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Year : 2016  |  Volume : 13  |  Issue : 2  |  Page : 89-91

Diffuse coronary vasospasm in a patient with hypothyroidism

1 Department of Cardiology, Dr. Siyami Ersek Thoracic and Cardiovascular Surgery Center, Training and Research Hospital, Istanbul, Turkey
2 Department of Internal Medicine, Rize Findikli Guatr Research Center, Rize, Turkey
3 Department of Cardiology, Trabzon Vakfıkebir State Hospital, Trabzon, Turkey

Date of Web Publication1-Jun-2016

Correspondence Address:
Dr. Altug Osken
Dr. Siyami Ersek Thoracic and Cardiovascular Surgery Center, Cardiology Clinic, Tibbiye Cad., No. 13, Haydarpasa, Istanbul
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0973-0354.183274

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Coronary vasospasm is an important etiology of ischemic heart disease. Sometimes thyroid disorders may be associated with cardiovascular disease. The major cardiovascular changes that occur in hypothyroidism include a decrease in cardiac output and cardiac contractility, a reduction in heart rate, and an increase in peripheral vascular resistance. There are also significant changes in modifiable atherosclerotic risk factors, including hypercholesterolemia, diastolic hypertension, carotid intimal media thickness, and endothelial derived relaxation factor (nitric oxide), which accompany overt hypothyroidism. Here, we present a case of diffuse coronary arterial vasospasm in a patient with hypothyroidism.

Keywords: Coronary vasospasm, hypothyroidism, thyroid disorders

How to cite this article:
Osken A, Yaylaci S, Aydin E, Kemaloglu Oz T, Ipek G, Atasoy I, Zehir R, Dayi SU. Diffuse coronary vasospasm in a patient with hypothyroidism. Thyroid Res Pract 2016;13:89-91

How to cite this URL:
Osken A, Yaylaci S, Aydin E, Kemaloglu Oz T, Ipek G, Atasoy I, Zehir R, Dayi SU. Diffuse coronary vasospasm in a patient with hypothyroidism. Thyroid Res Pract [serial online] 2016 [cited 2022 Dec 5];13:89-91. Available from: https://www.thetrp.net/text.asp?2016/13/2/89/183274

  Introduction Top

Coronary artery vasospasm or smooth muscle constriction of the coronary artery is an important cause of chest pain syndromes that can lead to myocardial infarction, ventricular arrhythmias, and sudden death. It also plays a key role in the development of atherosclerotic lesions. In many cases, coronary artery vasospasm can occur spontaneously without an identifiable cause.[1] Known triggers of spasm in susceptible patients include hyperventilation, cocaine or tobacco use, and administration of provocative agents such as acetylcholine, ergonovine, histamine, or serotonin.[2]

Nitric oxide (NO) is a cellular signaling molecule, which has many important roles in the body. NO deficiency is believed to play an important role in the development of coronary artery vasospasm.[3] In addition, available data existed on NO levels can be influenced on thyroid disorders; therefore, it can be a factor for those people with autoimmune thyroid conditions. In this respect, our case is the first indicating hypothyroidism with coronary vasospasm.

  Case Report Top

A 54-year-old female patient was admitted to the cardiology clinic with complaints of resting substernal chest pain radiating to the left arm and progressive exertional dyspnea for the last 6 months. On her history, she had hypertension for 4 years and was on the treatment of valsartan + hydrochlorothiazide. Therefore, she was on the follow-up of endocrinology clinic because of thyroid nodules and she was using l-thyroxine 50 µg/day.

On physical examination, heart rate was 60/min, arterial blood pressure was 136/74 mmHg, and respiratory rate was 18/min. Cardiovascular examination revealed apical 2/6 holosystolic murmur on auscultation and thyroid examination revealed approximately 1 cm regular palpable nodules. In laboratory investigations, thyroid stimulating hormone level was 1:23 µl/ml (0.55–4.78) and FT4 level was 0.99 mg/dL (0.74–2), she was on euthyroid state. Blood glucose, lipid profile, hepatobiliary-kidney function tests, and complete blood count values were within normal limits. 1 cm × 1.5 cm hypodense nodule on the left lobe of the thyroid watched at ultrasound examination. Normal left ventricular systolic and diastolic function and mild mitral regurgitation were detected on echocardiography and also 1 mm ST-segment depression in the inferolateral leads was detected on electrocardiogram monitoring. Therefore, stress myocardial perfusion scintigraphy was performed and revealed mild ischemia on the apical and mid-ventricular anteroseptal wall sections. Coronary angiographic examination was decided. Left coronary system were within normal limits, but 70% narrowing on the proximal right coronary artery was observed and thought to be connected to the catheter-induced vasospasm, so 100 µg intracoronary nitrate was administered to the patient. The lesions regressed completely in control angiography, diffuse increase in vessel diameter was observed. After discharge, diltiazem 30 mg 3 × 1 and 1 × 1 50 mg isosorbide mononitrate was added to the treatment.

