scholarly journals Coronary spasm and thrombosis associated with myocardial infarction in a patient with nearly normal coronary arteries.

Circulation ◽  
1983 ◽  
Vol 67 (5) ◽  
pp. 1147-1150 ◽  
Author(s):  
A Benacerraf ◽  
J M Scholl ◽  
F Achard ◽  
M Tonnelier ◽  
G Lavergne
Angiology ◽  
2001 ◽  
Vol 52 (5) ◽  
pp. 299-304 ◽  
Author(s):  
Aung Tun ◽  
Ijaz A. Khan

Myocardial infarction with normal coronary arteries is a syndrome resulting from numerous conditions but the exact cause in a majority of the patients remains unknown. Cigarette smokers and cocaine users are more prone to develop this condition. The possible mechanisms causing myocardial infarction with normal coronary arteries are hypercoagulable states, coronary embolism, an imbalance between oxygen demand and supply, intense sympathetic stimulation, non-atherosclerotic coronary diseases, coronary trauma, coronary vasospasm, coronary thrombosis, and endothelial dysfunction. It primarily affects younger individuals, and the clinical presentation is similar to that of myocardial infarction with coronary atherosclerosis. Thrombolytics, aspirin, nitrates, and beta blockers should be instituted as a standard therapy for acute myocardial infarction. Once normal coronary arteries are identified on subsequent angiography, the calcium channel blockers could be added since coronary vasospasm appears to play a major role in the pathophysiology of this condition. The beta blockers should be avoided in cocaine-induced myocardial infarction because the coronary spasm may worsen. In myocardial infarction with normal coronary arteries, complications such as malignant arrhythmia, heart failure, and hypotension are generally less common, and prognosis is usually good. Recurrent infarction, postinfarction angina, heart failure, and sudden cardiac death are rare. Stress electrocardiography and imaging studies are not useful prognostic tests and long- term survival mainly depends on the residual left ventricular function, which is usually good.


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.


2021 ◽  
Vol 10 (Supplement_1) ◽  
Author(s):  
RA Montone ◽  
F Gurgoglione ◽  
MG Del Buono ◽  
MC Meucci ◽  
G Iannaccone ◽  
...  

Abstract Funding Acknowledgements Type of funding sources: None. Background Myocardial bridging (MB) is associated with endothelial dysfunction and may represent a cause of angina in patients with non-obstructive coronary artery disease (NOCAD). Purpose  Herein, we assessed the interplay between MB and coronary vasomotor disorders, evaluating also their prognostic relevance in patients with myocardial infarction and non-obstructive coronary arteries (MINOCA) or stable NOCAD. Methods We prospectively enrolled consecutive NOCAD patients undergoing intracoronary acetylcholine provocative test to assess the presence of epicardial or microvascular spasm in patients with suspected angina or MINOCA. Myocardial bridging was diagnosed by coronary angiography. The incidence of major adverse cardiac events (MACE), defined as the composite of cardiac death, non-fatal MI and rehospitalisation for unstable angina, was assessed at follow-up. We also assessed angina status using Seattle Angina Questionnaires (SAQ). Results We enrolled 310 patients (mean age 60.6 ± 11.9; 136 [43.9%] men; 169 [54.5%] stable NOCAD and 141 [45.5%] MINOCA). MB was found in 53 (17.1%) patients. MB was an independent predictor of spasm and MINOCA (p < 0.05). At follow-up (median 22 months, interquartile range [13-32]), patients with MB had a higher rate of MACE and a lower SAQ score (all p < 0.001) compared with patients without MB. The rate of MACE was considerably higher in patients with both spasm and MB than in the remaining patients (12/42 [28.6%] vs. 13/268 [4.8%], p < 0.001). Conclusion Among patients with NOCAD coronary spasm associated with MB predicts a worse clinical presentation with MINOCA and a worse clinical outcome at medium-long term follow-up, thus identifying a high-risk subset of patients with MB with relevant therapeutic implications. MB and clinical outcomesCharacteristicsOverall population(n= 310)Presence of Myocardial bridging(n= 53)Absence of Myocardial bridging(n = 257)p valueMACE [n, (%)]25 (8.1)12 (22.6)13 (5.1)<0.001CV Death [n, (%)]1 (0.3)0 (0.0)1 (0.4)0.649MI occurrence [n, (%)]6 (1.9)2 (3.8)4 (1.6)0.286Hospitalization for unstable angina [n, (%)]18 (5.8)10 (18.9)8 (3.1)< 0.001Recurrent angina [n, (%)]70 (22.6)20 (37.7)50 (19.4)0.004SAQ [median (IQR)]82 [78; 88]78 [68; 84]84 [78; 88]< 0.001Follow-up time [months, median (IQR)]22 [15;32]20 [15; 28]23 [15; 34]0.10CV Cardiovascular; MI: Myocardial Infarction; IQR: InterQuartile Range; MACE: Major Adverse Cardiovascular Event; SAQ: Seattle Angina Questionnaire.Abstract Figure Outcomes


1980 ◽  
Vol 99 (4) ◽  
pp. 506-509 ◽  
Author(s):  
Edward H. Schuster ◽  
Stephen C. Achuff ◽  
William R. Bell ◽  
Bernadine H. Bulkley

Angiology ◽  
2001 ◽  
Vol 52 (11) ◽  
pp. 785-788 ◽  
Author(s):  
Bruno Laganà ◽  
Luigi Baratta ◽  
Luigi Tubani ◽  
Vincenzina Golluscio ◽  
Massimo Delfino ◽  
...  

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