Author + information
- Received August 9, 2016
- Accepted August 11, 2016
- Published online December 12, 2016.
- Naddi Marah, MD∗ (, )
- Keisha Bryant, MD,
- Salman Haq, MD and
- Muhammad Khan, MD
- ↵∗Reprint requests and correspondence:
Dr. Naddi Marah, Department of Medicine, New York Methodist Hospital-Weill Cornell Medicine, 506 6th Street, Brooklyn, New York 11215.
- coronary vasospasm
- Graves’ disease
- thyroid peroxidase antibody
- thyroid-stimulating immunoglobulin
A 51-year-old woman presented to the emergency department with a 3-week history of intermittent palpitations, dyspnea, and substernal chest pain lasting 5 to 10 min with spontaneous resolution. She remained hemodynamically stable, and an electrocardiogram showed a 1.5-mm ST-segment elevation in lead V2 along with sinus tachycardia. Given the persistence of her symptoms, she underwent diagnostic angiography. Upon coronary vessel engagement with the coronary catheter, there was severe left main and right coronary ostial vasospasm, with dampening of the blood pressure tracings, both subsequently relieved with the administration of sublingual and intracoronary nitroglycerin (Figure 1).
Further investigation revealed an elevated serum-free thyroxine of 7.22 ng/dl (range: 0.76 to 1.46 ng/dl), suppressed thyroid-stimulating hormone of <0.005 μIU/ml (range: 0.36 to 3.74 μIU/ml), elevated thyroid peroxidase antibody titer of 87 IU/ml (normal value is <9 μIU/ml), and thyroid-stimulating immunoglobulin of 341 (normal value is <140 IU/ml), confirming the diagnosis of Graves’ disease. Although her clinical assessment, supported by a Burch-Wartofsky score of 20, indicated a low likelihood of thyrotoxicosis, she was started on methimazole and propanolol. Euthyroidism was restored thereafter, as well as symptomatic relief with the attenuation of her adrenergic drive.
Multiple hypothetical pathophysiological pathways have been proposed for the mechanism of thyroid hormone–induced coronary vasospasm. In a Korean study of 6,923 subjects undergoing coronary angiography for evaluation of chest pain, the incidence of coronary vasospasm was 5%, with 29% occurring in women under 50 years of age (1). During a thyrotoxic state, hypersensitivity to vasoconstrictive agents, decreased vasodilation, and general hypermetabolic state precipitates an imbalance between blood supply and oxygen demand (2). Controlling thyroid activity is in itself curative, obviating the need for unnecessary mechanical interventions and further antianginal therapy.
All authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received August 9, 2016.
- Accepted August 11, 2016.
- 2016 American College of Cardiology Foundation