ic pacemaker during repolarization and re-entry, along with enhancement of spontaneous depolar- ization of the ectopic pacemaker by the preceding beat.
I Case Reports
Bigeminal arrhythmia associated with hyperparathyroid crisis Molka Chaieb Chadli, MD Larbi Chaieb, MD Letaief Jemni, MD Najib Chatti, MD Moncef Allegue, MD Abdelkarim Zebidi, MD Abdelhamid Djaidane, MD
T he effects of hypercalcemia on the heart and the consequent modifications in the electrocardiogram (ECG) are well known. However, arrhythmias are an uncommon manifestation of hypercalcemia.1 An acute elevation of the serum calcium concentration may cause bradycardia and first-degree heart block.2 We present a case of hyperparathyroid crisis secondary to a cystic parathyroid adenoma in which ventricular bigeminal rhythm occurred. To our knowledge no similar arrhythmia has previously been reported. Case report A 44-year-old woman was admitted to hospital with a pathologic fracture of the left radius. She had had persistent low back pain for several years and recurrent bilateral renal calculi for 6 years; nephrolithotomy had been performed twice. In the last year she had suffered from headache, occasional generalized pruritus, increasing weakness and dizziness. Four months before admission she had begun to have nausea, vomiting and recurrent abdominal pain. She had lost 8 kg. Physical examination revealed evidence of weight loss and dehydration. She was lethargic. Her blood pressure was 130/70 mm Hg, pulse rate 120 beats/min and rhythm regular, and temperature normal. Two nodules were found over the right lobe of the thyroid gland: a firm mass about 4 cm in diameter at the lower pole, which pushed From the Department of Internal Medicine and the Endocrinology Section, h6pital universitaire Farhat Hached, Sousse, Tunisia
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the trachea to the left, and a mass about 3 cm in diameter at the upper pole. The remainder of the physical findings were within normal limits. The patient's hemoglobin level was 127 g/L, the hematocrit 40%, the leukocyte count 5.4 X 109/L and the serum glucose level 110 mg/dl (6.1 mmol/L). Abnormal serum levels were as follows: calcium 12.4 mg/dl (3.09 mmol/L) (normally 8.5 to 10.5 mg/dl [2.12 to 2.62 mmol/L]), alkaline phosphatase 1476 (normally 60 to 170) IU/L and chloride 114 (normally 95 to 105) mmol/L. The inorganic phosphorus level was normal, as were all the indices of thyroid function; however, the level of immunoreactive parathyroid hormone (iPTH) was elevated, at 8200 (normally 20 to 90) mlEq/L. A technetium thyroid scan showed enlargement of the right lobe and homogeneous uptake of the isotope. Grey-scale ultrasonography revealed that the nodule at the right lower pole was a multiloculated cyst (Fig. 1). The nodule at the right upper pole was solid. A skeletal radiographic survey showed generalized demineralization, with a "salt-and-pepper" pattern in the skull, subperiosteal resorption of the phalanges, and cystic lesions of the ribs and left radius. Dental x-ray films revealed a loss of the lamina dura. An ECG the day of admission showed sinus tachycardia (rate 120 beats/min), normal PR and QT, intervals, and P waves typical of right atrial enlargement. On the fourth hospital day the patient complained of weakness and anorexia and began to vomit frequently. The weakness became extreme, and occasional muscle twitches and exaggerated reflexes were noted. Her temperature was normal. The ECG revealed bigeminal rhythm (Fig. 2). The serum calcium level rose to 15 mg/dl (3.74 mmol/L); the serum inorganic phosphorus level had fallen to a low-normal value (2.7 mg/dl [0.87 CMAJ, VOL. 138, JUNE 15,1988
1115
