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Communications to the Editor |

ECG Abnormalities Associated With Hypocalcemia FREE TO VIEW

Basil M. RuDusky, MD, FCCP
Author and Funding Information

Wilkes-Barre, PA

Correspondence to: Basil M. RuDusky, MD, FCCP, 15 Public Square, Wilkes-Barre, PA 18701



Chest. 2001;119(2):668-669. doi:10.1378/chest.119.2.668-a
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Published online

To the Editor:

The recently published case report in CHEST (July 2000)1 concerning the ECG manifestations of severe hypocalcemia producing injury current mimicking acute myocardial infarction merits additional clinical commentary. The authors also deserve to be complimented on the excellence of their presentation and discussion of the pathophysiology involved and their astute conclusion regarding the most likely cause of the dramatic ECG abnormalities as being due to coronary vasospasm. The report has the possibility of being a landmark article. The central issue discussed revolves around the production of an acute anterior wall injury pattern on the ECG resembling that of an acute anterior wall myocardial infarction with reciprocal ST-segment depression in the inferior leads, a very rare situation in patients with sole hypocalcemia (although compounded in this patient, as is frequently the case, by hypomagnesemia and hypokalemia). The myocardial dyskinesia noted by echocardiography and cardiac catheterization is also an expected finding, as are the marked improvements of the ECG abnormalities following replacement of calcium and vitamin D.

The ECG hallmark of hypocalcemia remains the prolongation of the QTc interval because of lengthening of the ST segment, which is directly proportional to the degree of hypocalcemia or, as otherwise stated, inversely proportional to the serum calcium level. The exact opposite holds true for hypercalcemia.

Considerable controversy still exists concerning other ECG abnormalities. The T waves are normal in > 50% of patients, but decreased T-wave voltage and even negative to deeply negative T waves have been said to occur.2 It is doubtful, however, that these cases were evaluated as completely as was this patient. Peaked T waves have been reported with ST-segment elevation in patients with combined hypocalcemia and hyperkalemia (often renal dialysis patients). Cardiac arrhythmias are also rarely reported, including torsade de pointes.

Reddy et al3in 1974 and Khardori et al4 in 1985 each described a single patient with an acute anteroseptal injury pattern on the ECG with no proven subsequent infarction, which they associated with hypocalcemia. In both instances, the patients involved had complicated coexisting medical problems with associated electrolyte imbalance. It is commonly accepted that hypocalcemia with its accompanying increase in the QTc interval does not affect the QRS complex, and therefore does not produce an intraventricular conduction defect. It must be remembered that a prolonged QT interval can be associated with other conditions, such as hypokalemia (broad T and U waves), hypoglycemia, diabetic acidosis, alkalosis, beriberi, heart failure, cardiomegaly, heart block, bundle-branch block and, importantly, with quinidine use. In some of these situations, the QT may be normal; therefore, both a QT measurement and a corrected QT interval must be obtained.

Hypomagnesemia may, in some instances, accompany primary hypocalcemia. However, when hypomagnesemia is independently present, it is known to exaggerate the ECG effects of hypocalcemia, thereby contributing to the development of tachycardia, hypertension, and vasomotor changes. Severe hypocalcemia may depress myocardial function to such an extent that congestive heart failure ensues.5

Hypocalcemia generally does not cause T-wave changes because it does not affect phase 3 of the action potential. Since these changes have been reported, however, it is best to evaluate each individual for some additional coexisting process if ST-segment or T-wave changes are noted on the ECG, as was done in this case. This holds true especially if there is persistent evidence for myocardial injury. As medical science and technology continue to progress, our endeavors become increasingly more difficult and complex.

References

Lehmann, G, Deisenhofer, I, Ndrepepa, G, et al (2000) ECG changes in a 25-year old woman with hypocalcemia due to hypoparathyroidism: hypocalcemia mimicking acute myocardial infarctionChest118,260-262
 
Bronsky, D, Dubin, A, Waldstein, S Calcium and the electrocardiogram. Am J Cardiol. 1961;;7 ,.:833
 
Reddy, C, Gould, L, Gomprecht, R Unusual electrocardiographic manifestations of hypocalcemia.Angiology1974;25,764-768
 
Khardori, R, Cohen, B, Taylor, D, et al Electrocardiographic findings simulating acute myocardial infarction in a compound metabolic aberration.Am J Med1985;78,529-532
 
Kudoh, C, Tannaka, S, Marusaki, S, et al Hypocalcemic cardiomyopathy in a patient with idiopathic hypoparathyroidism.Intern Med1992;31,561-568
 

Figures

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References

Lehmann, G, Deisenhofer, I, Ndrepepa, G, et al (2000) ECG changes in a 25-year old woman with hypocalcemia due to hypoparathyroidism: hypocalcemia mimicking acute myocardial infarctionChest118,260-262
 
Bronsky, D, Dubin, A, Waldstein, S Calcium and the electrocardiogram. Am J Cardiol. 1961;;7 ,.:833
 
Reddy, C, Gould, L, Gomprecht, R Unusual electrocardiographic manifestations of hypocalcemia.Angiology1974;25,764-768
 
Khardori, R, Cohen, B, Taylor, D, et al Electrocardiographic findings simulating acute myocardial infarction in a compound metabolic aberration.Am J Med1985;78,529-532
 
Kudoh, C, Tannaka, S, Marusaki, S, et al Hypocalcemic cardiomyopathy in a patient with idiopathic hypoparathyroidism.Intern Med1992;31,561-568
 
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