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Acute myocardial infarction and subclinical hyperthyroidism without significant coronary stenoses
International Journal of Cardiology 134 (2009) e135 – e137 www.elsevier.com/locate/ijcard
Letter to the Editor
Acute myocardial infarction and subclinical hyperthyroidism without significant coronary stenoses Salvatore Patanè a,⁎, Filippo Marte a , Gianluca Di Bella b , Giuseppe Turiano c a
Cardiologia Nuovo Presidio Ospedaliero Cutroni Zodda-Barcellona P.d.G (Me), AUSL5 Messina, Italy Clinical and Experimental Department of Medicine and Pharmacology, University of Messina, Italy c Endocrinologia Azienda Ospedale Piemonte — Messina, Italy
b
Received 1 December 2007; accepted 1 March 2008 Available online 24 June 2008
Abstract Subclinical hyperthyroidism is an increasingly recognized entity that is defined as a normal serum free thyroxine and free triiodothyronine levels with a thyroid-stimulating hormone level suppressed below the normal range and usually undetectable. It has been reported that subclinical hyperthyroidism is not associated with CHD or mortality from cardiovascular causes but increased factor X activity in patients with subclinical hyperthyroidism represents a potential hypercoagulable state. It has been also reported an acute myocardial infarction with normal coronary arteries associated with iatrogenic hyperthyroidism and with a myocardial bridge too. Moreover, it has been reported that simply measuring maximum P wave duration and P wave dispersion values, may help to determine the patients with subclinical hyperthyroidism and high risk for the development of atrial fibrillation. We present a case of an acute myocardial infarction without significant coronary stenoses associated with subclinical hyperthyroidism. Also this case focuses attention on the importance of a correct evaluation of subclinical hyperthyroidism. © 2008 Elsevier Ireland Ltd. All rights reserved. Keywords: Acute myocardial infarction; Normal coronary arteries; Subclinical hyperthyroidism
1. Case report Subclinical hyperthyroidism is an increasingly recognized entity that is defined as a normal serum free thyroxine and free triiodothyronine levels with a thyroid-stimulating hormone level suppressed below the normal range and usually undetectable [1]. It has been reported that subclinical hyperthyroidism is not associated with CHD or mortality from cardiovascular causes [2] but increased factor × activity in patients with subclinical hyperthyroidism represents a potential hypercoagulable state [3]. It has been also reported an acute myocardial infarction with normal coronary arteries
⁎ Corresponding author. Cardiologia Nuovo Presidio Ospedaliero Cutroni Zodda-Barcellona P.d.G(Me) AUSL5 Messina, Via Cattafi 98051 Barcellona Pozzo di Gotto, Messina, Italy. E-mail address: [email protected] (S. Patanè). 0167-5273/$ - see front matter © 2008 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2008.03.011
associated with iatrogenic hyperthyroidism [4] and with a myocardial bridge too [5]. Moreover, it has been reported that simply measuring maximum P wave duration and P wave dispersion values, may help to determine the patients with subclinical hyperthyroidism and high risk for the development of atrial fibrillation [6]. We present a case of an acute myocardial infarction without significant coronary stenoses associated with subclinical hyperthyroidism. Also this case focuses attention on the importance of a correct evaluation of subclinical hyperthyroidism. On September 19th, 2007, a 67-year-old Italian woman was admitted to the emergency department. A history of chest pain was present. A history of paroxysmal supraventricular tachycardia and a history of current smoke were present. No current treatment for a history of a known subclinical hyperthyroidism was reported. Blood pressure values were 120/80 mmHg, the heart rate was 75 b/min, the oxygen saturation was normal. The ECG was performed (Fig. 1, Panel A). Troponin I was
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S. Patanè et al. / International Journal of Cardiology 134 (2009) e135–e137
Fig. 1. Panel A : ECG in the emergency department. Panel B : ECG with atrial fibrillation.
