While the majority of calcium in the body is within the skeletal system or bound to albumin in plasma, free calcium is tightly controlled by homeostasis effected by parathyroid hormone (PTH). Transmembrane gradients in calcium concentration drive membrane excitability in muscles, neurones and myocytes.1
Myocardial contraction is dependent on extracellular calcium because the myocardial sarcoplasmic reticulum cannot store sufficient quantities. As such, prolonged and significant hypocalcaemia can result in heart failure.
Among many causes of hypocalcaemia, thyroid surgery, with the inherent risk of parathyroid removal or injury, is a recognised cause of hypoparathyroidism and subsequent hypocalcaemia.2
Patients should undergo long term follow-up to ensure this complication does not present at a later date. Here, it presented 23 years after the initial surgery.
Acute cardiomyopathies have been induced by hypocalcaemia, and calcium replacement and vitamin D supplementation have been shown to reverse the heart failure.3
Furthermore, renal excretion of sodium is partially dependent on intracellular calcium concentrations, and hypocalcaemia may encourage salt and water retention, exacerbating heart failure.3
In our patient, a mild left ventricular hypokinesia was noted with chamber dilatation. However, clinical signs of heart failure did not occur and the ejection fraction remained normal.
Hypocalcaemia is a recognised cause of QT prolongation via prolongation of the plateau phase of the cardiac action potential.4,5
This causes calcium ion channels to remain open for a longer period, allowing a late calcium inflow and the formation of early after-depolarisations.6,7
If threshold for depolarisation is reached, new action potentials are induced, initiating a tachycardia and re-entry. Ventricular arrhythmias can follow, in particular torsades de pointes (TdP; polymorphic ventricular tachycardia) and ventricular fibrillation (VF).8
Therefore, ventricular arrhythmias are a known complication of hypocalcaemia and patients can present with exertional syncope representing TdP and loss of cardiac output.7–9
In contrast, hypercalcaemia and calcium infusions have been shown to reduce immediately the QTc with shortening of the ST segment but prolongation of the T wave; ventricular ectopics are suppressed but heart block and bradyarrhythmias can occur.1,4,5
Recent findings suggest that the disordered repolarisation characteristic of subjects with congenital long QT syndrome (LQTS) occurs in the atria as well as the ventricles.10
Electrophysiological studies showed that congenital LQTS patients had altered atrial electrical conduction such that atrial tachyarrhythmias, such as AF, were more easily induced and persisted for longer than in normal or other patients with AF.10
These induced episodes of AF often had a polymorphic undulating appearance, similar to TdP, and have led to the new term of ‘atrial torsades de pointes’.10
Two large studies have shown that early onset of atrial arrhythmias (typically AF) is 10-fold higher in those with genetically proven LQTS than the general population or matched controls.11
This coincides with genetic studies that suggest the genes that predispose to LQTS (KCNQ1
encoded potassium channels) also predispose to atrial arrhythmia in the general population.11
These new developments raise the possibility that long QTc triggered by acquired causes, as presented here, could create the same electrophysiological state present in congenital LQTS which destabilises atrial rhythms to trigger atrial arrhythmia. It is possible that hypocalcaemia prolongs atrial repolarisation and therefore triggers atrial arrhythmias with ‘atrial torsades de pointes’ being the underlying abnormality. This mechanism may explain the occurrence of atrial arrhythmia in our patient, though the possibility of a genetic LQTS has not formally been excluded. Furthermore, formal electrophysiological testing may be required because a 12 lead ECG is unlikely to visualise ‘atrial torsades de pointes’, with most previous reports relying on electrophysiology studies or atrial traces from automated defibrillators.
- Hypocalcaemia is a cause of QTc prolongation and this predisposes to ventricular arrhythmias.
- Atrial arrhythmias have an increased incidence in those with congenital long QTc syndrome. While a genetic basis may be involved, acquired causes of QTc prolongation may similarly predispose to atrial arrhythmias.
- Hypocalcaemia due to hypoparathyroidism is a known late complication of thyroid surgery. In our case, it presented 23 years after initial surgery.