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Extreme but not life-threatening QT interval prolongation? Take a closer look at the neck!
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Journal of Electrocardiology 46 (2013) 128 – 130 www.jecgonline.com
Extreme but not life-threatening QT interval prolongation? Take a closer look at the neck! Elias Rentoukas, MD, a George Lazaros, MD, b,⁎ Spiridon Sotiriou, MD, a Minas Athanassiou, MD, a Dimitris Tsiachris, MD, b Spiridon Deftereos, MD, a Christodoulos Stefanadis, MD b a
b
2nd Department of Cardiology, Amalia Fleming General Hospital, Athens, Greece 1st Department of Cardiology, University of Athens Medical School, Hippokration Hospital, Athens, Greece
Abstract
We present the case of a 82-year-old woman with a history of total thyroidectomy who was admitted in hospital with severe hypocalcemia. A 12-lead surface ECG revealed atrial fibrillation along with an extremely prolonged QT interval of approximately 730 ms. In the absence of any other possible cause of QT interval prolongation, hypocalcemia was attributed to surgical hypoparathyroidism and undue discontinuation of calcium supplementation. Surprisingly, no ventricular arrhythmias were recorded and calcium repletion was followed by normalization of QT interval. © 2013 Elsevier Inc. All rights reserved.
Keywords:
QT prolongation; Hypocalcaemia; Hypoparathyroidism; Torsades des pointes
Introduction
Case report
The QT interval on the surface electrocardiogram depicts ventricular depolarization and repolarization. In clinical practice QT measurement is clinically relevant since its abnormal prolongation or, as recently shown, its shortening have been both shown to predispose to malignant and potentially fatal ventricular arrhythmias. 1,2 Because the QT interval is prolonged at slower heart rates and shortened at faster heart rates, many formulas have been proposed to adjust for these variations. 3,4 The QTc interval is traditionally considered long in men when it is more than 440 ms and in women when it exceeds 460 ms, but some have suggested values up to 470 ms in males and 480 ms in females. 3,5 The term long QT syndrome refers to a genetic or acquired disorder of myocardial repolarization characterized by a prolonged QT interval associated with an increased risk of a peculiar life-threatening cardiac arrhythmia, known as torsades de pointes. 2,3 In clinical practice, the most frequent cause of the long QT syndrome is drug therapy, followed by electrolyte disorders. 5,6
A 82 year-old-female was admitted with worsening dyspnea, palpitations, weakness and muscle cramps. Her past medical history was remarkable for persistent atrial fibrillation, type II diabetes mellitus, arterial hypertension and mild cognitive impairment due to senile dementia. Her medicalsurgical history was notable for total thyroidectomy 14 years earlier, and for an internal fixation of an intertrochanteric fracture 3 months ago. Her medication regimen included warfarin, telmisartan 80 mg daily, atenolol 25 mg daily, levothyroxine 125mcg daily, nateglinide 120 mg daily and a combination of calcium 1000 mg and cholecalciferol 800 IU once daily. However, as afterwards was figured out, the above mentioned fixed combination was discontinued by the patient herself after the recent orthopedic surgery, without any apparent reason. On clinical examination the patient appeared anxious and in mildly impaired general condition. Apart from dyspnea which was her main complain, she reported paresthesias and numbness of the fingertips and perioral area. She was afebrile, her blood pressure was 120/60 mmHg, pulse rate was irregular at a rate of ~ 85 bpm, and respirations were 20 per minute. Lung auscultation revealed prolonged expiration and diffuse wheezing. Initial laboratory tests were remarkable for hypocalcemia with a calcium serum level of 3.4 mg/dL or 4.8 when corrected for albumin levels (2.6gr/dL). Serum potassium was 3.5 mg/dL, serum magnesium was 1.9 mg/dL, and parathormone levels were
⁎ Corresponding author. First Department of Cardiology, University of Athens Medical School, Hippokration Hospital, 114 Vas. Sofias Ave., Athens, Greece. E-mail address: [email protected] 0022-0736/$ – see front matter © 2013 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jelectrocard.2012.10.007
E. Rentoukas et al. / Journal of Electrocardiology 46 (2013) 128–130
129
Fig. 1. Admission electrocardiogram showing atrial fibrillation, diffuse T wave inversionand a markedly prolonged QT interval.