positive and the patient was admitted to the Cardiology Unit. Echocardiographic evaluation revealed a mild left atrial dilatation, a mild mitral regurgitation, a mild tricuspid regurgitation, a mild-moderate aortic regurgitation, a mild interventricular septal hypertrophy, an akinesia of the whole middle-apical portion of the interventricular septum, a medial segment akinesia of lateral wall with a medial segment hypokinesia of inferior wall. A pulmonary artery systolic pressure of 50 mmHg and an ejection fraction of 50% were observed. No pericardial effusion was observed. Initially the patient was treated with aspirin (1000 mg), intravenous heparin (bolus of 5000 IU and 1000 IU/h as a maintenance), nitroglycerin (5 mcg/kg/min), tirofiban, clopidogrel, bisoprolol. A new-onset of atrial fibrillation (Fig. 1, Panel B) and its pharmacological conversion to sinus rhythm were also observed. Over the following days the patient felt better and
ECG alterations evolved towards T-wave inversion in V2– V3–V4–V5–V6 (Fig. 2). Thyroglobulin autoantibodies were 190.78 U/ml (normal value 0–4.11), antithyroid peroxidase antibodies were 10.59 U/ml (normal value 0–5.61), thyroid– stimulating hormone was 0.009 μU/ml (normal value 0.350– 4.940), free triiodothyronine was 3.04 pg/ml (normal value 1.71–3.71), free thyroxine was 1.40 ng/dl (normal value 0.71–1.85) TropI peak was 2.80 ng/ml. In the cath-lab for coronary angiography no significant coronary stenoses were observed. References [1] Shrier DK, Burman KD. Subclinical hyperthyroidism: controversies in management. Am Fam Phys Feb 1 2002;65(3):431–8. [2] Singh S, Duggal J, Molnar J, Maldonado F, Barsano CP, Arora R. Impact of subclinical thyroid disorders on coronary heart disease,
S. Patanè et al. / International Journal of Cardiology 134 (2009) e135–e137
e137
Fig. 2. ECG without atrial fibrillation and with T-wave inversion in V2–V3–V4–V5–V6.
cardiovascular and all-cause mortality: a meta-analysis. Int J Cardiol 2008;125:41–8. [3] Erem C. Blood coagulation, fibrinolytic activity and lipid profile in subclinical thyroid disease: subclinical hyperthyroidism increases plasma factor X activity. Clin Endocrinol (Oxf) Mar 2006;64(3):323–9. [4] Gowda RM, Khan IA, Soodini G, Vasavada BC, Sacchi TJ. Acute myocardial infarction with normal coronary arteries associated with iatrogenic hyperthyroidism. Int J Cardiol Aug 2003;90(2–3):327–9.
[5] Patanè S, Marte F, Patanè F, et al. Acute myocardial infarction in a young patient with myocardial bridge and elevated levels of free triiodothyronine. Int J Cardiol 2009;132:140–2. [6] Aras D, Maden O, Ozdemir O, et al. Simple electrocardiographic markers for the prediction of paroxysmal atrial fibrillation in hyperthyroidism. Int J Cardiol Mar 10 2005;99(1):59–64.
Letter to the Editor
Acute myocardial infarction and subclinical hyperthyroidism without significant coronary stenoses Salvatore Patanè a,⁎, Filippo Marte a , Gianluca Di Bella b , Giuseppe Turiano c a
Cardiologia Nuovo Presidio Ospedaliero Cutroni Zodda-Barcellona P.d.G (Me), AUSL5 Messina, Italy Clinical and Experimental Department of Medicine and Pharmacology, University of Messina, Italy c Endocrinologia Azienda Ospedale Piemonte — Messina, Italy
b
Received 1 December 2007; accepted 1 March 2008 Available online 24 June 2008
Abstract Subclinical hyperthyroidism is an increasingly recognized entity that is defined as a normal serum free thyroxine and free triiodothyronine levels with a thyroid-stimulating hormone level suppressed below the normal range and usually undetectable. It has been reported that subclinical hyperthyroidism is not associated with CHD or mortality from cardiovascular causes but increased factor X activity in patients with subclinical hyperthyroidism represents a potential hypercoagulable state. It has been also reported an acute myocardial infarction with normal coronary arteries associated with iatrogenic hyperthyroidism and with a myocardial bridge too. Moreover, it has been reported that simply measuring maximum P wave duration and P wave dispersion values, may help to determine the patients with subclinical hyperthyroidism and high risk for the development of atrial fibrillation. We present a case of an acute myocardial infarction without significant coronary stenoses associated with subclinical hyperthyroidism. Also this case focuses attention on the importance of a correct evaluation of subclinical hyperthyroidism. © 2008 Elsevier Ireland Ltd. All rights reserved. Keywords: Acute myocardial infarction; Normal coronary arteries; Subclinical hyperthyroidism
