Thyroid dysfunction is a known cause of cardiovascular disturbance, both as a precipitant of cardiovascular pathology and a mimic of underlying heart disease. These can mostly be categorized under 3 headings: arrhythmias, heart failure (HF), and vascular dysfunction. New research has unearthed the mechanistic links of the thyro-cardiac axis to the pathophysiology of cardiac electrophysiology, myocardial function, and vascular biology. Hypothyroidism, both overt and subclinical, is associated with bradycardia and pacemaker disturbance, diastolic hypertension, dyslipidemia, and accelerated atherosclerosis. Hyperthyroidism, on the other hand, causes atrial fibrillation and hypercoagulable states, worsening the stroke risk of these patients. Thyroid hormone excess and deficiency can both exacerbate HF in different ways. Thyrotoxicosis induces high-output HF and tachyarrhythmias, whereas hypothyroidism promotes a low-output, HF with preserved ejection fraction phenotype with impaired relaxation. In this article, we have discussed the mechanisms, management, and incidence of these conditions as well as the current scope of research in these fields. We aim to inform future endocrinologists, cardiologists, and primary care physicians about the factors to keep in mind when confronted by these patients and the risk factors to consider to prevent worsening morbidity.
Tannous et al. (Mon,) studied this question.