11.3 pg/dL (normal values 15–65). The INR was 1.68. The rest of blood tests results were within or near the reference range. A 12-lead surface ECG revealed atrial fibrillation at a rate of 85 bpm, inverted T waves in most leads, and a markedly prolonged QT interval of 730 ms (Fig. 1). Since the patient was in atrial fibrillation, QT duration was established by averaging the measured QT intervals over 10 beats, as elsewhere described. 5 As preferred by other experts, QT interval was alternatively calculated by taking the average of QT intervals with shortest and longest preceding R-R intervals and results were fairly reproducible (~ 720 ms). 5 A chest X-ray was clear and an echocardiographic study revealed a normal sized, mildly hypertrophic left ventricle with globally depressed contractility (ejection fraction ~ 40%). The right ventricle was mildly dilated with mildly impaired contractility. The pulmonary artery systolic pressure was estimated at 45 mmHg whereas pulse wave Doppler of the transmitral inflow revealed absence of A wave. The patient's assessment throughout hospitalization included, among others, coronary angiography which did not reveal obstructive coronary artery disease, and a chest spiral
CT scan with radiocontrast agent which excluded pulmonary embolism (suspected in view of the recent hip fracture and the subtherapeutic levels of INR). The patient's management consisted of intravenous infusion of calcium gluconate until normalization of serum calcium levels as well as potassium and albumin repletion. The patient was discharged 12 days after admission in good condition. The pre-discharged ECG showed sinus rhythm (she converted spontaneously to sinus rhythm on hospital day 3), along with a QTc calculated with Fridericia's formula of 440 ms (Fig. 2). The serum calcium levels were normal (9.1 mg/dL) and left ventricular contractility improved (EF ~ 50%). Discussion This is the case of severe hypocalcemia in a patient with surgical hypoparathyroidism appearing after total thyroidectomy. We emphasize that the patient had mistakenly interrupted calcium and cholecalciferol few weeks before admission. Post-operative hypocalcemia is one of the most
Fig. 2. Electrocardiogram obtained at discharge showing sinus rhythm with supraventricular extrasystoles, normalization of QT interval and persisting T wave inversion.
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important complications after thyroidectomy, with reported incidence ranging from 1.6 to 50%. 7 Surgical trauma, devascularisation or inadvertent excision of parathyroid glands, and autoimmune fibrosis in patients with Grave's disease have been proposed as the possible pathophysiologic mechanisms underlying hypoparathyroidism. 7 Furthermore, any other possible causes of QT interval prolongation, such as use of medications known to prolong QT,ischemia, andabnormal renal function were excluded. 4–6 Major causes of long QT syndrome (and accordingly torsades de pointes) include congenital and acquired forms. The differential diagnosis of the latter forms include, among others, administration of pharmacological agents causing lengthening of QT interval (such as, certain antiarrhythmics, antibiotics, antipsychotics, antidepressants, etc.), electrolyte disturbances (particularly hypokalemia, hypomagnesemia, hypocalcemia), clinically significant bradycardia, myocardial injury and ischemia, renal and hepatic dysfunction, acute phase of stroke (ischemic stroke and intracerebral hemorrhage), cocaine abuse, starvation, anorexia nervosa, etc. 4 The main difficulty of QT interval measurement lies in identifying correctly the point where the descending limb of a positive T wave intersects the isoelectric line, which is often challenging in the presence of a positive earlyoccurring U wave. In the latter eventuality the duration of ventricular repolarization could be overestimated. 