© 2004 by European Society of Cardiology
CASE REPORT
Primary hyperparathyroidism and arrhythmic storm in a patient with an implantable cardioverter defibrillator for primary prevention of sudden death
Cardiology Division, Faculty of Medicine, University of Piemonte Orientale Novara, Italy
Manuscript submitted 12 November 2003. Accepted after revision 25 January 2004.
*Corresponding author. Divisione Clinicizzata di Cardiologia, Azienda Ospedaliera Maggiore della Carità, Corso Mazzini 18, 28100 Novara, Italy. Tel.: +39-0321-3733413; fax: +39-0321-3733407. E-mail addresses: occhetta{at}r-j.it, cardio1{at}maggioreosp.novara.it (E. Occhetta).
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Abstract |
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A case of a patient with an automatic cardioverter defibrillator (ICD) and recurrent ventricular arrhythmic storms related to primary hyperparathyroidism and hypercalcaemia is reported: medical therapy was ineffective and only surgical resection of the parathyroid adenoma resolved this complex clinical condition.
Key Words: hyperparathyroidism, arrhythmic storm, implantable cardioverter defibrillator
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Introduction |
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Primary hyperparathyroidism is a generalized disorder of calcium, phosphate, and bone metabolism due to an increased secretion of parathyroid hormone and consequent hypercalcaemia and hypophosphataemia. High calcium levels often result in fatigue, anorexia, reversible renal tubular defects, short QT interval and, rarely, cardiac arrhythmias [1]
. We report the case of a patient with coronary artery disease, implanted with an automatic cardioverter defibrillator (ICD) for primary prevention of sudden death, with multiple and ineffective ICD discharges, related to primary hyperparathyroidism and hypercalcaemia.
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Case report |
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In 1999, a 71-year-old man was admitted to the cardiac care unit for the treatment of antero-lateral acute myocardial infarction. Primary coronary angioplasty of the left anterior descending coronary artery was performed (TIMI 2 final flow grade) [2]
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Because of persistent left ventricular dysfunction (ejection fraction 0.30) the patient was enrolled in the BEST + ICD Trial [3] and randomized to electrophysiological evaluation, during which ventricular fibrillation was induced. The patient was then implanted with a single chamber VVI ICD (Mini IV 1790, Guidant Corporation, St. Paul, Minnesota, USA), programmed with ventricular fibrillation detection at 180 bpm (31 J shock therapies); he was discharged on metoprolol (25 mg) and digoxin (0.125 mg).
After 20 months without arrhythmias, the patient arrived in the emergency room complaining of palpitations and several ICD shocks. The ECG showed sinus rhythm with right bundle branch block, left anterior hemiblock and previous anterior myocardial infarction (same pattern as preimplant ECG) (Fig. 1).
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The stored ICD memories showed a wide QRS tachycardia (190 bpm), properly detected and treated with the complete programmed therapy (five 31 J shocks), without interrupting the tachycardia, which later spontaneously terminated (Fig. 2).
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Total calcium level was increased: 11.2 mg/dL (normal range 8.2–10 mg/dL); phosphate was decreased: 1.2 mg/dL (normal level 2.5–4.5 mg/dL); immunoactive parathyroid hormone level was very high: 873 pg/mL (normal range 12.0–72.0 pg/mL); potassium, sodium and myocardial enzymes were normal.
Ischaemic causes of the arrhythmic storm were excluded by coronary angiography and a myocardial single-photon emission computed tomography.
In order to verify correct ICD function, ventricular fibrillation was induced, properly detected and interrupted by ICD discharge (31 J; impedance 42 
); the ICD was permanently also programmed to give antitachycardia pacing.
The echo-sonograhy of the neck showed a hypoechoic mass of maximum diameter 14 mm located behind the right inferior portion of the thyroid gland, that was a parathyroid adenoma.
Therapy with calcitonin (100 UI twice daily), pamidronate (90 mg/once month), and prednisone (25 mg once daily) was started.
After one month, the patient returned to our service because of several more ICD discharges: the telemetric interrogation showed 15 new episodes of ICD activation, similar to the previous electrograms. Calcium level was 13 mg/dL and phosphate level 1.8 mg/dL.
Therapy with amiodarone intravenously was started. During the hospitalization the patient presented new ventricular tachycardias not interrupted by the programmed therapy and degenerating into ventricular fibrillation, treated by external DC shock. Radiofrequency ablation was not considered sufficiently effective or safe.
