Angina in thyrotoxicosis. Thyroid-related coronary artery spasm

University of Washington Seattle, Seattle, Washington, United States
Archives of Internal Medicine (Impact Factor: 17.33). 04/1983; 143(3):554-5. DOI: 10.1001/archinte.1983.00350030168028
Source: PubMed


Ischemic heart disease is a common complication of thyrotoxicosis, although the exact mechanism has not been defined. A case is reported of angina and thyrotoxicosis in which the angina was reproduced by coronary artery spasm induced by ergonovine maleate, relieved by thyroid ablation, and reactivated by postablative thyroid replacement. Coronary arteriography did not show significant stenoses prior to ergonovine injection. Possible mechanisms of coronary artery spasm in thyrotoxicosis are briefly discussed. Hyperthyroidism should be considered as a cause of angina in any patient with rest pain and normal coronary arteries.

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    • "Atrial fibrillation may further compromise left ventricular filling because of loss of the atrial contribution and a rapid ventricular response rate. In addition, increased myocardial oxygen demand may ensue myocardial ischemia, particularly in the presence of coronary artery disease or spasm, and may contribute to the occurrence of heart failure.5 Adverse cardiovascular effects of hyperthyroidism are well documented in literature.6–8 "
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    ABSTRACT: The objective of this report is to present a case of Graves' thyrotoxicosis-induced cardiomyopathy. This is a case of a 26 year old woman that presented with severe symptomatic congestive heart failure and was subsequently diagnosed with dilated cardiomyopathy secondary to Graves' disease. Despite an initial left ventricular systolic ejection fraction of 20% on echocardiography, treatment with anti-thyroid agents led to rapid improvement of her clinical status and normalization of her ejection fraction. The proposed mechanisms underlying the development of systolic dysfunction in thyrotoxicosis are discussed and the literature on similar cases previously reported is highlighted. Cardiomyopathy should be considered even in young patients with Graves' thyrotoxicosis.
    Clinical Medicine Insights: Case Reports 03/2013; 6:47-50. DOI:10.4137/CCRep.S10534
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    • "Es besteht die Gefahr, dass durch das Vorhofflimmern der atriale Beitrag zur ventrikulären Füllung fehlt und dadurch die linke Kammer ein geringeres Auswurfvolumen kompensieren muss [85]. Falls die erhöhte myokardiale Sauerstoffanforderung wegen der erhöhten zu erbringenden Leistung nicht durch eine Vasodilatation der Koronararterien gewährleistet werden kann, kann eine myokardiale Ischämie die Folge sein, vor allem, wenn eine koronare Herzkrankheit oder Koronarspasmen bestehen, was wiederum zum Herzversagen führen kann [23]. Folgen des Vorhofflimmerns können eine Kardiomyopathie, cerebrovaskuläre Erkrankungen oder Synkopen sein [31]. "
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    ABSTRACT: Zur Erhärtung der Bedeutung der latenten Hyperthyreose für das Auslösen von Vorhofflimmern wurden im Rahmen einer aus zwei Fall-Kontrollstudien kombinierten Analyse 295 Patienten mit Vorhofflimmern einer Kontrollgruppe mit 611 Patienten mit einem Sinusrhythmus gegenübergestellt. Der Schilddrüsenfunktionszustand beider Gruppen wurde beleuchtet. Bei 4,41 % der Patienten mit der Erstdiagnose eines Vorhofflimmerns und bei 1,84% der Patienten ohne Vorhofflimmern fand sich ein supprimiertes Serum-TSH bei normalen peripheren Schilddrüsenhormonen (Odds Ratio: 2,8). Patienten mit einer subklinischen Hyperthyreose (TSH-Werten <0,1 mU/l) hatten eine 2,8-fach höhere Wahrscheinlichkeit für Vorhofflimmern als Patienten mit einer normalen Schilddrüsenfunktion und sonst vergleichbarem Risikoprofil. Die Ergebnisse zeigen, dass eine subklinische Hyperthyreose ein von anderen Risikofaktoren unabhängiger und klinisch relevanter Risikofaktor für Vorhofflimmern darstellt.
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    ABSTRACT: The importance of cardiovascular system involvement in hyperthyroidism has been recognized for many years. In the middle-aged and elderly patient, often with mild but prolonged elevation of plasma thyroid hormones, symptoms and signs of heart failure and complicating atrial fibrillation may dominate the clinical picture and mask the more classical endocrine manifestations of the disease. Pitfalls in diagnosis and the importance of early recognition and treatment are discussed. Despite experimental evidence for a short-term inotropic action of thyroid hormone excess, clinical data support the existence of a reversible cardiomyopathy in hyperthyroidism with impaired contractile reserve. Enhanced myocardial performance at rest primarily reflects the peripheral actions of thyroid hormone excess. Most, if not all, of the cardiac abnormalities return to normal once a euthyroid state has been achieved, although atrial fibrillation may persist in a minority. Optimum treatment requires rapid and definitive antithyroid therapy, usually using a large dose of radio-iodine, and rapid control of heart failure. Systemic anticoagulation is indicated in the presence of atrial fibrillation and should be continued until sinus rhythm has been present for at least three months, either spontaneously or after cardioversion.
    Clinics in Endocrinology and Metabolism 06/1985; 14(2):491-508. DOI:10.1016/S0300-595X(85)80044-X
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