8 However, this is not the case of our patient, where the presence of negative T waves without any discernible U wave, allowed a clear-cut QT interval demarcation, which measured 730 ms.We wish to emphasize that such prolongation is rarely detected in clinical practice, especially in the presence of a single predisposing parameter (i.e. hypocalcemia). 6 Interestingly, despite marked QT prolongation, continuouscardiac rhythm monitoring did not reveal torsades de pointes
tachycardia or other life-threatening arrhythmias. Althougharrhythmogenicity in individual basis, is rather complex and probably multifactorial, it seems that hypocalcemia per se, even with extreme QT prolongation, rarely triggers torsades, for reasons not yet clarified. 6,9 On the contrary, it is well established that congenital long QT syndromes confer higher risk for sudden death compared with the acquired forms. 5 Conclusion Hypocalcemia due to inadvertent excision of parathyroid glands in the context of thyroidectomy is a possible and important complication. When physicians deal with a QT prolongation due to hypocalcemic state, a closer look at the neck may uncover the underlying cause. References 1. Napolitano C, Bloise R. Priori 1 SG. Long QT syndrome and short QT syndrome: how to make correct diagnosis and what about eligibility for sports activity. J Cardiov Med 2006;7:250. 2. Patanè S, Marte F, Di Bella G. QT interval prolongation and torsade de pointes. Int J Cardiol 2009;131:e51. 3. Corrado D, Pelliccia A, Heidbuchel H, et al. Recommendations for interpretation of 12-lead electrocardiogram in the athlete. Eur Heart J 2010;31:243. 4. Gowda RM, Khan IA, Wilbur SL, Vasavada BC, Sacchi TJ. Torsade de pointes: the clinical considerations. Int J Cardiol 2004;96:1. 5. Al-Khatib SM, LaPointe NM, Kramer JM, Califf RM. What clinicians should know about the QT interval. JAMA 2003;289:2120. 6. Dilaveris P, Giannopoulos G, Riga M, Synetos A, Stefanadis C. Beat by beat variations. Am J Med 2007;120:21. 7. Karefilakis CM, Mazokopakis EE. Management of post-thyroidectomy hypocalcaemia. Current trends ANZ J Surg 2009;79:574. 8. Goldenberg I, Moss AJ, Zareba W. QT interval: how to measure it and what is “normal”. J Cardiovasc Electrophysiol 2006;17:333. 9. Akiyama T, Batchelder J, Worsman J, Moses HW, Jedlinski M. Hypocalcemic torsades de pointes. J Electrocardiol 1989;22:89.
Journal of Electrocardiology 46 (2013) 128 – 130 www.jecgonline.com
Extreme but not life-threatening QT interval prolongation? Take a closer look at the neck! Elias Rentoukas, MD, a George Lazaros, MD, b,⁎ Spiridon Sotiriou, MD, a Minas Athanassiou, MD, a Dimitris Tsiachris, MD, b Spiridon Deftereos, MD, a Christodoulos Stefanadis, MD b a
b
2nd Department of Cardiology, Amalia Fleming General Hospital, Athens, Greece 1st Department of Cardiology, University of Athens Medical School, Hippokration Hospital, Athens, Greece
Abstract
We present the case of a 82-year-old woman with a history of total thyroidectomy who was admitted in hospital with severe hypocalcemia. A 12-lead surface ECG revealed atrial fibrillation along with an extremely prolonged QT interval of approximately 730 ms. In the absence of any other possible cause of QT interval prolongation, hypocalcemia was attributed to surgical hypoparathyroidism and undue discontinuation of calcium supplementation. Surprisingly, no ventricular arrhythmias were recorded and calcium repletion was followed by normalization of QT interval. © 2013 Elsevier Inc. All rights reserved.