As ventricular arrhythmias were possibly related to primary hyperparathyroidism the patient underwent right inferior parathyroidectomy and right hemithyroidectomy.
The pathological finding confirmed the adenomatous origin of the lesion (Fig. 3).
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The postoperative course was uneventful and the serum calcium and parathyroid hormone returned to normal levels.
During the following year no ventricular arrhythmias occurred despite worsening heart failure for which the patient died 12 months after operation.
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Discussion |
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Primary hyperparathyroidism is an uncommon disease which may exhibit multiple clinical manifestations; previous studies on rat hearts have shown that the parathyroid hormone has a direct positive inotropic and chronotropic effect [4,
5]. Moreover, hypercalcaemia is associated with major ECG changes such as prolongation of the PR and QRS intervals, shortening of QT interval and ST segment [6,7].
Voss and Drake [8] reported the case of a patient with a parathyroid adenoma exhibiting sick sinus syndrome and first-degree atrioventricular block; also ventricular tachyarrhythmias have been associated with primary hyperparathyroidism [9,10]. More recently, Chang et al. [11] described the case of a woman with primary hyperparathyroidism and spontaneous ventricular tachycardias, which could be induced after calcium–gluconate injection and terminated after verapamil infusion.
According to Kearney et al. [10] the arrhythmogenic effect of hypercalcaemia could be related to early afterdepolarizations; calcium overloading could also trigger delayed afterdepolarization through a shortening of action potential phase two [6]. Furthermore, hypercalcaemia can also shorten the effective refractory period and precipitate reentry [12].
The exact electrophysiological mechanism which caused refractory ventricular tachyarrhythmias in our patient is unknown; undoubtedly, hypercalcaemia in a compromised heart can trigger life-threatening ventricular arrhythmias. In our patient medical and electrical therapy was ineffective and only surgical right parathyroidectomy, which was initially not performed because it was considered at high risk, was able to resolve this rare and complex clinical situation.
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References |
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[1] Potts JT Jr. Disease of the parathyroid gland and other hyper- and hypocalcemic disorders. In Fauci AS and Braunwald E (Eds.). Harrison's principle of internal medicine 14th ed. 1998; New York, NY, USA The McGraw-Hill Companies, Inc pp. 2227–2241.
[2] The TIMI Study Group. The Thrombolysis in Myocardial Infarction (TIMI) Trial. N Engl J Med 1985; 312: 932–936.[Medline]
[3] Raviele A, Bongiorni MG, Brignole M, et al. Which strategy is "best" after myocardial infarction? The beta blocker strategy plus implantable cardioverter defibrillator trial: rationale and study design. Am J Cardiol 1999; 83:Suppl_5B 104D–111D.[CrossRef][ISI][Medline]
[4] Vogin E, Massry SG, Harary I. Effect of parathyroid hormone on rat heart cells. J Clin Invest 1981; 67: 1215–1227.[ISI][Medline]
[5] Katoh Y, Klein KL, Kaplan RA, et al. Parathyroid hormone has a positive inotropic action in the rat. Endocrinology 1981; 109: 2252–2254.[Abstract]
[6] Surawicz B. Relationship between electrocardiogram and electrolytes. Am Heart J 1967; 73: 814–834.[CrossRef][ISI][Medline]
[7] Chodack P, Attie JN, Groder MG, et al. Hypercalcemic crisis coincidental with hemorrhage in parathyroid adenoma. Arch Intern Med 1965; 116: 416–423.[Medline]
[8] Voss DM and Drake EH. Cardiac manifestations of hyperparathyroidism, with presentation of a previously unreported arrhythmia. Am Heart J 1967; 72: 235–239.
[9] Hewson JS. Parathyroid crisis. A cause of sudden death. Arch Intern Med 1959; 102: 199–203.
[10] Kearney P, Reardon M, O'Hare J. Primary hyperparathyroidism presenting as torsade de pointes. Br Heart J 1993; 70: 473.
[11] Chang CJ, Chen SA, Tai CT, et al. Ventricular tachycardia in a patient with primary hyperparathyroidism. Pacing Clin Electrophysiol 2000; 23: 534–537.[CrossRef][Medline]
[12] Surawicz B. Role of electrolytes in etiology and management of cardiac arrhythmia. Prog Cardiovasc Dis 1966; 8: 364–385.[CrossRef][Medline]
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