Cardiovascular Events in Patients With Thyroid Storm

Zainulabedin Waqar; Sindhu Avula; Jay Shah; Syed Sohail Ali


J Endo Soc. 2021;5(6) 

In This Article


Hyperthyroidism is due to excessive endogenous thyroid hormone production and thyrotoxicosis as a result of excess thyroid hormone, which can be secondary to either endogenous thyroid hormone production (hyperthyroidism) or due to exogenous thyroid hormone replacement.[5]

Thyroid crisis or thyroid storm, on the other hand, is an extreme manifestation of thyrotoxicosis, which is characterized by amplified manifestations. It is most commonly caused by Grave's disease or toxic multinodular goiter, but in rare occasions can be from subacute thyroiditis or due to intentional thyroid hormone overdose.[9]

Thyroid storm can occur with solitary toxic adenoma or toxic multinodular goiter and less commonly with thyroid-secreting pituitary adenomas, hypersecretory thyroid carcinomas, teratomas, and with hydatiform moles. It can also be associated with thyrotoxicosis induced by interleukin-2 or α-interferon.[10] Several other conditions such as diabetic ketoacidosis, myocardial infarction, congestive heart failure, trauma, surgery, infection, and intense emotional stress can serve as triggers for thyroid storm in patients with thyrotoxicosis.[11]

Thyroid storm is a clinical emergency, with a mortality rate of 20% to 30%.[12] Its incidence rate was 0.57 to 0.76 per 100 000 persons and 4.8 to 5.6 per 100 000 hospitalized patients per year, as found in a US-based survey.[13] It constituted 16% of patients hospitalized with thyrotoxicosis and has 12 times the mortality compared with thyrotoxicosis without storm.[13] The study showed that although its incidence rate did not change significantly spanning the years 2003 to 2014, the hospitalization costs had increased. Our analysis, which included the interval years 2012 to 2015, showed that among hospitalized patients with thyroid storm, any CE was associated with higher mortality, length of stay (LOS), and hospitalization costs. The longer LOS and hospitalization costs remained significant even upon conducting a subgroup analysis among various subtypes of CEs, such as ischemic events, heart failure, or arrhythmias. There were significantly more patients with obesity, liver disease, and smoking in the group that had CV events, which is not unexpected, as these are the traditional CV risk factors.

Thyroid disorders, both thyroid hormone excess or deficiency, are well known to have myriad effects on the CV system. These include heart failure, atrial and ventricular arrhythmias, and atherosclerosis.[14] There is growing evidence that suggests that even subclinical thyrotoxicosis or hypothyroidism could be associated with CV risk and arrhythmias.[14,15] Cardiovascular manifestations are the most severe demonstration of thyrotoxicosis.[16] There is a hyperdynamic state that consists of an increased resting heart rate, increased blood volume, and enhanced left ventricular contractility, but reduced systemic vascular resistance.[17,18] Reduced exercise tolerance is the most common manifestation, though in rare cases patients can have severe symptomatic congestive heart failure.[19,20] Previous studies have shown that about 6% of patients with thyrotoxicosis develop heart failure and that reduced ejection fraction occurs in about 1% of patients. In our study, about 8% of thyroid storm patients had acute heart failure. However, the type of heart failure, whether with or without reduced ejection fraction, could not be deciphered. Isolated right heart failure can also occur with thyrotoxicosis, which is usually a result of pulmonary hypertension.[18] However, both right and left heart failure can be reversed with the rapid treatment of thyrotoxicosis.[21,22] A small rise in troponin in thyroid storm may be due to tachycardia,[23] coronary artery spasm,[24] or Takotsubo cardiomyopathy[25,26] and not necessarily due to atherosclerotic coronary artery disease.

Sinus tachycardia is the most common abnormal rhythm, which is found in a majority of patients with hyperthyroidism.[27,28] Atrial fibrillation is the most commonly identified arrhythmia in patients with thyrotoxicosis, with a prevalence rate of 13.8% compared with 2.3% in euthyroid patients.[29,30] From the Danish registry data, it was found that male gender, congestive heart failure, ischemic and valvular heart disease were at highest risk for atrial fibrillation. However, in unselected patients with atrial fibrillation, the prevalence of overt hyperthyroidism was <1%.[5,31] In our study, atrial fibrillation was the commonly associated arrhythmia followed by nonspecific tachycardia. As sinus tachycardia is a rather benign finding, there is a good chance that several cases of sinus tachycardia might not have been coded into a patient's diagnoses list. Atrial flutter was the next most commonly found arrhythmia, followed by ectopy, including parosyxmal atria complexes (PACs) or parosyxmal ventricular arrhythmias (PVCs).

Thyrotoxicosis has traditionally been known to cause supraventricular arrhythmias, whereas hypothyroidism has been indicted in ventricular arrhythmias, albeit with lesser evidence to its support.[30] Ventricular arrhythmias tend to occur in patients with intrinsic cardiac disease and are rarely associated with isolated thyrotoxicosis.[12] There are a few isolated case reports where thyrotoxicosis was associated with ventricular fibrillation.[32–34] Of these, 2 case reports had negative cardiac work-up that ruled out any intrinsic cardiac disease.[33,34] In our study, ventricular tachycardia was the 5th most common arrhythmia after PACs/PVCs.

About 150 cardiac arrests were registered, but only 20 observations were ventricular fibrillation, which was also the least common arrhythmia seen in the database.

Limitations to the data include not having data to subclassify heart failure with or without preserved ejection fraction, and subclassification of arrhythmias was based on documented ICD-9 codes and could not be further stratified. ICD-9 codes were available but not ICD-10 codes. Due to the nature of the data used, it was not possible to decipher if the same patient had multiple hospitalizations, which could potentially skew the data. Exact levels of thyroid stimulating hormone (TSH), free T3, and free thyroxine T4 were not readily available, nor was any analysis of the Burch-Wartofsky scale in any patients analyzed in this data.