  Discussion Top

Coronary arterial vasospasm is usually caused by focal spasm (of the smooth muscle layer of the arterial wall) of a major coronary artery resulting in a high-grade obstruction. Spasm occurs in the absence of any preceding increase in myocardial oxygen demand (e.g., exercise) and in normal or diseased vessels. It is usually focal in its anatomic distribution, although spasm in more than one site and diffuse spasm have been described.[1],[2],[3]

NO is a cellular signaling molecule which has many important roles in the body. Not only it is important for maintaining normal blood pressure, but also it is important for neurotransmission, the health of the mitochondria, it plays a role in platelet function, and it can modulate the immune system, which, therefore, can be a factor for those people with autoimmune thyroid conditions. There are three different forms of NO: Neuronal NO synthase (nNOS), endothelial NOS (eNOS), and inducible NOS (iNOS). eNOS is found in the lining of the blood vessels and it has numerous biological properties which help to maintain vascular homeostasis, including modulating the tone of the blood vessels, supporting blood flow, and it protects the vessel from injury. Thus, NO deficiency is believed to play an important role in the development of coronary artery vasospasm. This may also explain the correlation between coronary artery vasospasm and increased intimal thickening: NO deficiency results in enhanced activity of potent vasoconstrictors and stimulators of vascular smooth muscle proliferation, such as angiotensin II and endothelin.[4]

Hypothyroidism is characterized by a decrease in oxygen and substrate utilization by all the major organ systems of the body. As a result, the demands for cardiac output decrease; in addition, hypothyroidism directly alters cardiac function through changes in myocyte-specific gene expression. Hypothyroidism predominantly causes exertional dyspnea, exercise intolerance, bradycardia, hypertension resulting from the increase in vascular resistance and the fall in endothelial-derived relaxing factor, cardiac dysfunction with poor contractility, dilatation or pericardial effusion, and often nonpitting edema. The occurrence of anginal-like pain in some hypothyroid patients and the frequent occurrence of hypercholesterolemia, diastolic hypertension, and elevated homocysteine levels have led to suggestions that hypothyroidism is associated with accelerated coronary artery disease.[5] Numerous publications were available in literature about thyroid function disorders. They may be predisposing factors for atherosclerosis related to cardiovascular disease. Our case is the first in literature in terms of showing the coronary vasospasm associated with hypothyroidism.

It is important to understand that thyroid hormones can affect the formation of NO. With regards to the immune system, NO plays a role in eradicating pathogens and it also influences the Th1/Th2 balance, which relates to autoimmunity. If NO is too high or too low, then this not only can decrease the body's ability to eradicate pathogens, but also it can shift someone to a Th1 or Th2 dominant state, which in turn can increase the risk of developing an autoimmune condition such as Graves' disease or Hashimoto's thyroiditis. Most people with autoimmune thyroid conditions have higher levels of iNOS, which is pro-inflammatory, and therefore they need to decrease the levels of iNOS while increasing the levels of nNOs and eNOS.

We believe that the changes in NO metabolism depending on the patient's thyroid dysfunction may have caused the coronary vasospasm.

  Conclusion Top

Especially in young female patients, coronary vasospasm is an entity which may degrade the quality of life and cause symptoms. In these patients, there is no net benefit in coronary invasive procedures, detailed examination should be made to avoid incorrect diagnosis and unnecessary interventions, thus appropriate medical treatment choices should be initiated to the patients.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Yasue H, Nakagawa H, Itoh T, Harada E, Mizuno Y. Coronary artery spasm – Clinical features, diagnosis, pathogenesis, and treatment. J Cardiol 2008;51:2-17.  Back to cited text no. 1
Ajani AE, Yan BP. The mystery of coronary artery spasm. Heart Lung Circ 2007;16:10-5.  Back to cited text no. 2
Okumura K, Yasue H, Matsuyama K, Ogawa H, Kugiyama K, Ishizaka H, et al. Diffuse disorder of coronary artery vasomotility in patients with coronary spastic angina. Hyperreactivity to the constrictor effects of acetylcholine and the dilator effects of nitroglycerin. J Am Coll Cardiol 1996;27:45-52.  Back to cited text no. 3
Kaneda H, Taguchi J, Kuwada Y, Hangaishi M, Aizawa T, Yamakado M, et al. Coronary artery spasm and the polymorphisms of the endothelial nitric oxide synthase gene. Circ J 2006;70:409-13.  Back to cited text no. 4
Klein I, Danzi S. Thyroid disease and the heart. Circulation 2007;116:1725-35.  Back to cited text no. 5


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