional variations in myocardial repolarization and an increased QT dispersion has been found to be strongly associated with an increase in ventricular arrhythmias and sudden cardiac death . Lastly, an improvement in heart rate variability have also been documented in treated hypothyroidism .
Thirdly, hypothyroidism can affect cardiac structure [11–13]. These structural effects manifests clinically in hypothyroidism as an increase in myocardial echoreflectivity [13, 14], perhaps an explanation for the observed electrocardiographic abnormalities observed in hypothyroidism?
In conclusion, a case is presented showing the presence of cardiac late potentials in a patient with overt hypothyroidism. Disappearance of these late potentials with only T4 treatment is shown. It is proposed that undiagnosed and/or untreated hypothyroidism poses a threat of sudden cardiac death and that this concept is worthwhile to be studied in a proper randomized trial.
- Klein I, Ojamaa K: Thyroid hormone and the cardiovascular system. N Engl J Med 2001, 344: 501–509. 10.1056/NEJM200102153440707PubMedView Article
- Kweon KH, Park BH, Cho CG: The effects of L-thyroxine treatment on QT dispersion in primary hypothyroidism. J Korean Med Sci 2007, 22: 114–116. 10.3346/jkms.2007.22.1.114PubMed CentralPubMedView Article
- Klein I, Ojamaa K: Werner & Ingbar`s The Thyroid. In A Fundamental and Clinical Text, edit. 8. Edited by: Braverman LE, Utiger RD. Lippincott Williams & Wilkins, Philadelphia; 2000:777–782.
- Obuobie K, Smith J, Evans LM: Increased central arterial stiffness in hypothyroidism. J Clin Endocrinol Metab 2002, 87: 4662–4666. 10.1210/jc.2002-020493PubMedView Article
- Wieshammer S, Keck FS, Waitzinger J: Acute hypothyroidism slows the rate of left ventricular diastolic relaxation. Can J Physiol Pharmacol 1989, 67: 1007–1010. 10.1139/y89-158PubMedView Article
- Yamanaka S, Kumon Y, Matsumura Y, Kamioka M, Takeuchi H, Sugiura T: Link between pericardial effusion and attenuation of QRS voltage in patients with hypothyroidism. Cardiology 2010, 116: 32–36. 10.1159/000313464PubMedView Article
- Schenck JB, Rizvi AA, Lin T: Severe primary hypothyroidism manifesting with torsades de pointes. Am J Med Sci 2006, 331: 154–156. 10.1097/00000441-200603000-00008PubMedView Article
- Jarrett JR, Flowers NC: Signal-averaged electrocardiography: History, techniques and clinical applications. Clin Cardiol 1991, 14: 984–994. 10.1002/clc.4960141209PubMedView Article
- Nathaniel C, Caleb L, Azrin MA: QTc prolongation in hypothyroidism. J Am Coll Cardiol 1994, 23: 36A.
- Altun A, Altun G, Ozkan B, Kaya M, Ozbay G: The relationship between ventricular repolarization and thyroid stimulating hormone. Ann Noninvasive Electrocardiogr 1998, 3: 19.
- Kahaly GJ, Dillmann WH: Thyroid hormone action in the heart. Endocr Rev 2005,26(5):704–728. 10.1210/er.2003-0033PubMedView Article
- Klein I, Danzi S: Thyroid disease and the heart. Circulation 2007,116(15):1725–1735. 10.1161/CIRCULATIONAHA.106.678326PubMedView Article
- Romano MMD, Maciel LMZ, Almeida-Filho OC, Pazin-Filho A, Schmidt A, Maciel BC: Myocardial ultrasonic tissue characterization in patients with thyroid dysfunction. Cardiovascular Ultrasound 2010, 8: 15. 10.1186/1476-7120-8-15PubMed CentralPubMedView Article
- Ciulla MM, Paliotti R, Cortelazzi D, Tortora G, Barelli MV, Buonamici V, Magrini F, Beck-Peccoz P: Effects of thyroid hormones on cardiac structure: a tissue characterization study in patients with thyroid disorders before and after treatment. Thyroid 2001, 11: 613–619. 10.1089/105072501750362673PubMedView Article
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.