mmol/L]). The serum chloride level was still high, at 113 mmol/L. Treatment with saline solution and furosemide markedly improved the patient's clinical status. The serum calcium level gradually decreased, and when it was 11 mg/dl (2.74 mmol/L) the heart rhythm returned to normal. The nodule at the right lower pole of the thyroid was then removed; it proved to be a cystic parathyroid adenoma 4.5 X 3 cm that contained serosanguineous fluid. The microscopic findings were consistent with cystic degeneration. The nodule at the right upper pole, a solitary thyroid adenoma, was also removed. Postoperatively the serum calcium concentration gradually retumed to normal, and after 7 months the serum iPTH level had fallen to 75 mlEq/L. Skeletal x-ray films revealed evidence of recalcification, which was quite apparent in the skull and long bones. All subsequent ECGs were normal. Comments
Hypercalcemia decreases the plateau, or second, phase of the cardiac action potential; this may be reflected in a shortened ST segment and, consequently, a reduced QT interval.' Hypercalcemia can also affect depolarization (phase 4), but the magnitude of the change is usually not sufficient to induce arrhythmias.1 However, with acute
elevation of the serum calcium level, bradycardia and first-degree atrioventricular (AV) block may occur.' Also, sinus arrest with a slow ventricular rate, first-degree AV block and episodes of paroxysmal atrial fibrillation have been reported among patients with hypercalcemia secondary to a parathyroid adenoma.2 Moreover, it has been postulated that sudden death during hyperparathyroid crisis may be caused by ventricular fibrillation.3 The toxic effects of hyperparathyroid crisis on the myocardium are similar to those of digitalis intoxication. Our patient had never received digitalis. Parathyroid hormone has a positive chronotropic effect on rat myocardial cells in culture, and its action is mimicked by calcium ionophore and blocked by verapamil.4 Parathyroid hormone also has a positive inotropic effect on the rat heart at physiologic concentrations; this action too is blocked by verapamil.5 These experimental data suggest that parathyroid hormone has a direct effect on the myocardium that is mediated by an influx of calcium. Bigeminy probably results from several mechanisms, including electrical instability of the ectopic pacemaker during repolarization and re-entry, along with enhancement of spontaneous depolarization of the ectopic pacemaker by the preceding beat. The effect of chronic hypercalcemia on the heart may be relevant. Dystrophic myocardial calcification and deposits of calcium in the cardiac annuli and valvular cusps were found at autopsy among patients who had had ventricular arrhythmias, including premature beats and tachycardia.6 Acute cystic degeneration of a parathyroid adenoma can result in acute elevation of the serum parathyroid hormone level and subsequent hypercalcemia.78 However, the pathogenesis of parathyroid cysts is probably multifactorial. Nevertheless, our case suggests that hyperparathyroid crisis may produce or precipitate ectopic ventricular bigeminy.
References
Fig. 1 - Multiloculated cyst at right lower pole of thyroid.
Fig. 2 -Ventricular premature beats with bigeminy, in lead II. 1116
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1. Surawicz B: Relationship between electrocardiogram and electrolytes. Am HeartJ 1967; 73: 815-834 2. Voss DM, Drake EH: Cardiac manifestations of hyperparathyroidism, with presentation of previously unreported arrhythmia. Ibid: 235-239 3. Naik BK, Sarma RN, Capalrao V et al: Acute hyperparathyroidism. Arch Intemn Med 1963; 111: 729-731 4. Bogin E, Massry SG, Harary I: Effect of parathyroid hormone on rat heart cells. J Clin Invest 1981; 67: 1215-1227 5. Katoh Y, Klein KL, Kaplan RA et al: Parathyroid hormone has a positive inotropic action in the rat. Endocrinology 1981; 109: 2252-2254 6. Roberts WC, Waller BF: Effect of chronic hypercalcemia on the heart. An analysis of 18 necropsy patients. Am J Med 1981; 71: 371-384 7. Albertson DA, Marshall RB, Jarman WT: Hypercalcemic crisis secondary to a functioning parathyroid cyst. Am J Surg 1981; 141: 175-177 8. Calandra DB, Shah KH, Prinz RA et al: Parathyroid cysts: a report of eleven cases including two associated with hyperparathyroid crisis. Surgery 1983; 96: 887-891
