Beat by Beat Variations
Article Outline
Presentation
A 58-year-old female with no prior history of cardiovascular disease or symptoms was admitted with diarrhea, fatigue, irritability, and muscle cramps. She had undergone total thyroidectomy 5 years earlier for multinodular goiter, and at that time, the parathyroid glands were inadvertently removed. The patient was on levothyroxine, 150 mcg once daily. Her regimen also included oral calcium supplementation for surgical hypoparathyroidism, but she had mistakenly interrupted therapy a few days earlier. She was not using antiarrhythmics, antibiotics, psychotropic or narcotic medications, or any other medication known to prolong the QT-interval. Her medical-surgical history was otherwise unremarkable.
Assessment
On examination, the patient had circumoral paresthesia and muscle spasms upon flexion of the metacarpophalangeal joints and wrists, and with extension of the fingers. Her systolic blood pressure was 90 mm Hg, with a heart rate of 105 beats per minute, and her body temperature was normal. Auscultation of the lung fields disclosed severe bilateral bronchospasm.
Laboratory tests showed hypocalcemia, with a serum calcium level of 5.8 mg/dL. The corrected (adjusted for albumin) calcium level was 6.6 mg/dL. Her hemoglobin level was low at 10 g/dL. Other values were as follows: potassium, 3.2 mEq/L; magnesium, 2.1 mg/dL; total protein, 4.5 g/dL; and serum albumin, 3 g/dL. The rest of the biochemical markers were within reference ranges.
A 12-lead surface ECG indicated a sinus rhythm (100 beats per minute) and marked QT-interval prolongation. The QT duration alternated between approximately 520 ms and 600 ms, with corresponding QTc values (using Fridericia’s formula) of 615 ms and 710 ms, respectively. Macroscopic T-wave alternans was also evident (Figure). An echocardiogram showed mild left ventricular dysfunction (ejection fraction
=50%), without valvular disease or segmental wall-motion abnormalities.
Figure.
On presentation, the patient’s ECG showed sinus rhythm with a heart rate of 100 beats per minute, macroscopically visible T-wave alternans, and a prolonged QT-interval.
Diagnosis
Our patient presented with isolated hypocalcemia, without any other severe electrolyte disorders. Her renal function was normal. However, the calcium deficit produced QT-prolongation and T-wave alternans, which is defined as a beat-to-beat change in the amplitude, polarity, and/or morphology of the T-wave on the surface ECG. Also known as repolarization alternans, the event represents alternation in repolarization of the ventricular myocyte and indicates a vulnerability to ventricular arrhythmia.1, 2
The exact cellular mechanism responsible for electrocardiographic T-wave alternans is not fully described, though a strong relationship with intracellular calcium cycling kinetics has been demonstrated. Mainly, T-wave alternans appears to be linked to impaired coupling between calcium released from the sarcoplasmic reticulum and that drawn from the sarcoplasm by Ca2+ ATPase; changes in extracellular calcium concentration also have been shown to result in alternations of the action potential duration.3
It should be noted that intracellular calcium depletion alone is not sufficient to explain the pathogenesis of T-wave alternans. In fact, blocking the sarcoplasmic reticulum with ryanodine leads to elimination of repolarization alternans.3 Rather, beat-to-beat changes in calcium handling apparently underlie the pathophysiology of this ECG phenomenon. An evident link between low serum calcium and repolarization alternans has been experimentally confirmed.4 In a recent report, T-wave alternans was observed in a patient with hypocalcemia due to surgical hypoparathyroidism, which was accompanied by hypomagnesemia and hypokalemia, in the context of chronic renal failure.5
Management
Calcium gluconate was infused intravenously for several days, and the clinical status of the patient became remarkably better. As serum calcium returned to normal values, 24-hour ECG monitoring exhibited the gradual disappearance of QT-interval prolongation and T-wave alternans. No ventricular arrhythmias were recorded. On echocardiography, the systolic function of the left ventricle gradually improved as well (ejection fraction reached 60%). The patient was discharged from the cardiology department with a normal ECG (QTc=446ms) and in good general condition.
In this case, correction of hypocalcemia led to disappearance of the T-wave alternans and QT prolongation. No other treatment was administered, and the rest of the clinical parameters were unaltered, which led us to conclude that the observed T-wave alternans was, beyond reasonable doubt, caused by the patient’s hypocalcemic state.
References
- . Electrical alternans and vulnerability to ventricular arrhythmias. N Engl J Med. 1994;330:235–241
- . Further observations to elucidate the role of interventricular dispersion of repolarization and early afterdepolarizations in the genesis of acquired torsade de pointes arrhythmias: a comparison between almokalant and d-sotalol using the dog as its own control. J Am Coll Cardiol. 1997;30:1575–1584
- . Cellular and ionic basis for T-wave alternans under long-QT conditions. Circulation. 1999;99:1499–1507
- . Isolated T wave alternans elicited by hypocalcemia in dogs. J Electrocardiol. 1978;11:103–108
- Reversible hypocalcemic heart failure with T wave alternans and increased QTc dispersion in a patient with chronic renal failure after parathyroidectomy. Clin Nephrol. 2006;65:65–70
Julia H. Indik, MD, PhD, Section Editor
PII: S0002-9343(06)01255-1
doi:10.1016/j.amjmed.2006.10.009
© 2007 Elsevier Inc. All rights reserved.
