Acute myocardial infarction with normal coronary arteries: Role of coronary artery spasm and arrhythmic complications

2007 ◽  
Vol 117 (1) ◽  
pp. 3-5 ◽  
Author(s):  
Enrico Romagnoli ◽  
Gaetano Antonio Lanza
2010 ◽  
Vol 2010 ◽  
pp. 1-4
Author(s):  
J. Gosai ◽  
C. J. Malkin ◽  
E. D. Grech

A 62-year-old lady was admitted with clinical and electrocardiograph features of acute myocardial infarction. Urgent coronary arteriography was performed, demonstrating a single discrete stenosis of one coronary artery. Following intracoronary injection of GTN, this stenosis completely resolved, as the symptoms did. The causes of acute myocardial infarction with normal coronary arteries are reviewed.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Basma Ataallah ◽  
Barjinder Buttar ◽  
Georgia Kulina ◽  
Alan Kaell

Abstract Background: Coronary artery vasospasm-induced myocardial infarction is a rare cardiac complication of untreated thyrotoxicosis. Diagnosis is difficult due to the transient and unpredictable occurrence of coronary spasm [1]. Clinical Case: A 47-year-old Hispanic female smoker presented with a one-week history of severe, intermittent substernal chest pain radiating to the left arm. The pain was associated with palpitations and shortness of breath. She was afebrile with a heart rate of 100, a blood pressure of 119/59, a fine tremor, and brisk reflexes. No lid lag or proptosis was appreciated. The thyroid was enlarged, non-tender, without palpable nodules. ECG showed T- Wave Inversions in leads V1-V2 and ST depressions in V4-V5. Chest pain was relieved by SL nitroglycerin. Lab results showed a peak Troponin of 0.20 (N < 0.06), TSH 0.01 mU/L (N > 0.45mU/L), free T4 5.54 (N < 1.46 ng/dl), total T3 4.50 pg/mL (N < 1.37 ng/mL), free T3 21.0 ng/mL (N < 4.4 pg/ml), TSI 3.61 IU/L (N < 0.55 IU/L), thyrotropin R Ab 7.47 IU/L (N < 1.75 IU/L) and thyroglobulin Ab 1.3 IU/ml (ULN < 0.9 IU/ml). Thyroid US showed a heterogeneous enlarged thyroid gland with increased vascularity. For her NSTEMI she was treated with a heparin drip, aspirin, clopidogrel, atorvastatin, propranolol, and isosorbide mononitrate. Methimazole was started to treat thyrotoxicosis. Cardiac catheterization revealed coronary vasospasm without evidence of valvular or coronary artery disease. Methimazole restored euthyroidism and she has not had recurrence of angina. Discussion: Rarely, hyperthyroidism can present with transient myocardial ischemia secondary to coronary artery vasospasm in patients with normal coronary arteries. The etiopathogenesis is unclear and may relate to a direct metabolic effect of excess thyroid hormone on the myocardium. In a Korean study evaluating chest pain in patients who underwent coronary angiography, the incidence of coronary vasospasm was 5%, occurring most frequently in women under 50 years of age with thyrotoxicosis [2]. Conclusion: Patients who present with angina and are thyrotoxic should be evaluated for vasospasm. Females under 50 years old with Graves’ disease are at highest risk. Treatment includes antithyroid medications along with nitroglycerin, and we can consider calcium channel blockers including diltiazem. Treatment of thyrotoxicosis eliminates recurrence of vasospasm [3]. References 1. Chudleigh RA, Davies JS: Grave’s thyrotoxicosis and coronary artery spasm. Postgrad Med J. 2007, 83(985):e1-e2. 2. Zheng W, Zhang YJ, Li SY, et al: Painless thyroiditis-induced acute myocardial infarction with normal coronary arteries. Am J Emerg Med. 2015, 33:5-10. 3. Marah N, Bryant K, Haq S, Khan M: Graves’ disease-induced coronary vasospasm. JACC: Cardiovascular Interventions. 2016, 9(23):2452-2453.


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