Hypercalcemia-Induced ST-Segment Elevation Mimicking Acute Myocardial Infarction

Written By: Sam Savage

Published Date: July 12, 2006 Last Edited: July 12, 2006

By Nishi, Shawn P E; Barbagelata, Nestor A; Atar, Shaul; Birnbaum, Yochai; Et al

Abstract

We describe a patient who presented with abdominal pain radiating to the chest and ST elevation in the precordial leads, mimicking acute myocardial infarction. Urgent coronary angiography revealed normal coronary arteries and his serum troponin has not increased. Subsequently, he was found to have severe hypercalcemia. ST segment elevation resolved after correction of hypercalcemia. This phenomenon of ST elevation secondary to hypercalcemia has been described only two times in the English literature to date.

Keywords: Hypercalcemia; Myocardial infarction; ST elevation; QTc interval; ECG; Arrhythmia

Introduction

It is well established that hypercalcemia causes shortening of the QT interval. However, other electrocardiographic (ECG) changes related to hypercalcemia have been less characterized. Review of literature suggested that hypercalcemia may cause ST-segment elevations, arrhythmias, atrioventricular blocks, and a variety of T- wave changes, including flattening, inversions, and notchings. We report a patient with severe hypercalcemia presented with chest pain and ST-segment elevation mimicking acute myocardial infarction.

Case report

A 31-year-old male Vietnamese was admitted for 5-day complaint of nausea, vomiting, lethargy, and diffuse abdominal pain radiating to his precordium. Medical history includes poorly controlled stage 2 hypertension that had been diagnosed and treated medically 5 years before admission, a recent diagnosis of hyperparathyroidism for which the patient had undergone parathyroidectomy 1 week before admission, and chronic kidney disease. The patient denied any other significant cardiac history of coronary artery disease, diabetes, or hyperlipidemia.

The patient presented to the emergency department in obvious distress. On evaluation, his blood pressure was 200/90 mm Hg, heart rate of 78 beats per minute, respirations at 18/min, and temperature of 36.2C. There was no jugular venous distension, lungs were clear to auscultation bilaterally, and cardiac auscultation yielded no murmur or friction rub. The abdomen was benign. An initial ECG showed normal sinus rhythm with marked ST elevations in leads VI through V5 and QTc of 415 milliseconds (Fig. 1). Chest x-ray revealed an enlarged heart with clear lungs.

Given the ECG findings and patient presentation, management included intravenous administration heparin, nitroglycerin, and β-blocker, and the patient was taken to the catheterization laboratory for urgent coronary angiography. Coronary angiography revealed normal coronary arteries.

Subsequently, the first set of cardiac enzymes showed elevated creatine kinase (337 U/L), mildly elevated creatine kinase-MB fraction (6.3 ng/mL), and normal troponin I levels (0.16 ng/mL). All other laboratory values were within normal range except for a serum calcium level of 17.8 mg/ dL, creatinine of 3.28 mg/dL, and serum urea nitrogen of 41 mg/dL. The second and third set of cardiac enzymes revealed serum creatine kinase of 218 and 114 mg/dL, respectively; serum creatine kinase-MB of 3.9 and 2.3 ng/ mL, respectively; and troponin I of 0.07 and 0.04 ng/mL, respectively.

Repeat ECGs showed persistent marked ST elevation in the precordial leads. Transthoracic echocardiographic examination demonstrated moderate left ventricular hypertrophy with normal left ventricular function, mild right ventricular hypertrophy, mild aortic dilation, and dilated left coronary sinus of Valsai va. The ejection fraction was 50% to 55% and without regional wall motion abnormalities. There was no pericardial effusion and the pericardium appeared normal.

Fig. 1. Initial ECG with serum calcium level of 17.8 mg/dt. showing diffuse ST elevations in V^sub 2^ through V^sub 5^ with QTc of 415 milliseconds.

The patient was treated with aggressive hydration and diuresis for hypercalceinia with a decrease in serum calcium to 10.1 mg/dL. Repeated ECG performed 3 weeks after discharge from the hospital showed resolution of the ST elevation without T-wave inversion or abnormal O waves. The QTc interval increased to 476 milliseconds (Fig. 2). At that time, his serum calcium level was 8.6 mg/dL.

Discussion

The patient presented with chest pain and ST-segment elevation compatible with ST-elevation acute myocardial infarction. However, coronary angiography revealed normal coronary arteries without obstruction and subsequent serum troponin I levels were within normal range. Moreover, ST-segment elevation resolved only after correction of his hypercalcemia. without evolution of abnormal Q waves or inverted T waves, and transthoracic echocardiogram did not show regional wall motion abnormalities or pericardial effusion. Thus, in our patient, ST-segment elevation was probably not caused by myocardial ischemia or acute pericarditis.

Fig. 2. Follow-up ECG of patient aller serum calcium levels normali/ed to preadmissions levels (serum calcium, 8.6 mg/dL) and QTc of 476 milliseconds.

