Management of Hypothyroidism in Patients with Acute Myocardial Infarction

Abstract

Background and Objectives: Thyroid hormones (TH) affect cardiac function through effects on cardiac contractility and systemic vascular resistance. While TH replacement for patients with hypothyroidism might be necessary for restoration of cardiac output after an acute myocardial infarction (AMI), it could theoretically lead to excessively rapid restoration of the metabolic rate. The appropriate management of hypothyroidism in patients with AMI is unknown. We describe the practice patterns in the management of hypothyroidism in the setting of AMI as well as patients’ clinical outcomes. Material and Methods: Retrospective study of patients that were admitted to a tertiary care hospital with AMI and newly diagnosed or uncontrolled hypothyroidism (TSH ≥ 10 mIU/L) between 2011–2018. Eligible patients were identified using diagnosis codes for AMI and laboratory values, followed by medical record review. We categorized patients according to treatment status with TH and by degree of hypothyroidism. Clinical outcomes included: 30-day mortality/readmission, bleeding, stroke, arrhythmia, sudden cardiac death, and new or worsening heart failure. Summary statistics and group comparisons are presented. Results: Sixty-four patients were included, their median age was 64 years and 61% (n = 39) were women. Most of the patients (59%) had a documented history of hypothyroidism. Of these, all were restarted on levothyroxine (LT4) during the index admission when compared to patients without a history of hypothyroidism, of which 54% received LT4 treatment (p = 0.001). The median TSH in those treated with LT4 was higher (25 mIU/L) when compared to those who were not (12 mIU/L), (p = 0.007). Patients who received intravenous LT4 had higher TSH levels and other variables suggesting worse clinical presentation, but these differences were not statistically significant. No statistically significant differences were noted on clinical outcomes according to LT4 treatment status. Conclusion: A history of hypothyroidism and the degree of TSH elevation seem to guide the management of hypothyroidism in patients with AMI. The clinical effect of correcting hypothyroidism in this setting requires further evaluation.

A Delayed Diagnosis of Myxedema Coma

“…Furthermore, treatment with thyroxine (T4) may be less effective due to impaired conversion of T4 into triiodothyronine (T3), which commonly occurs during severe illness and inadequate caloric intake [ 9 ]. Hypothyroidism generally has harmful effects on the cardiovascular system, including increased systemic vascular resistance, while cardiac output, heart rate, and myocardial contractility are decreased [ 6 ].…”

“…The treatment of myxedema coma involves supportive care with fluids, vasopressors, ventilation if necessary, passive warming, and glucocorticoids for potential concurrent adrenal insufficiency, followed by thyroid hormone replacement. Thyroid hormone replacement starts IV with 200-400 mcg daily for three to five days, followed by a daily oral dose based upon typical dosing of 1.6 mcg/kg (the IV dose is 75% of the oral dose) [3,[5][6][7][8].…”

“…Steroids are usually given as 100 mg IV hydrocortisone every eight hours until serum cortisol results are obtained and may be discontinued if random cortisol is greater than 18 mg/dL [3,[5][6][7][8].…”

“…Finally, even when successfully identified, special considerations must be made regarding treatment when the inciting event is cardiac in nature or the patient has a significant cardiac history, as thyroid hormones affect cardiac contractility and systemic vascular resistance. Particularly after myocardial infarction, IV levothyroxine can potentially cause the rapid restoration of metabolic homeostasis, increasing the strain on cardiac function and the risk of arrhythmias and further myocardial damage [ 6 ].…”

Cardiovascular and Neuronal Consequences of Thyroid Hormones Alterations in the Ischemic Stroke

“…Multiple studies have highlighted the correlation between the circulating T3 levels and the recovery ability of the ventricular function, indicating T3 as a significant predictor of myocardial ischemia outcome [ 132 , 133 , 134 , 135 ]. Accordingly, patients with elevated systemic rT3 or low T3 have been reported more prone to short and long-term mortality, unsuccessful cardiac rehabilitation and rising blood levels of indicators for acute cardiac distress, such as troponin T and N-terminal pro-brain natriuretic peptide [ 118 , 122 , 136 ]. Moreover, an inverse correlation exists between the reduction of serum T3 levels and the severity of the cardiac disease [ 137 ].…”