Keywords:
QT prolongation; Hypocalcaemia; Hypoparathyroidism; Torsades des pointes
Introduction
Case report
The QT interval on the surface electrocardiogram depicts ventricular depolarization and repolarization. In clinical practice QT measurement is clinically relevant since its abnormal prolongation or, as recently shown, its shortening have been both shown to predispose to malignant and potentially fatal ventricular arrhythmias. 1,2 Because the QT interval is prolonged at slower heart rates and shortened at faster heart rates, many formulas have been proposed to adjust for these variations. 3,4 The QTc interval is traditionally considered long in men when it is more than 440 ms and in women when it exceeds 460 ms, but some have suggested values up to 470 ms in males and 480 ms in females. 3,5 The term long QT syndrome refers to a genetic or acquired disorder of myocardial repolarization characterized by a prolonged QT interval associated with an increased risk of a peculiar life-threatening cardiac arrhythmia, known as torsades de pointes. 2,3 In clinical practice, the most frequent cause of the long QT syndrome is drug therapy, followed by electrolyte disorders. 5,6
A 82 year-old-female was admitted with worsening dyspnea, palpitations, weakness and muscle cramps. Her past medical history was remarkable for persistent atrial fibrillation, type II diabetes mellitus, arterial hypertension and mild cognitive impairment due to senile dementia. Her medicalsurgical history was notable for total thyroidectomy 14 years earlier, and for an internal fixation of an intertrochanteric fracture 3 months ago. Her medication regimen included warfarin, telmisartan 80 mg daily, atenolol 25 mg daily, levothyroxine 125mcg daily, nateglinide 120 mg daily and a combination of calcium 1000 mg and cholecalciferol 800 IU once daily. However, as afterwards was figured out, the above mentioned fixed combination was discontinued by the patient herself after the recent orthopedic surgery, without any apparent reason. On clinical examination the patient appeared anxious and in mildly impaired general condition. Apart from dyspnea which was her main complain, she reported paresthesias and numbness of the fingertips and perioral area. She was afebrile, her blood pressure was 120/60 mmHg, pulse rate was irregular at a rate of ~ 85 bpm, and respirations were 20 per minute. Lung auscultation revealed prolonged expiration and diffuse wheezing. Initial laboratory tests were remarkable for hypocalcemia with a calcium serum level of 3.4 mg/dL or 4.8 when corrected for albumin levels (2.6gr/dL). Serum potassium was 3.5 mg/dL, serum magnesium was 1.9 mg/dL, and parathormone levels were
⁎ Corresponding author. First Department of Cardiology, University of Athens Medical School, Hippokration Hospital, 114 Vas. Sofias Ave., Athens, Greece. E-mail address: [email protected] 0022-0736/$ – see front matter © 2013 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jelectrocard.2012.10.007
E. Rentoukas et al. / Journal of Electrocardiology 46 (2013) 128–130
129
Fig. 1. Admission electrocardiogram showing atrial fibrillation, diffuse T wave inversionand a markedly prolonged QT interval.
11.3 pg/dL (normal values 15–65). The INR was 1.68. The rest of blood tests results were within or near the reference range. A 12-lead surface ECG revealed atrial fibrillation at a rate of 85 bpm, inverted T waves in most leads, and a markedly prolonged QT interval of 730 ms (Fig. 1). Since the patient was in atrial fibrillation, QT duration was established by averaging the measured QT intervals over 10 beats, as elsewhere described. 5 As preferred by other experts, QT interval was alternatively calculated by taking the average of QT intervals with shortest and longest preceding R-R intervals and results were fairly reproducible (~ 720 ms). 5 A chest X-ray was clear and an echocardiographic study revealed a normal sized, mildly hypertrophic left ventricle with globally depressed contractility (ejection fraction ~ 40%). The right ventricle was mildly dilated with mildly impaired contractility. The pulmonary artery systolic pressure was estimated at 45 mmHg whereas pulse wave Doppler of the transmitral inflow revealed absence of A wave. The patient's assessment throughout hospitalization included, among others, coronary angiography which did not reveal obstructive coronary artery disease, and a chest spiral
CT scan with radiocontrast agent which excluded pulmonary embolism (suspected in view of the recent hip fracture and the subtherapeutic levels of INR). The patient's management consisted of intravenous infusion of calcium gluconate until normalization of serum calcium levels as well as potassium and albumin repletion. The patient was discharged 12 days after admission in good condition. The pre-discharged ECG showed sinus rhythm (she converted spontaneously to sinus rhythm on hospital day 3), along with a QTc calculated with Fridericia's formula of 440 ms (Fig. 2). The serum calcium levels were normal (9.1 mg/dL) and left ventricular contractility improved (EF ~ 50%). Discussion This is the case of severe hypocalcemia in a patient with surgical hypoparathyroidism appearing after total thyroidectomy. We emphasize that the patient had mistakenly interrupted calcium and cholecalciferol few weeks before admission. Post-operative hypocalcemia is one of the most
Fig. 2. Electrocardiogram obtained at discharge showing sinus rhythm with supraventricular extrasystoles, normalization of QT interval and persisting T wave inversion.