Although hypercalccmia has been well characterized to shorten the QT interval, few authors have been reported transient ST-segment elevation mimicking acute myocardial infarction in patients with hypcrcalcemia.'”4 Ashizawa et al5 described a similar “high takeoff of the ST segment” in leads Vl and V2 in a patient with hypercalcemia due to vitamin D intoxication, simulating an acute myocardial infarction. In addition, they reported flattened and biphasic/notched T waves that were not seen in our patient.’ Turhan et al1 reported on a patient with ST-segment elevation in leads I, II, and Vl through V^sub 2^. In addition, they observed transient Q waves in V^sub 2^ through V^sub 3^ with normal serum troponin T and creatine kinase-MB and no regional wall motion abnormalities by echocardiography.6 Others have observed that the T waves flatten, invert, or appear biphasic/notched in configuration, and the T-wave amplitude was shown to be inversely correlated with serum calcium levels.7,8

The characteristic electrocardiography changes found in association with hypercalcemia are prolongation of the PR interval and shortening of the QT interval mainly due to shortening of the ST segment. Ahmed and Hashiba1 further classified QT intervals due to the effect of the shortened ST segment and revealed the intervals Q- oTc (the interval from the beginning of the QRS complex to the beginning of the T wave) of less than 0.18 second, and Q-aTc of less than 0.30 second (measured from the beginning of the QRS complex to the apex of the T wave) as reliable indicators of clinically moderate to severe hypercalcemia. Ashizawa et al5 also showed that hypercalcemia caused shortening of the Q-aTc. Hypercalcemia decreases ventricular conduction velocity and shortens the effective refractory period. This property of shortened QT intervals can prove useful in distinguishing ST elevations of acute myocardial infarction from ST manifestations of hypercalcemia. However, other studies have found that shortening of the QT interval is an unreliable index of clinical hypercalcemia due to the wide distribution of normal values 9,10. In our patient, although the QTc interval prolonged after correction of hypercalcemia, it was still within normal range on presentation (Fig. 1 ).

A spectrum of other ECG findings associated with hypercalcemia have also been reported. Carpenter and May11 reported on a patient with hypercalcemia (serum calcium, 13-18 mg/dL) who developed a “tachycardiabradycardiaMike syndrome with episodes of sinus arrest and bouts of paroxysmal supraventricular tachycardia and first- degree atrioventricular block. Correction of the calcium levels led to resolution of the tachycardia-bradycardia syndrome; however, the atrioventricular block persisted. Rosenqvist12 went on to show a correlation between the severity of hypercalcemia and the degree of atrioventricular block. Kiewiet 13 first documented the development of ventricular fibrillation in a patient with hypercalcemic crisis and no other explanation. Others have also uniquely reported a normothermic Osborne or prominent J waves in at least 5 reported cases of hypercalcemia.8,14-16

Conclusions

In summary, we report a case of severe hypercalcemia with chest pain in which ECG changes mimicked myocardial and slowly resolved with correction of serum calcium. At least 2 other documented cases of hypercalcemic ST elevations mistaken for myocardial ischemia have also been reported in the English literature.5’6 Short QT intervals in low-risk patients with ST-segment elevation may suggest the diagnosis of hypercalcemia. However, normal QT intervals do not necessarily exclude the diagnosis as in our case report.

References

1. Ahmed R, Hashiba K. Reliability of QT intervals as indicators of clinical hypercalcemia. CHn Cardiol 1988; 11:395.

2. Douglas PS, Carmichael KA, Palevsky PM. Extreme hypercalcemia and electrocardiographic changes. Am J Cardiol 1984;54:674.

3. Nierenberg DW, Ransil BJ. Q-aTc interval as a clinical indicator of hypercalcemia. Am J Cardiol 1979;44:243.

4. Saikawa T, Tsumabuki S, Nakagawa M, Takakura T, Tamura M, Maeda T, et al. QT intervals as an index of high serum calcium in hypercalcemia. CHn Cardiol 1988; 11:75.

5. Ashizawa N, Arakawa S, Koide Y, Toda G, Seto S, Yano K. Hypercalcemia due to vitamin D intoxicationwith clinical features mimicking acute myocardial infarction. Intern Med 2003;42:340.

6. Turhan S, Kilickap M, Kilinc S. ST segment elevation mimicking acute myocardial infarction in hypercalcaemia. Heart 2005;91:999.

7. Ahmed R, Yano K, Mitsuoka T, Ikeda S, Ichimura M, Hashiba K.. Changes in T wave morphology during hypercalcemia and its relation to the severity of hypercalcemia. J Electrocardiol 1989;22:125.

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9. Wortsman J, Frank S. The QT interval in clinical hypercalcemia. CHn Cardiol 1981;4:87.

10. Rumancik WM, Denlinger JK, Nahrwold ML, FaIk Jr RB. The QT interval and serum ionized calcium. JAMA 1978;240:366.

11. Carpenter C, May ME. case report: cardiotoxic calcemia. Am J Med Sci 1994;307:43.

12. Rosenqvist M, Nordenstrom J, Andersson M, Edhag OK. Cardiac conduction in patients with hypercalcaemia due to primary hyperparathyroidism. CHn Endocrinol (Oxf) 1992;37:29.

13. Kiewiet RM, Ponssen HH, Janssens EN, Pels PW. Ventricular fibrillation in hypercalcaemic crisis due to primary hyperparathyroidism. Neth J Med 2004;62:94.

14. Otero J, Lenihan DJ. The “normothermic” Osborn wave induced by severe hypercalcemia. Tex Heart Inst J 2000;27:316.

15. Mitsunori M, Yoshinori K, Eitorah K, Yoshiyuki H, Hirotsugu A, Takao K, et al. Osborn waves: history and significance. Indian Pacing Electrophysiol J 2004;4:33.

16. Sridhara MR, Horan LG. Electrocardiographic J wave of hypercalcemia. Am J Cardiol 1984;54:672.

Shawn P.E. Nishi, MD, Nestor A. Barbagelata, MD, Shaul Atar, MD, Yochai Birnbaum, MD (Edward D. and Sally M. Futch Professor of Medicine, Medical Director)*, Enrique Tuero, MD

Division of Cardiology. Department of Internal Medicine, University of Texas Medical Branch, Galveston. TX 77555-0553, USA

Received 9 September 2005

* Corresponding author. Tel.: +1 409 772 2794; fax: +1 409 772 4982.

E-mail address: [email protected] (Y. Birnbaum).

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