scholarly journals Kounis Syndrome, a Case of Vancomycin Associated Coronary Artery Vasospasm Resulting in Myocardial Infarction

CJC Open ◽  
2021 ◽  
Author(s):  
Luke R. Gagnon ◽  
Yiming Huang ◽  
Robert Kay ◽  
Bibiana Cujec
2019 ◽  
Vol 72 (1) ◽  
pp. 137-141
Author(s):  
Olga Wajtryt ◽  
Tadeusz M Zielonka ◽  
Aleksandra Kaszyńska ◽  
Andrzej Falkowski ◽  
Katarzyna Życińska

Kounis syndrome or allergic myocardial infarction is an acute coronary syndrome in the course of an allergic reaction. In allergic patients in response to a specific condition - nourishment, inhalation, environmental substances, drug or insect bite there is an allergic reaction involving many different cells and mediators that can cause coronary artery spasm or initiate the process of rupture and activation of atherosclerotic plaque resulting in acute coronary syndrome. The paper describes a case of a young man with allergy to pollen and confirmed sensitization to nuts, who developed a full-blown anaphylactic shock after eating the nut mix and experienced a rapidly passing acute coronary syndrome with troponin up to 4.7 μg/L. An increased concentration of tryptase (15 μg/L), total IgE (> 3,000 IU/mL) and specific anti-nut IgE (55.1 kUA/L) were found. Based on the course of the disease and the results of allergic and cardiac tests, allergic type 1 myocardial infarction, i.e. caused by coronary artery spasm, was diagnosed. During the hospitalization, the patient’s condition improved quickly and after a few days he left the hospital without the signs of permanent damage to the heart muscle.


2018 ◽  
Vol 6 (5) ◽  
Author(s):  
Angelo Alencar Mello Savoldi ◽  
Alexandre Mello Savoldi ◽  
Gustavo Alexandre Dutra ◽  
Shirley Katherine Tinajero Enriquez ◽  
Gregue Marques Leite Costa

2018 ◽  
Vol 2018 ◽  
pp. 1-5
Author(s):  
Serena Sert Kim Khoo ◽  
Chong Mow Chu ◽  
Yin Khet Fung

Severe thyrotoxicosis can present with a myriad of cardiovascular complications. It may be mild features such as palpitations, tachycardia, and exertional dyspnea or may progress to life-threatening consequences such as atrial fibrillation, tachyarrhythmias, heart failure, myocardial infarction, and shock. In rare cases, they may present with myocardial ischemia secondary to coronary artery vasospasm. We report a case of a 59-year-old Malay gentleman who presented with fast atrial fibrillation and tachycardia-mediated heart failure that evolved to a silent myocardial infarction secondary to severe coronary artery vasospasm with undiagnosed severe thyrotoxicosis. He had complete resolution of heart failure and no further recurrence of coronary artery vasospasm once treatment for thyrotoxicosis was initiated and euthyroidism achieved. This life-threatening consequence has an excellent prognosis if recognised early and treated promptly.


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.


2018 ◽  
Vol 7 (1) ◽  
Author(s):  
Ankita Kulkarni ◽  
Hannah Anastasio ◽  
Alexandra Ward ◽  
Janelle Santos ◽  
Pamela Parker ◽  
...  

Abstract Background Acute myocardial infarction (AMI) in pregnancy is a rare event and of the causes, coronary artery vasospasm (CAV) is considered even more uncommon. Purpose We present a new case report of a woman at 32 weeks of pregnancy with an AMI from CAV with a normal coronary angiogram. We performed a systematic review of similar cases of spontaneous AMI related to CAV to better understand its characteristics and management. AMI was defined as elevated cardiac enzymes (troponin or CKMB) with chest pain and/or electrocardiogram (EKG) changes consistent with ischemia. Methods We use the terms “acute myocardial infarction”, “myocardial infarction”, “coronary artery vasospasm” and “pregnancy” for our PubMed review. We also evaluated all references in identified manuscripts. Six cases of AMI in pregnancy due to CAV have been reported as of November 2016, including ours. Results and conclusion Six cases of AMI due to CAV during pregnancy or postpartum are reported in the literature, including ours. Patients experiencing this condition tend to be of advanced maternal age, multigravida and in their third trimester or postpartum. Successful management with a combination of long acting nitrates and/or calcium channel blockers achieved symptomatic control in all published cases. Obstetric outcomes were mostly normal, with the majority experiencing uncomplicated deliveries at term.


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