1. Case report Subclinical hyperthyroidism is an increasingly recognized entity that is defined as a normal serum free thyroxine and free triiodothyronine levels with a thyroid-stimulating hormone level suppressed below the normal range and usually undetectable [1]. It has been reported that subclinical hyperthyroidism is not associated with CHD or mortality from cardiovascular causes [2] but increased factor × activity in patients with subclinical hyperthyroidism represents a potential hypercoagulable state [3]. It has been also reported an acute myocardial infarction with normal coronary arteries
⁎ Corresponding author. Cardiologia Nuovo Presidio Ospedaliero Cutroni Zodda-Barcellona P.d.G(Me) AUSL5 Messina, Via Cattafi 98051 Barcellona Pozzo di Gotto, Messina, Italy. E-mail address: [email protected] (S. Patanè). 0167-5273/$ - see front matter © 2008 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2008.03.011
associated with iatrogenic hyperthyroidism [4] and with a myocardial bridge too [5]. Moreover, it has been reported that simply measuring maximum P wave duration and P wave dispersion values, may help to determine the patients with subclinical hyperthyroidism and high risk for the development of atrial fibrillation [6]. We present a case of an acute myocardial infarction without significant coronary stenoses associated with subclinical hyperthyroidism. Also this case focuses attention on the importance of a correct evaluation of subclinical hyperthyroidism. On September 19th, 2007, a 67-year-old Italian woman was admitted to the emergency department. A history of chest pain was present. A history of paroxysmal supraventricular tachycardia and a history of current smoke were present. No current treatment for a history of a known subclinical hyperthyroidism was reported. Blood pressure values were 120/80 mmHg, the heart rate was 75 b/min, the oxygen saturation was normal. The ECG was performed (Fig. 1, Panel A). Troponin I was
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S. Patanè et al. / International Journal of Cardiology 134 (2009) e135–e137
Fig. 1. Panel A : ECG in the emergency department. Panel B : ECG with atrial fibrillation.
positive and the patient was admitted to the Cardiology Unit. Echocardiographic evaluation revealed a mild left atrial dilatation, a mild mitral regurgitation, a mild tricuspid regurgitation, a mild-moderate aortic regurgitation, a mild interventricular septal hypertrophy, an akinesia of the whole middle-apical portion of the interventricular septum, a medial segment akinesia of lateral wall with a medial segment hypokinesia of inferior wall. A pulmonary artery systolic pressure of 50 mmHg and an ejection fraction of 50% were observed. No pericardial effusion was observed. Initially the patient was treated with aspirin (1000 mg), intravenous heparin (bolus of 5000 IU and 1000 IU/h as a maintenance), nitroglycerin (5 mcg/kg/min), tirofiban, clopidogrel, bisoprolol. A new-onset of atrial fibrillation (Fig. 1, Panel B) and its pharmacological conversion to sinus rhythm were also observed. Over the following days the patient felt better and
ECG alterations evolved towards T-wave inversion in V2– V3–V4–V5–V6 (Fig. 2). Thyroglobulin autoantibodies were 190.78 U/ml (normal value 0–4.11), antithyroid peroxidase antibodies were 10.59 U/ml (normal value 0–5.61), thyroid– stimulating hormone was 0.009 μU/ml (normal value 0.350– 4.940), free triiodothyronine was 3.04 pg/ml (normal value 1.71–3.71), free thyroxine was 1.40 ng/dl (normal value 0.71–1.85) TropI peak was 2.80 ng/ml. In the cath-lab for coronary angiography no significant coronary stenoses were observed. References [1] Shrier DK, Burman KD. Subclinical hyperthyroidism: controversies in management. Am Fam Phys Feb 1 2002;65(3):431–8. [2] Singh S, Duggal J, Molnar J, Maldonado F, Barsano CP, Arora R. Impact of subclinical thyroid disorders on coronary heart disease,
S. Patanè et al. / International Journal of Cardiology 134 (2009) e135–e137
e137
Fig. 2. ECG without atrial fibrillation and with T-wave inversion in V2–V3–V4–V5–V6.
cardiovascular and all-cause mortality: a meta-analysis. Int J Cardiol 2008;125:41–8. [3] Erem C. Blood coagulation, fibrinolytic activity and lipid profile in subclinical thyroid disease: subclinical hyperthyroidism increases plasma factor X activity. Clin Endocrinol (Oxf) Mar 2006;64(3):323–9. [4] Gowda RM, Khan IA, Soodini G, Vasavada BC, Sacchi TJ. Acute myocardial infarction with normal coronary arteries associated with iatrogenic hyperthyroidism. Int J Cardiol Aug 2003;90(2–3):327–9.
[5] Patanè S, Marte F, Patanè F, et al. Acute myocardial infarction in a young patient with myocardial bridge and elevated levels of free triiodothyronine. Int J Cardiol 2009;132:140–2. [6] Aras D, Maden O, Ozdemir O, et al. Simple electrocardiographic markers for the prediction of paroxysmal atrial fibrillation in hyperthyroidism. Int J Cardiol Mar 10 2005;99(1):59–64.