130
E. Rentoukas et al. / Journal of Electrocardiology 46 (2013) 128–130
important complications after thyroidectomy, with reported incidence ranging from 1.6 to 50%. 7 Surgical trauma, devascularisation or inadvertent excision of parathyroid glands, and autoimmune fibrosis in patients with Grave's disease have been proposed as the possible pathophysiologic mechanisms underlying hypoparathyroidism. 7 Furthermore, any other possible causes of QT interval prolongation, such as use of medications known to prolong QT,ischemia, andabnormal renal function were excluded. 4–6 Major causes of long QT syndrome (and accordingly torsades de pointes) include congenital and acquired forms. The differential diagnosis of the latter forms include, among others, administration of pharmacological agents causing lengthening of QT interval (such as, certain antiarrhythmics, antibiotics, antipsychotics, antidepressants, etc.), electrolyte disturbances (particularly hypokalemia, hypomagnesemia, hypocalcemia), clinically significant bradycardia, myocardial injury and ischemia, renal and hepatic dysfunction, acute phase of stroke (ischemic stroke and intracerebral hemorrhage), cocaine abuse, starvation, anorexia nervosa, etc. 4 The main difficulty of QT interval measurement lies in identifying correctly the point where the descending limb of a positive T wave intersects the isoelectric line, which is often challenging in the presence of a positive earlyoccurring U wave. In the latter eventuality the duration of ventricular repolarization could be overestimated. 8 However, this is not the case of our patient, where the presence of negative T waves without any discernible U wave, allowed a clear-cut QT interval demarcation, which measured 730 ms.We wish to emphasize that such prolongation is rarely detected in clinical practice, especially in the presence of a single predisposing parameter (i.e. hypocalcemia). 6 Interestingly, despite marked QT prolongation, continuouscardiac rhythm monitoring did not reveal torsades de pointes
tachycardia or other life-threatening arrhythmias. Althougharrhythmogenicity in individual basis, is rather complex and probably multifactorial, it seems that hypocalcemia per se, even with extreme QT prolongation, rarely triggers torsades, for reasons not yet clarified. 6,9 On the contrary, it is well established that congenital long QT syndromes confer higher risk for sudden death compared with the acquired forms. 5 Conclusion Hypocalcemia due to inadvertent excision of parathyroid glands in the context of thyroidectomy is a possible and important complication. When physicians deal with a QT prolongation due to hypocalcemic state, a closer look at the neck may uncover the underlying cause. References 1. Napolitano C, Bloise R. Priori 1 SG. Long QT syndrome and short QT syndrome: how to make correct diagnosis and what about eligibility for sports activity. J Cardiov Med 2006;7:250. 2. Patanè S, Marte F, Di Bella G. QT interval prolongation and torsade de pointes. Int J Cardiol 2009;131:e51. 3. Corrado D, Pelliccia A, Heidbuchel H, et al. Recommendations for interpretation of 12-lead electrocardiogram in the athlete. Eur Heart J 2010;31:243. 4. Gowda RM, Khan IA, Wilbur SL, Vasavada BC, Sacchi TJ. Torsade de pointes: the clinical considerations. Int J Cardiol 2004;96:1. 5. Al-Khatib SM, LaPointe NM, Kramer JM, Califf RM. What clinicians should know about the QT interval. JAMA 2003;289:2120. 6. Dilaveris P, Giannopoulos G, Riga M, Synetos A, Stefanadis C. Beat by beat variations. Am J Med 2007;120:21. 7. Karefilakis CM, Mazokopakis EE. Management of post-thyroidectomy hypocalcaemia. Current trends ANZ J Surg 2009;79:574. 8. Goldenberg I, Moss AJ, Zareba W. QT interval: how to measure it and what is “normal”. J Cardiovasc Electrophysiol 2006;17:333. 9. Akiyama T, Batchelder J, Worsman J, Moses HW, Jedlinski M. Hypocalcemic torsades de pointes. J Electrocardiol 1989;22:89.